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1. A structural variation reference for medical and population genetics

Author: Collins, Ryan L, Brand, Harrison, Karczewski, Konrad J, Zhao, Xuefang, Alföldi, Jessica, Francioli, Laurent C, Khera, Amit V, Lowther, Chelsea, Gauthier, Laura D, Wang, Harold, Watts, Nicholas A, Solomonson, Matthew, O’Donnell-Luria, Anne, Baumann, Alexander, Munshi, Ruchi, Walker, Mark, Whelan, Christopher W, Huang, Yongqing, Brookings, Ted, Sharpe, Ted, Stone, Matthew R, Valkanas, Elise, Fu, Jack, Tiao, Grace, Laricchia, Kristen M, Ruano-Rubio, Valentin, Stevens, Christine, Gupta, Namrata, Cusick, Caroline, Margolin, Lauren, Taylor, Kent D, Lin, Henry J, Rich, Stephen S, Post, Wendy S, Chen, Yii-Der Ida, Rotter, Jerome I, Nusbaum, Chad, Philippakis, Anthony, Lander, Eric, Gabriel, Stacey, Neale, Benjamin M, Kathiresan, Sekar, Daly, Mark J, Banks, Eric, MacArthur, Daniel G, and Talkowski, Michael E
Subjects: Biological Sciences, Bioinformatics and Computational Biology, Genetics, Biotechnology, Human Genome, Generic health relevance, Disease, Female, Genetic Testing, Genetic Variation, Genetics, Medical, Genetics, Population, Genome, Human, Genotyping Techniques, Humans, Male, Middle Aged, Mutation, Polymorphism, Single Nucleotide, Racial Groups, Reference Standards, Selection, Genetic, Whole Genome Sequencing, Genome Aggregation Database Production Team, Genome Aggregation Database Consortium, General Science & Technology
Abstract: Structural variants (SVs) rearrange large segments of DNA1 and can have profound consequences in evolution and human disease2,3. As national biobanks, disease-association studies, and clinical genetic testing have grown increasingly reliant on genome sequencing, population references such as the Genome Aggregation Database (gnomAD)4 have become integral in the interpretation of single-nucleotide variants (SNVs)5. However, there are no reference maps of SVs from high-coverage genome sequencing comparable to those for SNVs. Here we present a reference of sequence-resolved SVs constructed from 14,891 genomes across diverse global populations (54% non-European) in gnomAD. We discovered a rich and complex landscape of 433,371 SVs, from which we estimate that SVs are responsible for 25-29% of all rare protein-truncating events per genome. We found strong correlations between natural selection against damaging SNVs and rare SVs that disrupt or duplicate protein-coding sequence, which suggests that genes that are highly intolerant to loss-of-function are also sensitive to increased dosage6. We also uncovered modest selection against noncoding SVs in cis-regulatory elements, although selection against protein-truncating SVs was stronger than all noncoding effects. Finally, we identified very large (over one megabase), rare SVs in 3.9% of samples, and estimate that 0.13% of individuals may carry an SV that meets the existing criteria for clinically important incidental findings7. This SV resource is freely distributed via the gnomAD browser8 and will have broad utility in population genetics, disease-association studies, and diagnostic screening.
Published: 2020

2. Stone tools in northern Europe made by Homo sapiens 45,000 years ago

Author: Banks, William E., primary
Published: 2024
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3. Analysis of protein-coding genetic variation in 60,706 humans.

Author: Lek, Monkol, Karczewski, Konrad J, Minikel, Eric V, Samocha, Kaitlin E, Banks, Eric, Fennell, Timothy, O'Donnell-Luria, Anne H, Ware, James S, Hill, Andrew J, Cummings, Beryl B, Tukiainen, Taru, Birnbaum, Daniel P, Kosmicki, Jack A, Duncan, Laramie E, Estrada, Karol, Zhao, Fengmei, Zou, James, Pierce-Hoffman, Emma, Berghout, Joanne, Cooper, David N, Deflaux, Nicole, DePristo, Mark, Do, Ron, Flannick, Jason, Fromer, Menachem, Gauthier, Laura, Goldstein, Jackie, Gupta, Namrata, Howrigan, Daniel, Kiezun, Adam, Kurki, Mitja I, Moonshine, Ami Levy, Natarajan, Pradeep, Orozco, Lorena, Peloso, Gina M, Poplin, Ryan, Rivas, Manuel A, Ruano-Rubio, Valentin, Rose, Samuel A, Ruderfer, Douglas M, Shakir, Khalid, Stenson, Peter D, Stevens, Christine, Thomas, Brett P, Tiao, Grace, Tusie-Luna, Maria T, Weisburd, Ben, Won, Hong-Hee, Yu, Dongmei, Altshuler, David M, Ardissino, Diego, Boehnke, Michael, Danesh, John, Donnelly, Stacey, Elosua, Roberto, Florez, Jose C, Gabriel, Stacey B, Getz, Gad, Glatt, Stephen J, Hultman, Christina M, Kathiresan, Sekar, Laakso, Markku, McCarroll, Steven, McCarthy, Mark I, McGovern, Dermot, McPherson, Ruth, Neale, Benjamin M, Palotie, Aarno, Purcell, Shaun M, Saleheen, Danish, Scharf, Jeremiah M, Sklar, Pamela, Sullivan, Patrick F, Tuomilehto, Jaakko, Tsuang, Ming T, Watkins, Hugh C, Wilson, James G, Daly, Mark J, MacArthur, Daniel G, and Exome Aggregation Consortium
Subjects: Exome Aggregation Consortium, Humans, Rare Diseases, Proteome, Sample Size, DNA Mutational Analysis, Phenotype, Genetic Variation, Exome, Datasets as Topic, Clinical Research, Biotechnology, Human Genome, Genetics, Genetic Testing, 2.1 Biological and endogenous factors, Aetiology, Generic health relevance, General Science & Technology
Abstract: Large-scale reference data sets of human genetic variation are critical for the medical and functional interpretation of DNA sequence changes. Here we describe the aggregation and analysis of high-quality exome (protein-coding region) DNA sequence data for 60,706 individuals of diverse ancestries generated as part of the Exome Aggregation Consortium (ExAC). This catalogue of human genetic diversity contains an average of one variant every eight bases of the exome, and provides direct evidence for the presence of widespread mutational recurrence. We have used this catalogue to calculate objective metrics of pathogenicity for sequence variants, and to identify genes subject to strong selection against various classes of mutation; identifying 3,230 genes with near-complete depletion of predicted protein-truncating variants, with 72% of these genes having no currently established human disease phenotype. Finally, we demonstrate that these data can be used for the efficient filtering of candidate disease-causing variants, and for the discovery of human 'knockout' variants in protein-coding genes.
Published: 2016

4. Thresholds for adding degraded tropical forest to the conservation estate

Author: Ewers, Robert M., Orme, C. David L., Pearse, William D., Zulkifli, Nursyamin, Yvon-Durocher, Genevieve, Yusah, Kalsum M., Yoh, Natalie, Yeo, Darren C. J., Wong, Anna, Williamson, Joseph, Wilkinson, Clare L., Wiederkehr, Fabienne, Webber, Bruce L., Wearn, Oliver R., Wai, Leona, Vollans, Maisie, Twining, Joshua P., Turner, Edgar C., Tobias, Joseph A., Thorley, Jack, Telford, Elizabeth M., Teh, Yit Arn, Tan, Heok Hui, Swinfield, Tom, Svátek, Martin, Struebig, Matthew, Stork, Nigel, Sleutel, Jani, Slade, Eleanor M., Sharp, Adam, Shabrani, Adi, Sethi, Sarab S., Seaman, Dave J. I., Sawang, Anati, Roxby, Gabrielle Briana, Rowcliffe, J. Marcus, Rossiter, Stephen J., Riutta, Terhi, Rahman, Homathevi, Qie, Lan, Psomas, Elizabeth, Prairie, Aaron, Poznansky, Frederica, Pillay, Rajeev, Picinali, Lorenzo, Pianzin, Annabel, Pfeifer, Marion, Parrett, Jonathan M., Noble, Ciar D., Nilus, Reuben, Mustaffa, Nazirah, Mullin, Katherine E., Mitchell, Simon, Mckinlay, Amelia R., Maunsell, Sarah, Matula, Radim, Massam, Michael, Martin, Stephanie, Malhi, Yadvinder, Majalap, Noreen, Maclean, Catherine S., Mackintosh, Emma, Luke, Sarah H., Lewis, Owen T., Layfield, Harry J., Lane-Shaw, Isolde, Kueh, Boon Hee, Kratina, Pavel, Konopik, Oliver, Kitching, Roger, Kinneen, Lois, Kemp, Victoria A., Jotan, Palasiah, Jones, Nick, Jebrail, Evyen W., Hroneš, Michal, Heon, Sui Peng, Hemprich-Bennett, David R., Haysom, Jessica K., Harianja, Martina F., Hardwick, Jane, Gregory, Nichar, Gray, Ryan, Gray, Ross E. J., Granville, Natasha, Gill, Richard, Fraser, Adam, Foster, William A., Folkard-Tapp, Hollie, Fletcher, Robert J., Fikri, Arman Hadi, Fayle, Tom M., Faruk, Aisyah, Eggleton, Paul, Edwards, David P., Drinkwater, Rosie, Dow, Rory A., Döbert, Timm F., Didham, Raphael K., Dickinson, Katharine J. M., Deere, Nicolas J., de Lorm, Tijmen, Dawood, Mahadimenakbar M., Davison, Charles W., Davies, Zoe G., Davies, Richard G., Dančák, Martin, Cusack, Jeremy, Clare, Elizabeth L., Chung, Arthur, Chey, Vun Khen, Chapman, Philip M., Cator, Lauren, Carpenter, Daniel, Carbone, Chris, Calloway, Kerry, Bush, Emma R., Burslem, David F. R. P., Brown, Keiron D., Brooks, Stephen J., Brasington, Ella, Brant, Hayley, Boyle, Michael J. W., Both, Sabine, Blackman, Joshua, Bishop, Tom R., Bicknell, Jake E., Bernard, Henry, Basrur, Saloni, Barclay, Maxwell V. L., Barclay, Holly, Atton, Georgina, Ancrenaz, Marc, Aldridge, David C., Daniel, Olivia Z., Reynolds, Glen, and Banks-Leite, Cristina
Abstract: Logged and disturbed forests are often viewed as degraded and depauperate environments compared with primary forest. However, they are dynamic ecosystems1that provide refugia for large amounts of biodiversity2,3, so we cannot afford to underestimate their conservation value4. Here we present empirically defined thresholds for categorizing the conservation value of logged forests, using one of the most comprehensive assessments of taxon responses to habitat degradation in any tropical forest environment. We analysed the impact of logging intensity on the individual occurrence patterns of 1,681 taxa belonging to 86 taxonomic orders and 126 functional groups in Sabah, Malaysia. Our results demonstrate the existence of two conservation-relevant thresholds. First, lightly logged forests (<29% biomass removal) retain high conservation value and a largely intact functional composition, and are therefore likely to recover their pre-logging values if allowed to undergo natural regeneration. Second, the most extreme impacts occur in heavily degraded forests with more than two-thirds (>68%) of their biomass removed, and these are likely to require more expensive measures to recover their biodiversity value. Overall, our data confirm that primary forests are irreplaceable5, but they also reinforce the message that logged forests retain considerable conservation value that should not be overlooked.
Published: 2024
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5. Geographic variation of mutagenic exposures in kidney cancer genomes

Author: Senkin, Sergey, Moody, Sarah, Díaz-Gay, Marcos, Abedi-Ardekani, Behnoush, Cattiaux, Thomas, Ferreiro-Iglesias, Aida, Wang, Jingwei, Fitzgerald, Stephen, Kazachkova, Mariya, Vangara, Raviteja, Le, Anh Phuong, Bergstrom, Erik N., Khandekar, Azhar, Otlu, Burçak, Cheema, Saamin, Latimer, Calli, Thomas, Emily, Atkins, Joshua Ronald, Smith-Byrne, Karl, Cortez Cardoso Penha, Ricardo, Carreira, Christine, Chopard, Priscilia, Gaborieau, Valérie, Keski-Rahkonen, Pekka, Jones, David, Teague, Jon W., Ferlicot, Sophie, Asgari, Mojgan, Sangkhathat, Surasak, Attawettayanon, Worapat, Świątkowska, Beata, Jarmalaite, Sonata, Sabaliauskaite, Rasa, Shibata, Tatsuhiro, Fukagawa, Akihiko, Mates, Dana, Jinga, Viorel, Rascu, Stefan, Mijuskovic, Mirjana, Savic, Slavisa, Milosavljevic, Sasa, Bartlett, John M. S., Albert, Monique, Phouthavongsy, Larry, Ashton-Prolla, Patricia, Botton, Mariana R., Silva Neto, Brasil, Bezerra, Stephania Martins, Curado, Maria Paula, Zequi, Stênio de Cássio, Reis, Rui Manuel, Faria, Eliney Ferreira, de Menezes, Nei Soares, Ferrari, Renata Spagnoli, Banks, Rosamonde E., Vasudev, Naveen S., Zaridze, David, Mukeriya, Anush, Shangina, Oxana, Matveev, Vsevolod, Foretova, Lenka, Navratilova, Marie, Holcatova, Ivana, Hornakova, Anna, Janout, Vladimir, Purdue, Mark P., Rothman, Nathaniel, Chanock, Stephen J., Ueland, Per Magne, Johansson, Mattias, McKay, James, Scelo, Ghislaine, Chanudet, Estelle, Humphreys, Laura, de Carvalho, Ana Carolina, Perdomo, Sandra, Alexandrov, Ludmil B., Stratton, Michael R., and Brennan, Paul
Abstract: International differences in the incidence of many cancer types indicate the existence of carcinogen exposures that have not yet been identified by conventional epidemiology make a substantial contribution to cancer burden1. In clear cell renal cell carcinoma, obesity, hypertension and tobacco smoking are risk factors, but they do not explain the geographical variation in its incidence2. Underlying causes can be inferred by sequencing the genomes of cancers from populations with different incidence rates and detecting differences in patterns of somatic mutations. Here we sequenced 962 clear cell renal cell carcinomas from 11 countries with varying incidence. The somatic mutation profiles differed between countries. In Romania, Serbia and Thailand, mutational signatures characteristic of aristolochic acid compounds were present in most cases, but these were rare elsewhere. In Japan, a mutational signature of unknown cause was found in more than 70% of cases but in less than 2% elsewhere. A further mutational signature of unknown cause was ubiquitous but exhibited higher mutation loads in countries with higher incidence rates of kidney cancer. Known signatures of tobacco smoking correlated with tobacco consumption, but no signature was associated with obesity or hypertension, suggesting that non-mutagenic mechanisms of action underlie these risk factors. The results of this study indicate the existence of multiple, geographically variable, mutagenic exposures that potentially affect tens of millions of people and illustrate the opportunities for new insights into cancer causation through large-scale global cancer genomics.
Published: 2024
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6. Nicotinamide N-methyltransferase knockdown protects against diet-induced obesity

Author: Kraus, Daniel, Yang, Qin, Kong, Dong, Banks, Alexander S, Zhang, Lin, Rodgers, Joseph T, Pirinen, Eija, Pulinilkunnil, Thomas C, Gong, Fengying, Wang, Ya-chin, Cen, Yana, Sauve, Anthony A, Asara, John M, Peroni, Odile D, Monia, Brett P, Bhanot, Sanjay, Alhonen, Leena, Puigserver, Pere, and Kahn, Barbara B
Subjects: Biochemistry and Cell Biology, Biological Sciences, Nutrition, Obesity, Diabetes, Liver Disease, Digestive Diseases, Aetiology, 2.1 Biological and endogenous factors, Stroke, Cancer, Oral and gastrointestinal, Metabolic and endocrine, Cardiovascular, Acetyltransferases, Adipocytes, Adipose Tissue, Adipose Tissue, White, Animals, Diabetes Mellitus, Type 2, Diet, Energy Metabolism, Fatty Liver, Gene Knockdown Techniques, Glucose Intolerance, Glucose Transporter Type 4, Insulin Resistance, Liver, Male, Mice, Mice, Inbred C57BL, NAD, Niacinamide, Nicotinamide N-Methyltransferase, Ornithine Decarboxylase, Oxidoreductases Acting on CH-NH Group Donors, S-Adenosylmethionine, Sirtuin 1, Spermine, Thinness, Polyamine Oxidase, General Science & Technology
Abstract: In obesity and type 2 diabetes, Glut4 glucose transporter expression is decreased selectively in adipocytes. Adipose-specific knockout or overexpression of Glut4 alters systemic insulin sensitivity. Here we show, using DNA array analyses, that nicotinamide N-methyltransferase (Nnmt) is the most strongly reciprocally regulated gene when comparing gene expression in white adipose tissue (WAT) from adipose-specific Glut4-knockout or adipose-specific Glut4-overexpressing mice with their respective controls. NNMT methylates nicotinamide (vitamin B3) using S-adenosylmethionine (SAM) as a methyl donor. Nicotinamide is a precursor of NAD(+), an important cofactor linking cellular redox states with energy metabolism. SAM provides propylamine for polyamine biosynthesis and donates a methyl group for histone methylation. Polyamine flux including synthesis, catabolism and excretion, is controlled by the rate-limiting enzymes ornithine decarboxylase (ODC) and spermidine-spermine N(1)-acetyltransferase (SSAT; encoded by Sat1) and by polyamine oxidase (PAO), and has a major role in energy metabolism. We report that NNMT expression is increased in WAT and liver of obese and diabetic mice. Nnmt knockdown in WAT and liver protects against diet-induced obesity by augmenting cellular energy expenditure. NNMT inhibition increases adipose SAM and NAD(+) levels and upregulates ODC and SSAT activity as well as expression, owing to the effects of NNMT on histone H3 lysine 4 methylation in adipose tissue. Direct evidence for increased polyamine flux resulting from NNMT inhibition includes elevated urinary excretion and adipocyte secretion of diacetylspermine, a product of polyamine metabolism. NNMT inhibition in adipocytes increases oxygen consumption in an ODC-, SSAT- and PAO-dependent manner. Thus, NNMT is a novel regulator of histone methylation, polyamine flux and NAD(+)-dependent SIRT1 signalling, and is a unique and attractive target for treating obesity and type 2 diabetes.
Published: 2014

7. Xiphoid nucleus of the midline thalamus controls cold-induced food seeking

Author: Lal, Neeraj K., primary, Le, Phuong, additional, Aggarwal, Samarth, additional, Zhang, Alan, additional, Wang, Kristina, additional, Qi, Tianbo, additional, Pang, Zhengyuan, additional, Yang, Dong, additional, Nudell, Victoria, additional, Yeo, Gene W., additional, Banks, Alexander S., additional, and Ye, Li, additional
Published: 2023
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8. Controlling organization and forces in active matter through optically defined boundaries

Author: Ross, Tyler D., Lee, Heun Jin, Qu, Zijie, Banks, Rachel A., Phillips, Rob, and Thomson, Matt
Subjects: Chemical research, Microtubules -- Observations, Biomolecules -- Observations, Molecular motors (Biochemistry) -- Observations, Asters -- Observations, Environmental issues, Science and technology, Zoology and wildlife conservation
Abstract: Living systems are capable of locomotion, reconfiguration and replication. To perform these tasks, cells spatiotemporally coordinate the interactions of force-generating, 'active' molecules that create and manipulate non-equilibrium structures and force fields of up to millimetre length scales.sup.1-3. Experimental active-matter systems of biological or synthetic molecules are capable of spontaneously organizing into structures.sup.4,5 and generating global flows.sup.6-9. However, these experimental systems lack the spatiotemporal control found in cells, limiting their utility for studying non-equilibrium phenomena and bioinspired engineering. Here we uncover non-equilibrium phenomena and principles of boundary-mediated control by optically modulating structures and fluid flow in an engineered system of active biomolecules. Our system consists of purified microtubules and light-activatable motor proteins that crosslink and organize the microtubules into distinct structures upon illumination. We develop basic operations--defined as sets of light patterns--to create, move and merge the microtubule structures. By combining these operations, we create microtubule networks that span several hundred micrometres in length and contract at speeds up to an order of magnitude higher than the speed of an individual motor protein. We manipulate these contractile networks to generate and sculpt persistent fluid flows. The principles of boundary-mediated control that we uncover may be used to study emergent cellular structures and forces and to develop programmable active-matter devices. Light is used to guide the behaviour of an engineered active-matter system, producing structures and properties that can be dynamically manipulated and controlled., Author(s): Tyler D. Ross [sup.1] , Heun Jin Lee [sup.2] , Zijie Qu [sup.1] , Rachel A. Banks [sup.1] , Rob Phillips [sup.1] [sup.2] [sup.3] , Matt Thomson [sup.1] Author [...]
Published: 2019
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9. A genomic mutational constraint map using variation in 76,156 human genomes.

Author: Chen, Siwei, Francioli, Laurent C., Goodrich, Julia K., Collins, Ryan L., Kanai, Masahiro, Wang, Qingbo, Alföldi, Jessica, Watts, Nicholas A., Vittal, Christopher, Gauthier, Laura D., Poterba, Timothy, Wilson, Michael W., Tarasova, Yekaterina, Phu, William, Grant, Riley, Yohannes, Mary T., Koenig, Zan, Farjoun, Yossi, Banks, Eric, and Donnelly, Stacey
Abstract: The depletion of disruptive variation caused by purifying natural selection (constraint) has been widely used to investigate protein-coding genes underlying human disorders1–4, but attempts to assess constraint for non-protein-coding regions have proved more difficult. Here we aggregate, process and release a dataset of 76,156 human genomes from the Genome Aggregation Database (gnomAD)—the largest public open-access human genome allele frequency reference dataset—and use it to build a genomic constraint map for the whole genome (genomic non-coding constraint of haploinsufficient variation (Gnocchi)). We present a refined mutational model that incorporates local sequence context and regional genomic features to detect depletions of variation. As expected, the average constraint for protein-coding sequences is stronger than that for non-coding regions. Within the non-coding genome, constrained regions are enriched for known regulatory elements and variants that are implicated in complex human diseases and traits, facilitating the triangulation of biological annotation, disease association and natural selection to non-coding DNA analysis. More constrained regulatory elements tend to regulate more constrained protein-coding genes, which in turn suggests that non-coding constraint can aid the identification of constrained genes that are as yet unrecognized by current gene constraint metrics. We demonstrate that this genome-wide constraint map improves the identification and interpretation of functional human genetic variation.A genomic constraint map for the human genome constructed using data from 76,156 human genomes from the Genome Aggregation Database shows that non-coding constrained regions are enriched for regulatory elements and variants associated with complex diseases and traits. [ABSTRACT FROM AUTHOR]
Published: 2024
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10. Creation of forest edges has a global impact on forest vertebrates

Author: Pfeifer, M., Lefebvre, V., Peres, C. A., Banks-Leite, C., Wearn, O. R., Marsh, C. J., Butchart, S. H. M., Arroyo-Rodrguez, V., Barlow, J., Cerezo, A., Cisneros, L., DCruze, N., Faria, D., Hadley, A., Harris, S. M., Klingbeil, B. T., Kormann, U., Lens, L., Medina-Rangel, G. F., Morante-Filho, J. C., Olivier, P., Peters, S. L., Pidgeon, A., Ribeiro, D. B., Scherber, C., Schneider-Maunoury, L., Struebig, M., Urbina-Cardona, N., Watling, J. I., Willig, M. R., Wood, E. M., and Ewers, R. M.
Subjects: Habitat destruction -- Research, Forests -- Natural history -- Environmental aspects -- United Kingdom, Ecological research, Vertebrates -- Distribution -- Environmental aspects, Company distribution practices, Environmental issues, Science and technology, Zoology and wildlife conservation
Abstract: Forest edges influence more than half of the worlds forests and contribute to worldwide declines in biodiversity and ecosystem functions. However, predicting these declines is challenging in heterogeneous fragmented landscapes. Here we assembled a global dataset on species responses to fragmentation and developed a statistical approach for quantifying edge impacts in heterogeneous landscapes to quantify edge-determined changes in abundance of 1,673 vertebrate species. We show that the abundances of 85% of species are affected, either positively or negatively, by forest edges. Species that live in the centre of the forest (forest core), that were more likely to be listed as threatened by the International Union for Conservation of Nature (IUCN), reached peak abundances only at sites farther than 200400m from sharp high-contrast forest edges. Smaller-bodied amphibians, larger reptiles and medium-sized non-volant mammals experienced a larger reduction in suitable habitat than other forest-core species. Our results highlight the pervasive ability of forest edges to restructure ecological communities on a global scale., Author(s): M. Pfeifer (corresponding author) [1, 2]; V. Lefebvre [2, 3]; C. A. Peres [4]; C. Banks-Leite [2]; O. R. Wearn [5]; C. J. Marsh [6]; S. H. M. Butchart [...]
Published: 2017
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11. Challenging the high-dose paradigm for cancer drugs

Author: Banks, Marcus A., primary
Published: 2022
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12. Challenging the high-dose paradigm for cancer drugs

Author: Marcus A. Banks
Subjects: Multidisciplinary
Published: 2022

13. Convection in a volatile nitrogen-ice-rich layer drives Plutos geological vigour

Author: McKinnon, William B., Nimmo, Francis, Wong, Teresa, Schenk, Paul M., White, Oliver L., Roberts, J. H., Moore, J. M., Spencer, J. R., Howard, A. D., Umurhan, O. M., Stern, S. A., Weaver, H. A., Olkin, C. B., Young, L. A., Smith, K. E., McKinnon, W. B., Beyer, R., Buie, M., Buratti, B., Cheng, A., Cruikshank, D., Dalle Ore, C., Gladstone, R., Grundy, W., Lauer, T., Linscott, I., Olkin, C., Parker, J., Porter, S., Reitsema, H., Reuter, D., Robbins, S., Schenk, P. M., Showalter, M., Singer, K., Strobel, D., Summers, M., Tyler, L., Weaver, H., White, O. L., Banks, M., Barnouin, O., Bray, V., Carcich, B., Chaikin, A., Chavez, C., Conrad, C., Hamilton, D., Howett, C., Hofgartner, J., Kammer, J., Lisse, C., Marcotte, A., Parker, A., Retherford, K., Saina, M., Runyon, K., Schindhelm, E., Stansberry, J., Steffl, A., Stryk, T., Throop, H., Tsang, C., Verbiscer, A., Winters, H., and Zangari, A.
Subjects: Pluto (Dwarf planet) -- Observations, Astrogeology -- Methods, Environmental issues, Science and technology, Zoology and wildlife conservation
Abstract: Author(s): William B. McKinnon (corresponding author) [1]; Francis Nimmo [2]; Teresa Wong [1]; Paul M. Schenk [3]; Oliver L. White [4]; J. H. Roberts [5]; J. M. Moore [4]; J. [...]
Published: 2016
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14. Disorder in convergent floral nanostructures enhances signalling to bees

Author: Moyroud, Edwige, Wenzel, Tobias, Middleton, Rox, Rudall, Paula J., Banks, Hannah, Reed, Alison, Mellers, Greg, Killoran, Patrick, Westwood, Murphy M., Steiner, Ullrich, Vignolini, Silvia, and Glover, Beverley J.
Published: 2017
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15. An ERK/Cdk5 axis controls the diabetogenic actions of PPAR[gamma]

Author: Banks, Alexander S., McAllister, Fiona E., Camporez, João Paulo G., Zushin, Peter-James H., Jurczak, Michael J., Laznik-Bogoslavski, Dina, Shulman, Gerald I., Gygi, Steven P., and Spiegelman, Bruce M.
Subjects: Peroxisomes -- Physiological aspects, Physiological research, Protein kinases -- Physiological aspects, Cellular signal transduction -- Research, Cell receptors -- Physiological aspects, Environmental issues, Science and technology, Zoology and wildlife conservation
Abstract: Blocking ERK/MAP kinases improves insulin sensitivity thorough a mechanism similar to the actions of the anti-diabetic thiazolidinediones drugs on PPAR[gamma]. Role of MEK/ERK pathway in glucose metabolism The nuclear receptor PPAR[gamma] is required for glucose metabolism and is a drug target in diabetes. Earlier work has suggested that PPAR[gamma] phosphorylation has an adverse effect on insulin sensitivity and that the kinase Cdk5 is the main kinase responsible for phosphorylation at this site. Now Bruce Spiegelman and colleagues report the paradoxical observation that insulin resistance is worsened in mice lacking Cdk5 in adipose tissue. The authors further show that Cdk5 suppresses the MEK/ERK signalling pathway that is central to the regulation of cell growth and proliferation, and that ERK directly phosphorylates PPAR[gamma]. MEK/ERK inhibitors can improve insulin resistance in obese wild-type and ob/ob mice. This work suggests that MEK/ERK inhibitors -- already approved for cancer treatment -- might also be effective against diabetes. Obesity-linked insulin resistance is a major precursor to the development of type 2 diabetes. Previous work has shown that phosphorylation of PPAR[gamma] (peroxisome proliferator-activated receptor [gamma]) at serine 273 by cyclin-dependent kinase 5 (Cdk5) stimulates diabetogenic gene expression in adipose tissues.sup.1. Inhibition of this modification is a key therapeutic mechanism for anti-diabetic drugs that bind PPAR[gamma], such as the thiazolidinediones and PPAR[gamma] partial agonists or non-agonists.sup.2. For a better understanding of the importance of this obesity-linked PPAR[gamma] phosphorylation, we created mice that ablated Cdk5 specifically in adipose tissues. These mice have both a paradoxical increase in PPAR[gamma] phosphorylation at serine 273 and worsened insulin resistance. Unbiased proteomic studies show that extracellular signal-regulated kinase (ERK) kinases are activated in these knockout animals. Here we show that ERK directly phosphorylates serine 273 of PPAR[gamma] in a robust manner and that Cdk5 suppresses ERKs through direct action on a novel site in MAP kinase/ERK kinase (MEK). Importantly, pharmacological inhibition of MEK and ERK markedly improves insulin resistance in both obese wild-type and ob/ob mice, and also completely reverses the deleterious effects of the Cdk5 ablation. These data show that an ERK/Cdk5 axis controls PPAR[gamma] function and suggest that MEK/ERK inhibitors may hold promise for the treatment of type 2 diabetes., Author(s): Alexander S. Banks [sup.1] , Fiona E. McAllister [sup.2] , João Paulo G. Camporez [sup.3] , Peter-James H. Zushin [sup.1] , Michael J. Jurczak [sup.3] , Dina Laznik-Bogoslavski [sup.4] [...]
Published: 2015
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16. γδ T cells and adipocyte IL-17RC control fat innervation and thermogenesis

Author: Bhavna N. Desai, Bradford B. Lowell, Chengcheng Jin, Mark P. Jedrychowski, Bo Hu, Zongfang Yang, Xing Zeng, Alexander S. Banks, Jon M. Resch, Diane Mathis, and Bruce M. Spiegelman
Subjects: Male, 0301 basic medicine, Sympathetic nervous system, Sympathetic Nervous System, T-Lymphocytes, Adipose tissue, Biology, Article, Transforming Growth Factor beta1, Mice, 03 medical and health sciences, chemistry.chemical_compound, 0302 clinical medicine, Adipose Tissue, Brown, Neurotrophic factors, Adipocyte, Adipocytes, medicine, Animals, Parenchymal Tissue, Mice, Knockout, Multidisciplinary, Interleukin-17, Thermogenesis, Hedgehog signaling pathway, Cell biology, 030104 developmental biology, medicine.anatomical_structure, Adipose Tissue, chemistry, Organ Specificity, Signal transduction, 030217 neurology & neurosurgery, Homeostasis, Signal Transduction
Abstract: The sympathetic nervous system innervates peripheral organs to regulate their function and maintain homeostasis, whereas target cells also produce neurotrophic factors to promote sympathetic innervation1,2. The molecular basis of this bi-directional communication remains to be fully determined. Here we use thermogenic adipose tissue from mice as a model system to show that T cells, specifically γδ T cells, have a crucial role in promoting sympathetic innervation, at least in part by driving the expression of TGFβ1 in parenchymal cells via the IL-17 receptor C (IL-17RC). Ablation of IL-17RC specifically in adipose tissue reduces expression of TGFβ1 in adipocytes, impairs local sympathetic innervation and causes obesity and other metabolic phenotypes that are consistent with defective thermogenesis; innervation can be fully rescued by restoring TGFβ1 expression. Ablating γδ Τ cells and the IL-17RC signalling pathway also impairs sympathetic innervation in other tissues such as salivary glands. These findings demonstrate coordination between T cells and parenchymal cells to regulate sympathetic innervation. Vγ6+ Vδ1+ γδ T cells control tolerance to cold by activating adipocyte IL-17RC and promoting sympathetic innervation of thermogenic adipose tissue in mice.
Published: 2020

17. Global conservation outcomes depend on marine protected areas with five key features

Author: Edgar, Graham J., Stuart-Smith, Rick D., Willis, Trevor J., Kininmonth, Stuart, Baker, Susan C., Banks, Stuart, Barrett, Neville S., Becerro, Mikel A., Bernard, Anthony T.F., Berkhout, Just, Buxton, Colin D., Campbell, Stuart J., Cooper, Antonia T., Davey, Marlene, Edgar, Sophie C., Forsterra, Gunter, Galvan, David E., Irigoyen, Alejo J., Kushner, David J., Moura, Rodrigo, Parnell, P. Ed, Shears, Nick T., Soler, German, Strain, Elisabeth M.A., and Thomson, Russell J.
Subjects: Marine resources conservation -- Research, Environment -- Research, Environmental issues, Science and technology, Zoology and wildlife conservation
Abstract: In line with global targets agreed under the Convention on Biological Diversity, the number of marine protected areas (MPAs) is increasing rapidly, yet socio-economic benefits generated by MPAs remain difficult to predict and under debate (1,2). MPAs often fail to reach their full potential as a consequence of factors such as illegal harvesting, regulations that legally allow detrimental harvesting, or emigration of animals outside boundaries because of continuous habitat or inadequate size of reserve (3-5). Here we show that the conservation benefits of 87 MPAs investigated worldwide increase exponentially with the accumulation of five key features: no take, well enforced, old (> 10 years), large (> 100 [km.sup.2]), and isolated by deep water or sand. Using effective MPAs with four or five key features as an unfished standard, comparisons of underwater survey data from effective MPAs with predictions based on survey data from fished coasts indicate that total fish biomass has declined about two-thirds from historical baselines as a result of fishing. Effective MPAs also had twice as many large (>250 mm total length) fish species per transect, five times more large fish biomass, and fourteen times more shark biomass than fished areas. Most (59%) of the MPAs studied had only one or two key features and were not ecologically distinguishable from fished sites. Our results show that global conservation targets based on area alone will not optimize protection of marine biodiversity. More emphasis is needed on better MPA design, durable management and compliance to ensure that MPAs achieve their desired conservation value., A multitude of socio-economic and biological factors influence the responses of species to protection within MPA networks, adding considerable uncertainty when making specific predictions regarding the conservation benefits of new [...]
Published: 2014

18. A polygenic burden of rare disruptive mutations in schizophrenia

Author: Purcell, Shaun M., Moran, Jennifer L., Fromer, Menachem, Ruderfer, Douglas, Solovieff, Nadia, Roussos, Panos, O'Dushlaine, Colm, Chambert, Kimberly, Bergen, Sarah E., Kahler, Anna, Duncan, Laramie, Stahl, Eli, Genovese, Giulio, Fernandez, Esperanza, Collins, Mark O., Komiyama, Noboru H., Choudhary, Jyoti S., Magnusson, Patrik K.E., Banks, Eric, Shakir, Khalid, Garimella, Kiran, Fennell, Tim, DePristo, Mark, Grant, Seth G.N., Haggarty, Stephen J., Gabriel, Stacey, Scolnick, Edward M., Lander, Eric S., Hultman, Christina M., Sullivan, Patrick F., McCarroll, Steven A., and Sklar, Pamela
Subjects: Gene mutations -- Psychological aspects -- Health aspects, Schizophrenia -- Genetic aspects, Multifactorial traits -- Psychological aspects -- Health aspects, Environmental issues, Science and technology, Zoology and wildlife conservation
Abstract: Schizophrenia is a common disease with a complex aetiology, probably involving multiple and heterogeneous genetic factors. Here, by analysing the exome sequences of 2,536 schizophrenia cases and 2,543 controls, we demonstrate a polygenic burden primarily arising from rare (less than 1 in 10,000), disruptive mutations distributed across many genes. Particularly enriched gene sets include the voltage-gated calcium ion channel and the signalling complex formed by the activity-regulated cytoskeleton-associated scaffold protein (ARC) of the postsynaptic density, sets previously implicated by genome-wide association and copy-number variation studies. Similar to reports in autism, targets of the fragile X mental retardation protein (FMRP, product of FMRl) are enriched for case mutations. No individual gene-based test achieves significance after correction for multiple testing and we do not detect any alleles of moderately low frequency (approximately 0.5 to 1 per cent) and moderately large effect. Taken together, these data suggest that population-based exome sequencing can discover risk alleles and complements established gene-mapping paradigms in neuropsychiatric disease., Genetic studies of schizophrenia (MIM 181500) have demonstrated a substantial heritability (1,2) that reflects common and rare alleles at many loci. Genome-wide association studies (GWAS) continue to uncover common single [...]
Published: 2014
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19. De novo mutations in schizophrenia implicate synaptic networks

Author: Fromer, Menachem, Pocklington, Andrew J., Kavanagh, David H., Williams, Hywel J., Dwyer, Sarah, Gormley, Padhraig, Georgieva, Lyudmila, Rees, Elliott, Palta, Priit, Ruderfer, Douglas M., Carrera, Noa, Humphreys, Isla, Johnson, Jessica S., Roussos, Panos, Barker, Douglas D., Banks, Eric, Milanova, Vihra, Grant, Seth G., Hannon, Eilis, Rose, Samuel A., Chambert, Kimberly, Mahajan, Milind, Scolnick, Edward M., Moran, Jennifer L., Kirov, George, Palotie, Aarno, McCarroll, Steven A., Holmans, Peter, Sklar, Pamela, Owen, Michael J., Purcell, Shaun M., and O'Donovan, Michael C.
Subjects: Gene mutations -- Health aspects -- Psychological aspects, Neural circuitry -- Genetic aspects, Schizophrenia -- Genetic aspects, Synapses -- Genetic aspects, Environmental issues, Science and technology, Zoology and wildlife conservation
Abstract: Inherited alleles account for most of the genetic risk for schizophrenia. However, new (de novo) mutations, in the form of large chromosomal copy number changes, occur in a small fraction of cases and disproportionally disrupt genes encoding postsynaptic proteins. Here we show that small de novo mutations, affecting one or a few nucleotides, are overrepresented among glutamatergic postsynaptic proteins comprising activity-regulated cytoskeleton-associated protein (ARC) and N-methyl-D-aspartate receptor (NMDAR) complexes. Mutations are additionally enriched in proteins that interact with these complexes to modulate synaptic strength, namely proteins regulating actin filament dynamics and those whose messenger RNAs are targets of fragile X mental retardation protein (FMRP). Genes affected by mutations in schizophrenia overlap those mutated in autism and intellectual disability, as do mutation-enriched synaptic pathways. Aligning our findings with a parallel case-control study, we demonstrate reproducible insights into aetiological mechanisms for schizophrenia and reveal pathophysiology shared with other neurodevelopmental disorders., Schizophrenia is a disorder whose pathophysiology is largely unknown. It has a lifetime risk of about 1%, is frequently chronic and socially disabling, and is associated with an average reduction [...]
Published: 2014
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20. A global reference for human genetic variation

Author: Altshuler, David M., (Co-Chair), Durbin, Richard M., (Co-Chair, Principal Investigator), Donnelly, Peter, Green, Eric D., Nickerson, Deborah A., Boerwinkle, Eric, Doddapaneni, Harsha, Han, Yi, Korchina, Viktoriya, Kovar, Christie, Lee, Sandra, Muzny, Donna, Reid, Jeffrey G., Zhu, Yiming, Wang, Jun, (Principal Investigator), Chang, Yuqi, Feng, Qiang, Fang, Xiaodong, Guo, Xiaosen, Jian, Min, Jiang, Hui, Jin, Xin, Lan, Tianming, Li, Guoqing, Li, Jingxiang, Li, Yingrui, Liu, Shengmao, Liu, Xiao, Lu, Yao, Ma, Xuedi, Tang, Meifang, Wang, Bo, Wang, Guangbiao, Wu, Honglong, Wu, Renhua, Xu, Xun, Yin, Ye, Zhang, Dandan, Zhang, Wenwei, Zhao, Jiao, Zhao, Meiru, Zheng, Xiaole, Lander, Eric S., (Principal Investigator), Gabriel, Stacey B., (Co-Chair), Gupta, Namrata, Gharani, Neda, Toji, Lorraine H., Gerry, Norman P., Resch, Alissa M., Barker, Jonathan, Gil, Laurent, Hunt, Sarah E., Kelman, Gavin, Kulesha, Eugene, Leinonen, Rasko, McLaren, William M., Radhakrishnan, Rajesh, Roa, Asier, Smirnov, Dmitriy, Smith, Richard E., Streeter, Ian, Thormann, Anja, Toneva, Iliana, Vaughan, Brendan, Zheng-Bradley, Xiangqun, Bentley, David R., (Principal Investigator), Grocock, Russell, Humphray, Sean, James, Terena, Kingsbury, Zoya, Lehrach, Hans, (Principal Investigator), Sudbrak, Ralf, (Project Leader), Albrecht, Marcus W., Amstislavskiy, Vyacheslav S., Borodina, Tatiana A., Lienhard, Matthias, Mertes, Florian, Sultan, Marc, Timmermann, Bernd, Yaspo, Marie-Laure, Mardis, Elaine R., (Co-Principal Investigator) (Co-Chair), Wilson, Richard K., (Co-Principal Investigator), Fulton, Lucinda, Fulton, Robert, Ananiev, Victor, Belaia, Zinaida, Beloslyudtsev, Dimitriy, Bouk, Nathan, Chen, Chao, Church, Deanna, Cohen, Robert, Cook, Charles, Garner, John, Hefferon, Timothy, Kimelman, Mikhail, Liu, Chunlei, Lopez, John, Meric, Peter, O’Sullivan, Chris, Ostapchuk, Yuri, Phan, Lon, Ponomarov, Sergiy, Schneider, Valerie, Shekhtman, Eugene, Sirotkin, Karl, Slotta, Douglas, Zhang, Hua, Balasubramaniam, Senduran, Burton, John, Danecek, Petr, Keane, Thomas M., Kolb-Kokocinski, Anja, McCarthy, Shane, Stalker, James, Quail, Michael, Schmidt, Jeanette P., (Principal Investigator), Davies, Christopher J., Gollub, Jeremy, Webster, Teresa, Wong, Brant, Zhan, Yiping, Auton, Adam, (Principal Investigator), Campbell, Christopher L., Kong, Yu, Marcketta, Anthony, Yu, Fuli, (Project Leader), Antunes, Lilian, Bainbridge, Matthew, Sabo, Aniko, Huang, Zhuoyi, Coin, Lachlan J. M., Fang, Lin, Li, Qibin, Li, Zhenyu, Lin, Haoxiang, Liu, Binghang, Luo, Ruibang, Shao, Haojing, Xie, Yinlong, Ye, Chen, Yu, Chang, Zhang, Fan, Zheng, Hancheng, Zhu, Hongmei, Alkan, Can, Dal, Elif, Kahveci, Fatma, Garrison, Erik P., (Project Lead), Kural, Deniz, Lee, Wan-Ping, Leong, Wen Fung, Stromberg, Michael, Ward, Alistair N., Wu, Jiantao, Zhang, Mengyao, Daly, Mark J., (Principal Investigator), DePristo, Mark A., (Project Leader), Handsaker, Robert E., (Project Leader), Banks, Eric, Bhatia, Gaurav, del Angel, Guillermo, Genovese, Giulio, Li, Heng, Kashin, Seva, Nemesh, James C., Poplin, Ryan E., Yoon, Seungtai C., (Principal Investigator), Lihm, Jayon, Makarov, Vladimir, Clark, Andrew G., (Principal Investigator), Gottipati, Srikanth, Keinan, Alon, Rodriguez-Flores, Juan L., Rausch, Tobias, (Project Leader), Fritz, Markus H., Stütz, Adrian M., Beal, Kathryn, Datta, Avik, Herrero, Javier, Ritchie, Graham R. S., Zerbino, Daniel, Sabeti, Pardis C., (Principal Investigator), Shlyakhter, Ilya, Schaffner, Stephen F., Vitti, Joseph, Cooper, David N., (Principal Investigator), Ball, Edward V., Stenson, Peter D., Barnes, Bret, Bauer, Markus, Cheetham, Keira R., Cox, Anthony, Eberle, Michael, Kahn, Scott, Murray, Lisa, Peden, John, Shaw, Richard, Kenny, Eimear E., (Principal Investigator), Batzer, Mark A., (Principal Investigator), Konkel, Miriam K., Walker, Jerilyn A., MacArthur, Daniel G., (Principal Investigator), Lek, Monkol, Herwig, Ralf, Koboldt, Daniel C., Larson, David, Ye, Kai, Gravel, Simon, Swaroop, Anand, Chew, Emily, Lappalainen, Tuuli, (Principal Investigator), Erlich, Yaniv, (Principal Investigator), Gymrek, Melissa, Willems, Thomas Frederick, Simpson, Jared T., Shriver, Mark D., (Principal Investigator), Rosenfeld, Jeffrey A., (Principal Investigator), Montgomery, Stephen B., (Principal Investigator), De La Vega, Francisco M., (Principal Investigator), Byrnes, Jake K., Carroll, Andrew W., DeGorter, Marianne K., Lacroute, Phil, Maples, Brian K., Martin, Alicia R., Moreno-Estrada, Andres, Shringarpure, Suyash S., Zakharia, Fouad, Halperin, Eran, (Principal Investigator), Baran, Yael, Cerveira, Eliza, Hwang, Jaeho, Malhotra, Ankit, (Co-Project Lead), Plewczynski, Dariusz, Radew, Kamen, Romanovitch, Mallory, Zhang, Chengsheng, (Co-Project Lead), Hyland, Fiona C. L., Craig, David W., (Principal Investigator), Christoforides, Alexis, Homer, Nils, Izatt, Tyler, Kurdoglu, Ahmet A., Sinari, Shripad A., Squire, Kevin, Xiao, Chunlin, Sebat, Jonathan, (Principal Investigator), Antaki, Danny, Gujral, Madhusudan, Noor, Amina, Ye, Kenny, Burchard, Esteban G., (Principal Investigator), Hernandez, Ryan D., (Principal Investigator), Gignoux, Christopher R., Haussler, David, (Principal Investigator), Katzman, Sol J., Kent, James W., Howie, Bryan, Ruiz-Linares, Andres, (Principal Investigator), Dermitzakis, Emmanouil T., (Principal Investigator), Devine, Scott E., (Principal Investigator), Abecasis, Gonçalo R., (Principal Investigator) (Co-Chair), Kang, Hyun Min, (Project Leader), Kidd, Jeffrey M., (Principal Investigator), Blackwell, Tom, Caron, Sean, Chen, Wei, Emery, Sarah, Fritsche, Lars, Fuchsberger, Christian, Jun, Goo, Li, Bingshan, Lyons, Robert, Scheller, Chris, Sidore, Carlo, Song, Shiya, Sliwerska, Elzbieta, Taliun, Daniel, Tan, Adrian, Welch, Ryan, Wing, Mary Kate, Zhan, Xiaowei, Awadalla, Philip, (Principal Investigator), Hodgkinson, Alan, Li, Yun, Shi, Xinghua, (Principal Investigator), Quitadamo, Andrew, Lunter, Gerton, (Principal Investigator), McVean, Gil A., (Principal Investigator) (Co-Chair), Marchini, Jonathan L., (Principal Investigator), Myers, Simon, (Principal Investigator), Churchhouse, Claire, Delaneau, Olivier, Gupta-Hinch, Anjali, Kretzschmar, Warren, Iqbal, Zamin, Mathieson, Iain, Menelaou, Androniki, Rimmer, Andy, Xifara, Dionysia K., Oleksyk, Taras K., (Principal Investigator), Fu, Yunxin, (Principal Investigator), Liu, Xiaoming, Xiong, Momiao, Jorde, Lynn, (Principal Investigator), Witherspoon, David, Xing, Jinchuan, Browning, Brian L., (Principal Investigator), Browning, Sharon R., (Principal Investigator), Hormozdiari, Fereydoun, Sudmant, Peter H., Khurana, Ekta, (Principal Investigator), Hurles, Matthew E., (Principal Investigator), Albers, Cornelis A., Ayub, Qasim, Chen, Yuan, Colonna, Vincenza, Jostins, Luke, Walter, Klaudia, Xue, Yali, Abyzov, Alexej, Balasubramanian, Suganthi, Chen, Jieming, Clarke, Declan, Fu, Yao, Harmanci, Arif O., Jin, Mike, Lee, Donghoon, Liu, Jeremy, Mu, Xinmeng Jasmine, Zhang, Jing, Zhang, Yan, McCarroll, Steven A., (Principal Investigator), Hartl, Chris, Shakir, Khalid, Degenhardt, Jeremiah, Korbel, Jan O., (Principal Investigator) (Co-Chair), Meiers, Sascha, Raeder, Benjamin, Casale, Francesco Paolo, Stegle, Oliver, Lameijer, Eric-Wubbo, Ding, Li, (Principal Investigator), Hall, Ira, Lee, Charles, (Principal Investigator) (Co-Chair), Bafna, Vineet, Michaelson, Jacob, Gardner, Eugene J., (Project Leader), Mills, Ryan E., (Principal Investigator), Dayama, Gargi, Chen, Ken, (Principle Investigator), Fan, Xian, Chong, Zechen, Chen, Tenghui, Eichler, Evan E., (Principal Investigator) (Co-Chair), Chaisson, Mark J., Huddleston, John, Malig, Maika, Nelson, Bradley J., Parrish, Nicholas F., Blackburne, Ben, Lindsay, Sarah J., Ning, Zemin, Zhang, Yujun, Lam, Hugo, Sisu, Cristina, Gibbs, Richard A., (Principal Investigator) (Co-Chair), Challis, Danny, Evani, Uday S., Lu, James, Nagaswamy, Uma, Yu, Jin, Li, Wangshen, Marth, Gabor T., (Principal Investigator) (Co-Chair), Habegger, Lukas, Yu, Haiyuan, (Principal Investigator), Cunningham, Fiona, Dunham, Ian, Lage, Kasper, (Principal Investigator), Jespersen, Jakob Berg, Horn, Heiko, Tyler-Smith, Chris, (Principal Investigator) (Co-Chair), Gerstein, Mark B., (Principal Investigator) (Co-Chair), Kim, Donghoon, Desalle, Rob, Narechania, Apurva, Wilson Sayres, Melissa A., Bustamante, Carlos D., (Principal Investigator) (Co-Chair), Mendez, Fernando L., Poznik, David G., Underhill, Peter A., Coin, Lachlan, (Principal Investigator), Mittelman, David, Banerjee, Ruby, Cerezo, Maria, Fitzgerald, Thomas W., Louzada, Sandra, Massaia, Andrea, Ritchie, Graham R., Yang, Fengtang, Kalra, Divya, Hale, Walker, Dan, Xu, Flicek, Paul, (Principal Investigator) (Co-Chair), Clarke, Laura, (Project Lead), Sherry, Stephen T., (Principal Investigator) (Co-Chair), Chakravarti, Aravinda, (Co-Chair), Knoppers, Bartha M., (Co-Chair), Barnes, Kathleen C., Beiswanger, Christine, Cai, Hongyu, Cao, Hongzhi, Henn, Brenna, Jones, Danielle, Kaye, Jane S., Kent, Alastair, Kerasidou, Angeliki, Mathias, Rasika, Ossorio, Pilar N., Parker, Michael, Rotimi, Charles N., Royal, Charmaine D., Sandoval, Karla, Su, Yeyang, Tian, Zhongming, Tishkoff, Sarah, Via, Marc, Wang, Yuhong, Yang, Ling, Zhu, Jiayong, Bodmer, Walter, Bedoya, Gabriel, Cai, Zhiming, Gao, Yang, Chu, Jiayou, Peltonen, Leena, Garcia-Montero, Andres, Orfao, Alberto, Dutil, Julie, Martinez-Cruzado, Juan C., Mathias, Rasika A., Hennis, Anselm, Watson, Harold, McKenzie, Colin, Qadri, Firdausi, LaRocque, Regina, Deng, Xiaoyan, Asogun, Danny, Folarin, Onikepe, Happi, Christian, Omoniwa, Omonwunmi, Stremlau, Matt, Tariyal, Ridhi, Jallow, Muminatou, Joof, Fatoumatta Sisay, Corrah, Tumani, Rockett, Kirk, Kwiatkowski, Dominic, Kooner, Jaspal, Hiê`n, Trâ`n Tinh, Dunstan, Sarah J., Hang, Nguyen Thuy, Fonnie, Richard, Garry, Robert, Kanneh, Lansana, Moses, Lina, Schieffelin, John, Grant, Donald S., Gallo, Carla, Poletti, Giovanni, Saleheen, Danish, Rasheed, Asif, Brooks, Lisa D., Felsenfeld, Adam L., McEwen, Jean E., Vaydylevich, Yekaterina, Duncanson, Audrey, Dunn, Michael, Schloss, Jeffery A., and Yang, Huanming
Published: 2015
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21. Antidiabetic actions of a non-agonist PPARγ ligand blocking Cdk5-mediated phosphorylation

Author: Choi, Jang Hyun, Banks, Alexander S., Kamenecka, Theodore M., Busby, Scott A., Chalmers, Michael J., Kumar, Naresh, Kuruvilla, Dana S., Shin, Youseung, He, Yuanjun, Bruning, John B., Marciano, David P., Cameron, Michael D., Laznik, Dina, Jurczak, Michael J., Schurer, Stephan C., Vidovic, Dusica, Shulman, Gerald I., Spiegelman, Bruce M., and Griffin, Patrick R.
Subjects: Cyclins -- Health aspects, Ligands (Biochemistry) -- Health aspects, Diabetes -- Drug therapy, Phosphotransferases -- Health aspects, Phosphorylation -- Research, Thiazolidinediones -- Chemical properties, Environmental issues, Science and technology, Zoology and wildlife conservation
Abstract: PPARγ is the functioning receptor for the thiazolidinedione (TZD) class of antidiabetes drugs including rosiglitazone and pioglitazone (1). These drugs are full classical agonists for this nuclear receptor, but recent data have shown that many PPARγ-based drugs have a separate biochemical activity, blocking the obesity-linked phosphorylation of PPARγ by Cdk5 (ref. 2). Here we describe novel synthetic compounds that have a unique mode of binding to PPARγ,completely lack classical transcriptional agonism and block the Cdk5-mediated phosphorylation in cultured adipocytes and in insulin-resistant mice. Moreover, one such compound, SR1664, has potent antidiabetic activity while not causing the fluid retention and weight gain that are serious side effects of many of the PPARγ drugs. Unlike TZDs, SR1664 also does not interfere with bone formation in culture. These data illustrate that new classes of antidiabetes drugs can be developed by specifically targeting the Cdk5-mediated phosphorylation of PPARγ., PPARγ is a member of the nuclear receptor family of transcription factors and is a dominant regulator of adipose cell differentiation and development (3,4). It is also the functioning receptor [...]
Published: 2011
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22. Anti-diabetic drugs inhibit obesity-linked phosphorylation of PPARγ by Cdk5

Author: Choi, Jang Hyun, Banks, Alexander S., Estall, Jennifer L., Kajimura, Shingo, Bostrom, Pontus, Laznik, Dina, Ruas, Jorge L., Chalmers, Michael J., Kamenecka, Theodore M., Bluher, Matthias, Griffin, Patrick R., and Spiegelman, Bruce M.
Subjects: Obesity -- Complications and side effects -- Genetic aspects -- Research -- Risk factors -- Drug therapy, Diabetes -- Risk factors -- Drug therapy -- Research -- Genetic aspects -- Complications and side effects, Hypoglycemic agents -- Dosage and administration -- Complications and side effects -- Research, Cell receptors -- Physiological aspects -- Genetic aspects -- Research
Abstract: Obesity induced in mice by high-fat feeding activates the protein kinase Cdk5 (cyclin-dependent kinase 5) in adipose tissues. This results in phosphorylation of the nuclear receptor PPARγ (peroxisome proliferator-activated receptor γ), a dominant regulator of adipogenesis and fat cell gene expression, at serine 273. This modification of PPARγ does not alter its adipogenic capacity, but leads to dysregulation of a large number of genes whose expression is altered in obesity, including a reduction in the expression of the insulin-sensitizing adipokine, adiponectin. The phosphorylation of PPARγ by Cdk5 is blocked by anti-diabetic PPARγ ligands, such as rosiglitazone and MRL24. This inhibition works both in vivo and in vitro, and is completely independent of classical receptor transcriptional agonism. Similarly, inhibition of PPARγ phosphorylation in obese patients by rosiglitazone is very tightly associated with the anti-diabetic effects of this drug. All these findings strongly suggest that Cdk5-mediated phosphorylation of PPARγ may be involved in the pathogenesis of insulin-resistance, and present an opportunity for development of an improved generation of anti-diabetic drugs through PPARγ., Adipose tissue is at the centre of metabolic syndrome. Excessive body fat defines obesity and leads to insulin resistance, dyslipidaemia, type 2 diabetes, certain cancers and cardiovascular disease. Understanding the [...]
Published: 2010
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23. Neurons that regulate mouse torpor

Author: Hanqi Yao, Sage Aronson, Elena G. Assad, Oren F Wilcox, Michaela E. Palmer, Alexander S. Banks, Senmiao Sun, Sinisa Hrvatin, Marcelo Cicconet, Eric C. Griffith, Michael E. Greenberg, and Aurora J. Lavin-Peter
Subjects: 0301 basic medicine, Male, Glutamine, Torpor, Population, Regulator, Hypothalamus, Biology, Article, Arousal, 03 medical and health sciences, Glutamatergic, Mice, 0302 clinical medicine, Neural Pathways, Homeothermy, Animals, education, Neurons, education.field_of_study, Multidisciplinary, Fasting, 030104 developmental biology, Pituitary Adenylate Cyclase-Activating Polypeptide, Female, Energy Metabolism, Food Deprivation, Neuroscience, 030217 neurology & neurosurgery, Homeostasis
Abstract: The advent of endothermy, which is achieved through the continuous homeostatic regulation of body temperature and metabolism1,2, is a defining feature of mammalian and avian evolution. However, when challenged by food deprivation or harsh environmental conditions, many mammalian species initiate adaptive energy-conserving survival strategies—including torpor and hibernation—during which their body temperature decreases far below its homeostatic set-point3–5. How homeothermic mammals initiate and regulate these hypothermic states remains largely unknown. Here we show that entry into mouse torpor, a fasting-induced state with a greatly decreased metabolic rate and a body temperature as low as 20 °C6, is regulated by neurons in the medial and lateral preoptic area of the hypothalamus. We show that restimulation of neurons that were activated during a previous bout of torpor is sufficient to initiate the key features of torpor, even in mice that are not calorically restricted. Among these neurons we identify a population of glutamatergic Adcyap1-positive cells, the activity of which accurately determines when mice naturally initiate and exit torpor, and the inhibition of which disrupts the natural process of torpor entry, maintenance and arousal. Taken together, our results reveal a specific neuronal population in the mouse hypothalamus that serves as a core regulator of torpor. This work forms a basis for the future exploration of mechanisms and circuitry that regulate extreme hypothermic and hypometabolic states, and enables genetic access to monitor, initiate, manipulate and study these ancient adaptations of homeotherm biology. A specific neuronal population in the medial and lateral preoptic area of the hypothalamus regulates entry into torpor in mice.
Published: 2020

24. Reorientation of Sputnik Planitia implies a subsurface ocean on Pluto

Author: Nimmo, F., Hamilton, D. P., McKinnon, W. B., Schenk, P. M., Binzel, R. P., Bierson, C. J., Beyer, R. A., Moore, J. M., Stern, S. A., Weaver, H. A., Olkin, C. B., Young, L. A., Smith, K. E., Spencer, J. R., Beyer, R., Buie, M., Buratti, B., Cheng, A., Cruikshank, D., Ore, C. Dalle, Earle, A., Gladstone, R., Grundy, W., Howard, A. D., Lauer, T., Linscott, I., Parker, J., Porter, S., Reitsema, H., Reuter, D., Roberts, J. H., Robbins, S., Showalter, M., Singer, K., Strobel, D., Summers, M., Tyler, L., White, O. L., Umurhan, O. M., Banks, M., Barnouin, O., Bray, V., Carcich, B., Chaikin, A., Chavez, C., Conrad, C., Howett, C., Hofgartner, J., Kammer, J., Lisse, C., Marcotte, A., Parker, A., Retherford, K., Saina, M., Runyon, K., Schindhelm, E., Stansberry, J., Steffl, A., Stryk, T., Throop, H., Tsang, C., Verbiscer, A., Winters, H., and Zangari, A.
Subjects: Pluto (Dwarf planet) -- Observations, Environmental issues, Science and technology, Zoology and wildlife conservation
Abstract: Author(s): F. Nimmo (corresponding author) [1]; D. P. Hamilton [2]; W. B. McKinnon [3]; P. M. Schenk [4]; R. P. Binzel [5]; C. J. Bierson [1]; R. A. Beyer [6]; [...]
Published: 2016
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25. Creation of forest edges has a global impact on forest vertebrates

Author: Anna M. Pidgeon, Oliver R. Wearn, Luc Lens, Veronique Lefebvre, Marion Pfeifer, James I. Watling, Jos Barlow, Adam S. Hadley, Carlos A. Peres, Cristina Banks-Leite, Víctor Arroyo-Rodríguez, Robert M. Ewers, Deborah Faria, Laura M. Cisneros, Eric M. Wood, Pieter Ignatius Olivier, José Carlos Morante-Filho, Sandra L. Peters, Danilo Bandini Ribeiro, Stuart H. M. Butchart, Urs G. Kormann, Christoph Scherber, Alexis Cerezo, Neil D'Cruze, J. Nicolás Urbina-Cardona, Guido Fabian Medina-Rangel, S.M. Harris, Brian T. Klingbeil, Michael R. Willig, L. Schneider-Maunoury, Matthew J. Struebig, Charles J. Marsh, and Natural Environment Research Council (NERC)
Subjects: 0106 biological sciences, General Science & Technology, Population Dynamics, Biodiversity, Geographic Mapping, QH75, FRAGMENTED LANDSCAPES, Forests, Biology, 010603 evolutionary biology, 01 natural sciences, TERRESTRIAL MAMMALS, Article, Amphibians, Birds, Abundance (ecology), PLANTATION FORESTS, QH541, Animals, Body Size, IUCN Red List, Intact forest landscape, ANOLIS-LIMIFRONS, BODY-SIZE, Mammals, geography, GE, Science & Technology, Multidisciplinary, Habitat fragmentation, geography.geographical_feature_category, Ecology, 010604 marine biology & hydrobiology, Reptiles, RAIN-FOREST, 15. Life on land, Old-growth forest, EXTINCTION RISK, Multidisciplinary Sciences, HABITAT FRAGMENTATION, Habitat, 13. Climate action, Threatened species, EUCALYPTUS-MARGINATA FOREST, Science & Technology - Other Topics, TROPICAL FOREST
Abstract: Forest edges influence more than half of the world’s forests and contribute to worldwide declines in biodiversity and ecosystem functions. However, predicting these declines is challenging in heterogeneous fragmented landscapes. Here we assembled a global dataset on species responses to fragmentation and developed a statistical approach for quantifying edge impacts in heterogeneous landscapes to quantify edge-determined changes in abundance of 1,673 vertebrate species. We show that the abundances of 85% of species are affected, either positively or negatively, by forest edges. Species that live in the centre of the forest (forest core), that were more likely to be listed as threatened by the International Union for Conservation of Nature (IUCN), reached peak abundances only at sites farther than 200–400 m from sharp high-contrast forest edges. Smaller-bodied amphibians, larger reptiles and medium-sized non-volant mammals experienced a larger reduction in suitable habitat than other forest-core species. Our results highlight the pervasive ability of forest edges to restructure ecological communities on a global scale.
Published: 2017

26. STAT3 signalling is required for leptin regulation of energy balance but not reproduction

Author: Bates, Sarah H., Stearns, Walter H., Dundon, Trevor A., Schubert, Markus, Tso, Annette W. K., Wang, Yongping, Banks, Alexander S., Lavery, Hugh J., Haq, Asma K., Maratos-Flier, Eleftheria, Neel, Benjamin G., Schwartz, Michael W., and Myers, Jr, Martin G.
Subjects: Environmental issues, Science and technology, Zoology and wildlife conservation
Abstract: Author(s): Sarah H. Bates [1]; Walter H. Stearns [1]; Trevor A. Dundon [1]; Markus Schubert [1]; Annette W. K. Tso [1]; Yongping Wang [2]; Alexander S. Banks [1]; Hugh J. [...]
Published: 2003
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27. An integrated map of genetic variation from 1,092 human genomes

Author: McVean, Gil A., Altshuler, David M., Durbin, Richard M., Abecasis, Gonçalo R., Bentley, David R., Chakravarti, Aravinda, Clark, Andrew G., Donnelly, Peter, Eichler, Evan E., Flicek, Paul, Gabriel, Stacey B., Gibbs, Richard A., Green, Eric D., Hurles, Matthew E., Knoppers, Bartha M., Korbel, Jan O., Lander, Eric S., Lee, Charles, Lehrach, Hans, Mardis, Elaine R., Marth, Gabor T., Nickerson, Deborah A., Schmidt, Jeanette P., Sherry, Stephen T., Wang, Jun, Wilson, Richard K., Dinh, Huyen, Kovar, Christie, Lee, Sandra, Lewis, Lora, Muzny, Donna, Reid, Jeff, Wang, Min, Wang, Jun, Fang, Xiaodong, Guo, Xiaosen, Jian, Min, Jiang, Hui, Jin, Xin, Li, Guoqing, Li, Jingxiang, Li, Yingrui, Li, Zhuo, Liu, Xiao, Lu, Yao, Ma, Xuedi, Su, Zhe, Tai, Shuaishuai, Tang, Meifang, Wang, Bo, Wang, Guangbiao, Wu, Honglong, Wu, Renhua, Yin, Ye, Zhang, Wenwei, Zhao, Jiao, Zhao, Meiru, Zheng, Xiaole, Zhou, Yan, Lander, Eric S., Gabriel, Stacey B., Gupta, Namrata, Flicek, Paul, Clarke, Laura, Leinonen, Rasko, Smith, Richard E., Zheng-Bradley, Xiangqun, Bentley, David R., Grocock, Russell, Humphray, Sean, James, Terena, Kingsbury, Zoya, Lehrach, Hans, Sudbrak, Ralf, Albrecht, Marcus W., Amstislavskiy, Vyacheslav S., Borodina, Tatiana A., Lienhard, Matthias, Mertes, Florian, Sultan, Marc, Timmermann, Bernd, Yaspo, Marie-Laure, Sherry, Stephen T., McVean, Gil A., Mardis, Elaine R., Wilson, Richard K., Fulton, Lucinda, Fulton, Robert, Weinstock, George M., Durbin, Richard M., Balasubramaniam, Senduran, Burton, John, Danecek, Petr, Keane, Thomas M., Kolb-Kokocinski, Anja, McCarthy, Shane, Stalker, James, Quail, Michael, Schmidt, Jeanette P., Davies, Christopher J., Gollub, Jeremy, Webster, Teresa, Wong, Brant, Zhan, Yiping, Auton, Adam, Yu, Fuli, Bainbridge, Matthew, Challis, Danny, Evani, Uday S., Lu, James, Nagaswamy, Uma, Sabo, Aniko, Wang, Yi, Yu, Jin, Coin, Lachlan J. M., Fang, Lin, Li, Qibin, Li, Zhenyu, Lin, Haoxiang, Liu, Binghang, Luo, Ruibang, Qin, Nan, Shao, Haojing, Wang, Bingqiang, Xie, Yinlong, Ye, Chen, Yu, Chang, Zhang, Fan, Zheng, Hancheng, Zhu, Hongmei, Garrison, Erik P., Kural, Deniz, Lee, Wan-Ping, Fung Leong, Wen, Ward, Alistair N., Wu, Jiantao, Zhang, Mengyao, Lee, Charles, Griffin, Lauren, Hsieh, Chih-Heng, Mills, Ryan E., Shi, Xinghua, von Grotthuss, Marcin, Zhang, Chengsheng, Daly, Mark J., DePristo, Mark A., Banks, Eric, Bhatia, Gaurav, Carneiro, Mauricio O., del Angel, Guillermo, Genovese, Giulio, Handsaker, Robert E., Hartl, Chris, McCarroll, Steven A., Nemesh, James C., Poplin, Ryan E., Schaffner, Stephen F., Shakir, Khalid, Yoon, Seungtai C., Lihm, Jayon, Makarov, Vladimir, Jin, Hanjun, Kim, Wook, Cheol Kim, Ki, Korbel, Jan O., Rausch, Tobias, Beal, Kathryn, Cunningham, Fiona, Herrero, Javier, McLaren, William M., Ritchie, Graham R. S., Clark, Andrew G., Gottipati, Srikanth, Keinan, Alon, Rodriguez-Flores, Juan L., Sabeti, Pardis C., Grossman, Sharon R., Tabrizi, Shervin, Tariyal, Ridhi, Cooper, David N., Ball, Edward V., Stenson, Peter D., Barnes, Bret, Bauer, Markus, Keira Cheetham, R., Cox, Tony, Eberle, Michael, Kahn, Scott, Murray, Lisa, Peden, John, Shaw, Richard, Ye, Kai, Batzer, Mark A., Konkel, Miriam K., Walker, Jerilyn A., MacArthur, Daniel G., Lek, Monkol, Sudbrak, Herwig, Ralf, Shriver, Mark D., Bustamante, Carlos D., Byrnes, Jake K., De La Vega, Francisco M., Gravel, Simon, Kenny, Eimear E., Kidd, Jeffrey M., Lacroute, Phil, Maples, Brian K., Moreno-Estrada, Andres, Zakharia, Fouad, Halperin, Eran, Baran, Yael, Craig, David W., Christoforides, Alexis, Homer, Nils, Izatt, Tyler, Kurdoglu, Ahmet A., Sinari, Shripad A., Squire, Kevin, Xiao, Chunlin, Sebat, Jonathan, Bafna, Vineet, Ye, Kenny, Burchard, Esteban G., Hernandez, Ryan D., Gignoux, Christopher R., Haussler, David, Katzman, Sol J., James Kent, W., Howie, Bryan, Ruiz-Linares, Andres, Dermitzakis, Emmanouil T., Lappalainen, Tuuli, Devine, Scott E., Liu, Xinyue, Maroo, Ankit, Tallon, Luke J., Rosenfeld, Jeffrey A., Min Kang, Hyun, Anderson, Paul, Angius, Andrea, Bigham, Abigail, Blackwell, Tom, Busonero, Fabio, Cucca, Francesco, Fuchsberger, Christian, Jones, Chris, Jun, Goo, Li, Yun, Lyons, Robert, Maschio, Andrea, Porcu, Eleonora, Reinier, Fred, Sanna, Serena, Schlessinger, David, Sidore, Carlo, Tan, Adrian, Kate Trost, Mary, Awadalla, Philip, Hodgkinson, Alan, Lunter, Gerton, McVean, Gil A., Marchini, Jonathan L., Myers, Simon, Churchhouse, Claire, Delaneau, Olivier, Gupta-Hinch, Anjali, Iqbal, Zamin, Mathieson, Iain, Rimmer, Andy, Xifara, Dionysia K., Oleksyk, Taras K., Fu, Yunxin, Liu, Xiaoming, Xiong, Momiao, Jorde, Lynn, Witherspoon, David, Xing, Jinchuan, Eichler, Evan E., Browning, Brian L., Alkan, Can, Hajirasouliha, Iman, Hormozdiari, Fereydoun, Ko, Arthur, Sudmant, Peter H., Mardis, Elaine R., Chen, Ken, Chinwalla, Asif, Ding, Li, Dooling, David, Koboldt, Daniel C., McLellan, Michael D., Wallis, John W., Wendl, Michael C., Zhang, Qunyuan, Hurles, Matthew E., Tyler-Smith, Chris, Albers, Cornelis A., Ayub, Qasim, Chen, Yuan, Coffey, Alison J., Colonna, Vincenza, Huang, Ni, Jostins, Luke, Li, Heng, Scally, Aylwyn, Walter, Klaudia, Xue, Yali, Zhang, Yujun, Gerstein, Mark B., Abyzov, Alexej, Balasubramanian, Suganthi, Chen, Jieming, Clarke, Declan, Fu, Yao, Habegger, Lukas, Harmanci, Arif O., Jin, Mike, Khurana, Ekta, Jasmine Mu, Xinmeng, Sisu, Cristina, Lee, Charles, McCarroll, Steven A., Degenhardt, Jeremiah, Korbel, Jan O., Stütz, Adrian M., Church, Deanna, Michaelson, Jacob J., Eichler, Evan E., Hurles, Matthew E., Blackburne, Ben, Lindsay, Sarah J., Ning, Zemin, DePristo, Mark A., Min Kang, Hyun, Mardis, Elaine R., Yu, Fuli, Michelson, Leslie P., Tyler-Smith, Chris, Frankish, Adam, Harrow, Jennifer, Fowler, Gerald, Hale, Walker, Kalra, Divya, Flicek, Paul, Clarke, Laura, Barker, Jonathan, Kelman, Gavin, Kulesha, Eugene, Radhakrishnan, Rajesh, Roa, Asier, Smirnov, Dmitriy, Streeter, Ian, Toneva, Iliana, Vaughan, Brendan, Sherry, Stephen T., Ananiev, Victor, Belaia, Zinaida, Beloslyudtsev, Dimitriy, Bouk, Nathan, Chen, Chao, Cohen, Robert, Cook, Charles, Garner, John, Hefferon, Timothy, Kimelman, Mikhail, Liu, Chunlei, Lopez, John, Meric, Peter, OʼSullivan, Chris, Ostapchuk, Yuri, Phan, Lon, Ponomarov, Sergiy, Schneider, Valerie, Shekhtman, Eugene, Sirotkin, Karl, Slotta, Douglas, Zhang, Hua, Chakravarti, Aravinda, Knoppers, Bartha M., Barnes, Kathleen C., Beiswanger, Christine, Burchard, Esteban G., Bustamante, Carlos D., Cai, Hongyu, Cao, Hongzhi, Durbin, Richard M., Gharani, Neda, Henn, Brenna, Jones, Danielle, Jorde, Lynn, Kaye, Jane S., Kent, Alastair, Kerasidou, Angeliki, Mathias, Rasika, Ossorio, Pilar N., Parker, Michael, Reich, David, Rotimi, Charles N., Royal, Charmaine D., Sandoval, Karla, Su, Yeyang, Sudbrak, Ralf, Tian, Zhongming, Tishkoff, Sarah, Toji, Lorraine H., Tyler-Smith, Chris, Via, Marc, Wang, Yuhong, Yang, Huanming, Yang, Ling, Zhu, Jiayong, Bodmer, Walter, Bedoya, Gabriel, Ruiz-Linares, Andres, Zhi Ming, Cai, Yang, Gao, Jia You, Chu, Peltonen, Leena, Garcia-Montero, Andres, Orfao, Alberto, Dutil, Julie, Martinez-Cruzado, Juan C., Oleksyk, Taras K., Brooks, Lisa D., Felsenfeld, Adam L., McEwen, Jean E., Clemm, Nicholas C., Duncanson, Audrey, Dunn, Michael, Guyer, Mark S., Peterson, Jane L., Abecasis, Goncalo R., and Auton, Adam
Published: 2012
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28. Humans integrate visual and haptic information in a statistically optimal fashion

Author: Ernst, Marc O. and Banks, Martin S.
Subjects: Environmental issues, Science and technology, Zoology and wildlife conservation
Abstract: Author(s): Marc O. Ernst (corresponding author) [1]; Martin S. Banks When a person looks at an object while exploring it with their hand, vision and touch both provide information for [...]
Published: 2002
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29. Patterns and rates of exonic de novo mutations in autism spectrum disorders

Author: Neale, Benjamin M., Kou, Yan, Liu, Li, Maʼayan, Avi, Samocha, Kaitlin E., Sabo, Aniko, Lin, Chiao-Feng, Stevens, Christine, Wang, Li-San, Makarov, Vladimir, Polak, Paz, Yoon, Seungtai, Maguire, Jared, Crawford, Emily L., Campbell, Nicholas G., Geller, Evan T., Valladares, Otto, Schafer, Chad, Liu, Han, Zhao, Tuo, Cai, Guiqing, Lihm, Jayon, Dannenfelser, Ruth, Jabado, Omar, Peralta, Zuleyma, Nagaswamy, Uma, Muzny, Donna, Reid, Jeffrey G., Newsham, Irene, Wu, Yuanqing, Lewis, Lora, Han, Yi, Voight, Benjamin F., Lim, Elaine, Rossin, Elizabeth, Kirby, Andrew, Flannick, Jason, Fromer, Menachem, Shakir, Khalid, Fennell, Tim, Garimella, Kiran, Banks, Eric, Poplin, Ryan, Gabriel, Stacey, DePristo, Mark, Wimbish, Jack R., Boone, Braden E., Levy, Shawn E., Betancur, Catalina, Sunyaev, Shamil, Boerwinkle, Eric, Buxbaum, Joseph D., Cook, Edwin H., Jr, Devlin, Bernie, Gibbs, Richard A., Roeder, Kathryn, Schellenberg, Gerard D., Sutcliffe, James S., and Daly, Mark J.
Published: 2012
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30. Neurons that regulate mouse torpor

Author: Hrvatin, Sinisa, primary, Sun, Senmiao, additional, Wilcox, Oren F., additional, Yao, Hanqi, additional, Lavin-Peter, Aurora J., additional, Cicconet, Marcelo, additional, Assad, Elena G., additional, Palmer, Michaela E., additional, Aronson, Sage, additional, Banks, Alexander S., additional, Griffith, Eric C., additional, and Greenberg, Michael E., additional
Published: 2020
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31. γδ T cells and adipocyte IL-17RC control fat innervation and thermogenesis

Author: Hu, Bo, primary, Jin, Chengcheng, additional, Zeng, Xing, additional, Resch, Jon M., additional, Jedrychowski, Mark P., additional, Yang, Zongfang, additional, Desai, Bhavna N., additional, Banks, Alexander S., additional, Lowell, Bradford B., additional, Mathis, Diane, additional, and Spiegelman, Bruce M., additional
Published: 2020
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32. Biochemical evidence of cannibalism at a prehistoric Puebloan site in southwestern Colorado

Author: Marlar, Richard A., Leonard, Banks L., Billman, Brian R., Lambert, Patricia M., and Marlar, Jennifer E.
Subjects: Environmental issues, Science and technology, Zoology and wildlife conservation
Abstract: Author(s): Richard A. Marlar (corresponding author) [1, 2]; Banks L. Leonard [3]; Brian R. Billman [3, 4]; Patricia M. Lambert [5]; Jennifer E. Marlar [2] The existence of cannibalism is [...]
Published: 2000
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33. A map of human genome variation from population-scale sequencing

Author: Durbin, Richard M., Altshuler, David L., Durbin, Richard M., Abecasis, Gonçalo R., Bentley, David R., Chakravarti, Aravinda, Clark, Andrew G., Collins, Francis S., De La Vega, Francisco M., Donnelly, Peter, Egholm, Michael, Flicek, Paul, Gabriel, Stacey B., Gibbs, Richard A., Knoppers, Bartha M., Lander, Eric S., Lehrach, Hans, Mardis, Elaine R., McVean, Gil A., Nickerson, Debbie A., Peltonen, Leena, Schafer, Alan J., Sherry, Stephen T., Wang, Jun, Wilson, Richard K., Gibbs, Richard A., Deiros, David, Metzker, Mike, Muzny, Donna, Reid, Jeff, Wheeler, David, Wang, Jun, Li, Jingxiang, Jian, Min, Li, Guoqing, Li, Ruiqiang, Liang, Huiqing, Tian, Geng, Wang, Bo, Wang, Jian, Wang, Wei, Yang, Huanming, Zhang, Xiuqing, Zheng, Huisong, Lander, Eric S., Altshuler, David L., Ambrogio, Lauren, Bloom, Toby, Cibulskis, Kristian, Fennell, Tim J., Gabriel, Stacey B., Jaffe, David B., Shefler, Erica, Sougnez, Carrie L., Bentley, David R., Gormley, Niall, Humphray, Sean, Kingsbury, Zoya, Koko-Gonzales, Paula, Stone, Jennifer, McKernan, Kevin J., Costa, Gina L., Ichikawa, Jeffry K., Lee, Clarence C., Sudbrak, Ralf, Lehrach, Hans, Borodina, Tatiana A., Dahl, Andreas, Davydov, Alexey N., Marquardt, Peter, Mertes, Florian, Nietfeld, Wilfiried, Rosenstiel, Philip, Schreiber, Stefan, Soldatov, Aleksey V., Timmermann, Bernd, Tolzmann, Marius, Egholm, Michael, Affourtit, Jason, Ashworth, Dana, Attiya, Said, Bachorski, Melissa, Buglione, Eli, Burke, Adam, Caprio, Amanda, Celone, Christopher, Clark, Shauna, Conners, David, Desany, Brian, Gu, Lisa, Guccione, Lorri, Kao, Kalvin, Kebbel, Andrew, Knowlton, Jennifer, Labrecque, Matthew, McDade, Louise, Mealmaker, Craig, Minderman, Melissa, Nawrocki, Anne, Niazi, Faheem, Pareja, Kristen, Ramenani, Ravi, Riches, David, Song, Wanmin, Turcotte, Cynthia, Wang, Shally, Mardis, Elaine R., Wilson, Richard K., Dooling, David, Fulton, Lucinda, Fulton, Robert, Weinstock, George, Durbin, Richard M., Burton, John, Carter, David M., Churcher, Carol, Coffey, Alison, Cox, Anthony, Palotie, Aarno, Quail, Michael, Skelly, Tom, Stalker, James, Swerdlow, Harold P., Turner, Daniel, De Witte, Anniek, Giles, Shane, Bainbridge, Matthew, Challis, Danny, Sabo, Aniko, Yu, Fuli, Yu, Jin, Fang, Xiaodong, Guo, Xiaosen, Li, Yingrui, Luo, Ruibang, Tai, Shuaishuai, Wu, Honglong, Zheng, Hancheng, Zheng, Xiaole, Zhou, Yan, Marth, Gabor T., Garrison, Erik P., Huang, Weichun, Indap, Amit, Kural, Deniz, Lee, Wan-Ping, Fung Leong, Wen, Quinlan, Aaron R., Stewart, Chip, Stromberg, Michael P., Ward, Alistair N., Wu, Jiantao, Lee, Charles, Mills, Ryan E., Shi, Xinghua, Daly, Mark J., DePristo, Mark A., Ball, Aaron D., Banks, Eric, Browning, Brian L., Garimella, Kiran V., Grossman, Sharon R., Handsaker, Robert E., Hanna, Matt, Hartl, Chris, Kernytsky, Andrew M., Korn, Joshua M., Li, Heng, Maguire, Jared R., McCarroll, Steven A., McKenna, Aaron, Nemesh, James C., Philippakis, Anthony A., Poplin, Ryan E., Price, Alkes, Rivas, Manuel A., Sabeti, Pardis C., Schaffner, Stephen F., Shlyakhter, Ilya A., Cooper, David N., Ball, Edward V., Mort, Matthew, Phillips, Andrew D., Stenson, Peter D., Sebat, Jonathan, Makarov, Vladimir, Ye, Kenny, Yoon, Seungtai C., Bustamante, Carlos D., Clark, Andrew G., Boyko, Adam, Degenhardt, Jeremiah, Gravel, Simon, Gutenkunst, Ryan N., Kaganovich, Mark, Keinan, Alon, Lacroute, Phil, Ma, Xin, Reynolds, Andy, Clarke, Laura, Flicek, Paul, Cunningham, Fiona, Herrero, Javier, Keenen, Stephen, Kulesha, Eugene, Leinonen, Rasko, McLaren, William M., Radhakrishnan, Rajesh, Smith, Richard E., Zalunin, Vadim, Zheng-Bradley, Xiangqun, Korbel, Jan O., Stütz, Adrian M., Humphray, Sean, Bauer, Markus, Cheetham, Keira R., Cox, Tony, Eberle, Michael, James, Terena, Kahn, Scott, Murray, Lisa, Ye, Kai, De La Vega, Francisco M., Fu, Yutao, Hyland, Fiona C. L., Manning, Jonathan M., McLaughlin, Stephen F., Peckham, Heather E., Sakarya, Onur, Sun, Yongming A., Tsung, Eric F., Batzer, Mark A., Konkel, Miriam K., Walker, Jerilyn A., Albrecht, Marcus W., Amstislavskiy, Vyacheslav S., Herwig, Ralf, Parkhomchuk, Dimitri V., Sherry, Stephen T., Agarwala, Richa, Khouri, Hoda M., Morgulis, Aleksandr O., Paschall, Justin E., Phan, Lon D., Rotmistrovsky, Kirill E., Sanders, Robert D., Shumway, Martin F., Xiao, Chunlin, McVean, Gil A., Auton, Adam, Iqbal, Zamin, Lunter, Gerton, Marchini, Jonathan L., Moutsianas, Loukas, Myers, Simon, Tumian, Afidalina, Desany, Brian, Knight, James, Winer, Roger, Craig, David W., Beckstrom-Sternberg, Steve M., Christoforides, Alexis, Kurdoglu, Ahmet A., Pearson, John V., Sinari, Shripad A., Tembe, Waibhav D., Haussler, David, Hinrichs, Angie S., Katzman, Sol J., Kern, Andrew, Kuhn, Robert M., Przeworski, Molly, Hernandez, Ryan D., Howie, Bryan, Kelley, Joanna L., Cord Melton, S., Abecasis, Gonçalo R., Li, Yun, Anderson, Paul, Blackwell, Tom, Chen, Wei, Cookson, William O., Ding, Jun, Min Kang, Hyun, Lathrop, Mark, Liang, Liming, Moffatt, Miriam F., Scheet, Paul, Sidore, Carlo, Snyder, Matthew, Zhan, Xiaowei, Zöllner, Sebastian, Awadalla, Philip, Casals, Ferran, Idaghdour, Youssef, Keebler, John, Stone, Eric A., Zilversmit, Martine, Jorde, Lynn, Xing, Jinchuan, Eichler, Evan E., Aksay, Gozde, Alkan, Can, Hajirasouliha, Iman, Hormozdiari, Fereydoun, Sahinalp, Cenk S., Sudmant, Peter H., Mardis, Elaine R., Chen, Ken, Chinwalla, Asif, Ding, Li, Koboldt, Daniel C., McLellan, Mike D., Wallis, John W., Wendl, Michael C., Zhang, Qunyuan, Albers, Cornelis A., Ayub, Qasim, Balasubramaniam, Senduran, Barrett, Jeffrey C., Chen, Yuan, Conrad, Donald F., Danecek, Petr, Dermitzakis, Emmanouil T., Hu, Min, Huang, Ni, Hurles, Matt E., Jin, Hanjun, Jostins, Luke, Keane, Thomas M., Quang Le, Si, Lindsay, Sarah, Long, Quan, MacArthur, Daniel G., Montgomery, Stephen B., Parts, Leopold, Tyler-Smith, Chris, Walter, Klaudia, Zhang, Yujun, Gerstein, Mark B., Snyder, Michael, Abyzov, Alexej, Balasubramanian, Suganthi, Bjornson, Robert, Du, Jiang, Grubert, Fabian, Habegger, Lukas, Haraksingh, Rajini, Jee, Justin, Khurana, Ekta, Lam, Hugo Y. K., Leng, Jing, Jasmine Mu, Xinmeng, Urban, Alexander E., Zhang, Zhengdong, Lee, Charles, McCarroll, Steven A., DePristo, Mark A., Korbel, Jan O., De La Vega, Francisco M., Blackwell, Tom, Eichler, Evan E., Kidd, Jeffrey M., Hurles, Matt E., Gibbs, Richard A., Coafra, Cristian, Dinh, Huyen, Kovar, Christie, Lee, Sandy, Nazareth, Lynne, Marth, Gabor T., Wilkinson, Jane, Flicek, Paul, Sherry, Stephen T., Abecasis, Gonçalo R., Mardis, Elaine R., Coffey, Allison, Scott, Carol, Gerstein, Mark B., Chakravarti, Aravinda, Knoppers, Bartha M., Bustamante, Carlos D., Gharani, Neda, Jorde, Lynn, Kaye, Jane S., Kent, Alastair, Li, Taosha, McGuire, Amy L., Ossorio, Pilar N., Rotimi, Charles N., Su, Yeyang, Toji, Lorraine H., Brooks, Lisa D., Felsenfeld, Adam L., McEwen, Jean E., Abdallah, Assya, Juenger, Christopher R., Clemm, Nicholas C., Duncanson, Audrey, Green, Eric D., Guyer, Mark S., and Peterson, Jane L.
Published: 2010
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34. International network of cancer genome projects

Author: Hudson, Thomas J., Anderson, Warwick, Aretz, Axel, Bell, Cindy, Bernabé, Rosa R., Bhan, M. K., Calvo, Fabien, Eerola, Iiro, Gerhard, Daniela S., Guttmacher, Alan, Guyer, Mark, Hemsley, Fiona M., Jennings, Jennifer L., Kerr, David, Klatt, Peter, Kolar, Patrik, Lane, David P., Laplace, Frank, Nettekoven, Gerd, Ozenberger, Brad, Peterson, Jane, Rao, T. S., Remacle, Jacques, Schafer, Alan J., Shibata, Tatsuhiro, Stratton, Michael R., Watanabe, Koichi, Yuen, Matthew M. F., Cambon-Thomsen, Anne, Dressler, Lynn G., Joly, Yann, Kennedy, Karen L., Parker, Michael J., Romeo-Casabona, Carlos M., Wallace, Susan, Wiesner, Georgia L., Zeps, Nikolajs, Biankin, Andrew V., Chabannon, Christian, de Alava, Enrique, Ferguson, Martin L., Geary, Peter, Hayes, Neil D., Johns, Amber L., Kasprzyk, Arek, Nakagawa, Hidewaki, Piris, Miguel A., van de Vijver, Marc, Aburatani, Hiroyuki, Bayés, Mónica, Bowtell, David D.L., Campbell, Peter J., Hirst, Martin, López-Otín, Carlos, Marra, Marco, Ning, Zemin, Puente, Xose S., Ruan, Yijun, Stunnenberg, Hendrik G., Swerdlow, Harold, Velculescu, Victor E., Xue, Hong H., Yang, Liu, Spellman, Paul T., Bader, Gary D., Boutros, Paul C., Flicek, Paul, Getz, Gad, Guigó, Roderic, Guo, Guangwu, Haussler, David, Hubbard, Tim J., Jiang, Tao, Jones, Steven M., Li, Qibin, López-Bigas, Nuria, Luo, Ruibang, Muthuswamy, Lakshmi, Ouellette, Francis B. F., Pearson, John V., Quesada, Victor, Raphael, Benjamin J., Sander, Chris, Stein, Lincoln D., Stuart, Joshua M., Teague, Jon W., Totoki, Yasushi, Tsunoda, Tatsuhiko, Valencia, Alfonso, Wheeler, David A., Wu, Honglong, Zhao, Shancen, Zhou, Guangyu, Lathrop, Mark, Axton, Myles, Dyke, Stephanie O. M., Gunter, Chris, McPherson, John D., Miller, Linda J., Zhang, Junjun, Haider, Syed A., Wang, Jianxin, Yung, Christina K., Cross, Anthony, Liang, Yong, Gnaneshan, Saravanamuttu, Guberman, Jonathan, Hsu, Jack, Bobrow, Martin, Chalmers, Don R. C., Hasel, Karl W., Kaan, Terry S. H., Knoppers, Bartha M., Lowrance, William W., Masui, Tohru, Nicolás, Pilar, Rial-Sebbag, Emmanuelle, Rodriguez, Laura Lyman, Vergely, Catherine, Grimmond, Sean M., Bowtell, David D. L., Cloonan, Nicole, deFazio, Anna, Eshleman, James R., Etemadmoghadam, Dariush, Gardiner, Brooke A., Kench, James G., Scarpa, Aldo, Sutherland, Robert L., Tempero, Margaret A., Waddell, Nicola J., Wilson, Peter J., Gallinger, Steve, Tsao, Ming-Sound, Shaw, Patricia A., Petersen, Gloria M., Mukhopadhyay, Debabrata, Chin, Lynda, DePinho, Ronald A., Thayer, Sarah, Shazand, Kamran, Beck, Timothy, Sam, Michelle, Timms, Lee, Ballin, Vanessa, Ji, Jiafu, Zhang, Xiuqing, Chen, Feng, Hu, Xueda, Yang, Qi, Tian, Geng, Zhang, Lianhai, Xing, Xiaofang, Li, Xianghong, Zhu, Zhenggang, Yu, Yingyan, Yu, Jun, Yang, Huanming, Tost, Jörg, Brennan, Paul, Holcatova, Ivana, Zaridze, David, Brazma, Alvis, Egevad, Lars, Prokhortchouk, Egor, Banks, Rosamonde Elizabeth, Uhlén, Mathias, Viksna, Juris, Ponten, Fredrik, Skryabin, Konstantin, Futreal, Andrew P., Birney, Ewan, Caldas, Carlos, Reis-Filho, Jorge S., Richardson, Andrea L., Sotiriou, Christos, Birnbaum, Daniel, Blanche, Hélène, Boucher, Pascal, Boyault, Sandrine, Masson-Jacquemier, Jocelyne D., Pauporté, Iris, Pivot, Xavier, Vincent-Salomon, Anne, Tabone, Eric, Theillet, Charles, Treilleux, Isabelle, Bioulac-Sage, Paulette, Clément, Bruno, Decaens, Thomas, Degos, Françoise, Franco, Dominique, Gut, Ivo, Gut, Marta, Heath, Simon, Samuel, Didier, Thomas, Gilles, Zucman-Rossi, Jessica, Eils, Roland, Brors, Benedikt, Korbel, Jan O., Korshunov, Andrey, Landgraf, Pablo, Lehrach, Hans, Pfister, Stefan, Radlwimmer, Bernhard, Reifenberger, Guido, Taylor, Michael D., von Kalle, Christof, Majumder, Partha P., Sarin, Rajiv, Pederzoli, Paolo, Lawlor, Rita T., Delledonne, Massimo, Bardelli, Alberto, Gress, Thomas, Klimstra, David, Zamboni, Giuseppe, Nakamura, Yusuke, Kusuda, Jun, Miyano, Satoru, Kato, Kazuto, Fujimoto, Akihiro, Yoshida, Teruhiko, Campo, Elias, Estivill, Xavier, de Sanjosé, Silvia, Montserrat, Emili, González-Díaz, Marcos, Jares, Pedro, Himmelbaue, Heinz, Bea, Silvia, Aparicio, Samuel, Borg, Ake, Børresen-Dale, Anne-Lise, Foekens, John A., vanʼt Veer, Laura, Easton, Douglas F., Martin, Sancha, Compton, Carolyn C., Lander, Eric S., Penny, Robert, Shaw, Kenna M., Speed, Terence P., Vockley, Joseph G., Lichter, Peter, Barker, Anna D., Burke, Wylie, Collins, Francis S., Green, Anthony R., Hamilton, Stanley R., Kallioniemi, Olli P., Ley, Timothy J., Liu, Edison T., Lu, Youyong, Majumder, Partha, Wainwright, Brandon J., and Wilson, Richard K.
Published: 2010
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35. Stone tools in northern Europe made by Homo sapiens45,000 years ago

Author: Banks, William E.
Abstract: DNA analyses of skeletal fragments from a site in Germany provide evidence that humans, rather than Neanderthals, were responsible for a particular stone-tool industry called the Lincombian–Ranisian–Jerzmanowician.
Published: 2024
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36. More ground work needed to prepare students for PhDs

Author: Banks-Leite, Cristina
Published: 2008
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37. NETWORKS & SUPPORT: Seeking a PhD abroad

Author: Banks, Michael
Published: 2007

38. Role of a p53 polymorphism in the development of human papillomavirus-associated cancer

Author: Storey, Alan, Thomas, Miranda, Kalita, Ann, Harwood, Catherine, Gardiol, Daniela, Mantovani, Fiamma, Breuer, Judith, Leigh, Irene M., Matlashewski, Greg, and Banks, Lawrence
Subjects: Papillomaviruses -- Research, Cervical cancer -- Causes of, Genetic polymorphisms -- Research, Environmental issues, Science and technology, Zoology and wildlife conservation
Abstract: New research on the role of the cellular tumour-suppressor protein p53 in the development of papillomavirus-associated cancer shows that the arginine form of p53 makes individuals seven times more susceptible to cervical carcinoma than the proline form. The p53 amino acid sequence commonly exists with either an arginine or a proline at position 72.
Published: 1998

39. Author Correction: A structural variation reference for medical and population genetics

Author: Anne H. O’Donnell-Luria, Chelsea Lowther, Christine Stevens, Elise Valkanas, Matthew R. Stone, Anthony A. Philippakis, Matthew Solomonson, Mark Walker, Yongqing Huang, Jack Fu, Jerome I. Rotter, Laurent C. Francioli, Wendy S. Post, Yii-Der Ida Chen, Kristen M. Laricchia, Amit Khera, Eric S. Lander, Kent D. Taylor, Mark J. Daly, Xuefang Zhao, Lauren Margolin, Ryan L. Collins, Henry J. Lin, Konrad J. Karczewski, Laura D. Gauthier, Ted Brookings, Jessica Alföldi, Benjamin M. Neale, Harrison Brand, Caroline N. Cusick, Eric Banks, Nicholas A. Watts, Stacey Gabriel, Harold Z. Wang, Valentin Ruano-Rubio, Michael E. Talkowski, Ruchi Munshi, Stephen S. Rich, Genome Aggregation Database Production Team, Sekar Kathiresan, Christopher W. Whelan, Daniel G. MacArthur, Namrata Gupta, Chad Nusbaum, Ted Sharpe, Grace Tiao, and Alexander Baumann
Subjects: Male, Genotyping Techniques, Genetics, Medical, MEDLINE, Population genetics, Computational biology, Biology, Genome informatics, Polymorphism, Single Nucleotide, Structural variation, Humans, Disease, Genetic Testing, Selection, Genetic, Author Correction, Multidisciplinary, Whole Genome Sequencing, Genome, Human, Published Erratum, Racial Groups, Genetic Variation, Chromosome abnormality, Genomics, Middle Aged, Reference Standards, Genetics, Population, Mutation, Female
Abstract: A Correction to this paper has been published: https://doi.org/10.1038/s41586-020-03176-6.
Published: 2021

40. Animal-rights zealots put wildlife welfare at risk

Author: Banks, Peter B.
Published: 2005

41. Uncoupling the agony from ecstasy

Author: Mills, Edward M., Banks, Matthew L., Sprague, Jon E., and Finkel, Toren
Published: 2003

42. The genetic architecture of type 2 diabetes

Author: Clement Ma, Liisa Hakaste, Claes Ladenvall, Massimo Mangino, Lars Lind, Aaron G. Day-Williams, Ryan Poplin, Thomas Schwarzmayr, Annette Peters, Thomas Meitinger, Satish Kumar, Kyong Soo Park, Ching-Yu Cheng, Farook Thameem, Kyle J. Gaulton, Olov Rolandsson, Yossi Farjoun, Neil Robertson, Mauricio O. Carneiro, Mark A. DePristo, Pierre Fontanillas, Ruth J. F. Loos, Heather M. Highland, Vilmantas Giedraitis, Gemma Buck, Fredrik Karpe, Mohammad Kamran Ikram, Alex S. F. Doney, Hae Kyung Im, Eric S. Lander, Johanna Kuusisto, Dorothée Thuillier, Denis Rybin, Jacquelyn Murphy, Benjamin M. Neale, Martina Müller-Nurasyid, Eric R. Gamazon, Johanne Marie Justesen, Tin Aung, Vincent K. L. Lam, John Danesh, Donna M. Lehman, Goo Jun, Marit E. Jørgensen, Christian Herder, Edmund Chan, Pamela J. Hicks, Todd Green, Claudia Langenberg, Yoon Shin Cho, James G. Wilson, Daniel E. Hale, Rector Arya, Giriraj R. Chandak, Juan Fernandez Tajes, Jaakko Tuomilehto, Christopher P. Jenkinson, Anders Rosengren, Torsten Lauritzen, Michael Griswold, Karen L. Mohlke, Amy J. Swift, Alena Stančáková, Christian Fuchsberger, Iksoo Huh, Nikhil Tandon, João Fadista, Christa Meisinger, Gonçalo R. Abecasis, Pål R. Njølstad, Dwaipayan Bharadwaj, Richard M. Watanabe, Shaun Purcell, Veikko Salomaa, Tim D. Spector, Paul W. Franks, Adam E. Locke, Sharon P. Fowler, Panos Deloukas, Reedik Mägi, Solomon K. Musani, Kee Seng Chia, Barbara Thorand, Soo Heon Kwak, Annemari Käräjämäki, Evelin Mihailov, John Blangero, Thomas Wieland, Christian Gieger, E. Shyong Tai, Jianjun Liu, James B. Meigs, Teemu Kuulasmaa, Martin Hrabé de Angelis, Francis S. Collins, Tim M. Strom, Tibor V. Varga, Juyoung Lee, Mark I. McCarthy, Domenico Palli, Jong-Young Lee, Benjamin Glaser, Tasha E. Fingerlin, Stephen O'Rahilly, Andrew T. Hattersley, Gil Atzmon, Manuel A. Rivas, Noël P. Burtt, Ivan Brandslund, Young-Jin Kim, Dorairaj Prabhakaran, Xu Wang, Taylor J. Maxwell, Valeriya Lyssenko, Frank B. Hu, Adolfo Correa, Khalid Shakir, Kathleen A. Jablonski, Yingchang Lu, Wei-Yen Lim, Min Jin Go, William R. Scott, Hanna E. Abboud, Leena Kinnunen, Inês Barroso, Gabriela L. Surdulescu, Peng Chen, Robert Sladek, Marju Orho-Melander, Xueling Sim, Robert A. Scott, Joanna M. M. Howson, Markku Laakso, David Altshuler, Vidya S. Farook, Harald Grallert, Janina S. Ried, Vineeta Agarwala, Philippe Froguel, Nicholas J. Wareham, Tiinamaija Tuomi, Joon Yoon, Heikki A. Koistinen, Toni I. Pollin, Heiner Boeing, Marie Loh, Nicola L. Beer, Joanne E. Curran, Lars Lannfelt, Dorota Pasko, Taesung Park, David Buck, Nir Barzilai, Stephen C. J. Parker, Michael Roden, Bok-Ghee Han, David Aguilar, Timothy Fennell, Sian-Tsung Tan, Gregory P. Wilson, Momoko Horikoshi, Cramer Christensen, Craig L. Hanis, Gilean McVean, Benjamin F. Voight, Wolfgang Rathmann, Jared Maguire, Ashok Kumar, Donald W. Bowden, Michael L. Stitzel, Yongkang Kim, Christine Blancher, Jason Carey, Min-Seok Kwon, Nicholette D. Palmer, Oluf Pedersen, Niels Grarup, Peter S. Chines, Cornelia Huth, James Scott, Torben Hansen, Konstantin Strauch, Erwin P. Bottinger, Andrew D. Morris, Anette P. Gjesing, Erik Ingelsson, Colin N. A. Palmer, Claudia H. T. Tam, Stacey Gabriel, Pablo Cingolani, Beverley Balkau, Michael Boehnke, Peter M. Nilsson, Wing-Yee So, Andrew R. Wood, Lili Milani, Ravindranath Duggirala, Qibin Qi, Mark Walker, Weiping Jia, Mark Seielstad, Narisu Narisu, Tien Yin Wong, Martijn van de Bunt, Anubha Mahajan, Davis J. McCarthy, Ann-Christine Syvänen, Jennifer Kriebel, N. William Rayner, Han Chen, Jinyan Huang, Chiea Chuen Khor, Richard N. Bergman, Shah Ebrahim, Dylan Hodgkiss, Weihua Zhang, Manjinder S. Sandhu, Richard D. Pearson, Juliana C.N. Chan, Rainer Rauramaa, Ralph A. DeFronzo, Andrew Farmer, Yoshihiko Nagai, Allan Linneberg, Herman A. Taylor, Jose C. Florez, Jaspal S. Kooner, Lori L. Bonnycastle, Jeroen R. Huyghe, Leif Groop, Joseph Trakalo, Sobha Puppala, Bong-Jo Kim, Kathleen Stirrups, Kerrin S. Small, Cecilia M. Lindgren, Jennifer E. Below, Heung Man Lee, Inga Prokopenko, Liming Liang, Timothy M. Frayling, Uzma Afzal, Mark J. Daly, Yik Ying Teo, Andrew P. Morris, Phoenix Kwan, Yvonne T. van der Schouw, Cheng Hu, Katharine R. Owen, Alisa K. Manning, Christopher J. Groves, Josée Dupuis, Ryan P. Welch, Loukas Moutsianas, Joshua D. Smith, Tanya M. Teslovich, Robert C. Onofrio, Maggie C.Y. Ng, Peter Donnelly, Tõnu Esko, Matt Neville, Bo Isomaa, Anne U. Jackson, Jette Bork-Jensen, Barry I. Freedman, Yi Chen, Danish Saleheen, Lu Qi, Laura J. Scott, Jasmina Kravic, Paul Elliott, Mette Hollensted, Carmen Navarro, Selyeong Lee, Benjamin Lehne, Thomas Illig, Nancy J. Cox, Jonathan C. Levy, George B. Grant, John C. Chambers, Adam S. Butterworth, Ronald C.W. Ma, Teresa Ferreira, John R. B. Perry, Eleftheria Zeggini, Hyun Min Kang, Loic Yengo, Eric Banks, Jae-Hoon Lee, Anna L. Gloyn, Christopher Hartl, Wei Zhao, Andres Metspalu, Keng-Han Lin, Graeme I. Bell, Jason Flannick, Torben Jørgensen, Thomas W. Blackwell, Heather M. Stringham, Olle Melander, Omri Gottesman, Other departments, British Heart Foundation, Wellcome Trust, Medical Research Council (MRC), Massachusetts Institute of Technology. Department of Biology, Altshuler, David M, Internal Medicine, Perry, John [0000-0001-6483-3771], Butterworth, Adam [0000-0002-6915-9015], Howson, Joanna [0000-0001-7618-0050], Danesh, John [0000-0003-1158-6791], Johnson, Kathleen [0000-0002-6823-3252], O'Rahilly, Stephen [0000-0003-2199-4449], Langenberg, Claudia [0000-0002-5017-7344], Sandhu, Manjinder [0000-0002-2725-142X], Barroso, Ines [0000-0001-5800-4520], Wareham, Nicholas [0000-0003-1422-2993], and Apollo - University of Cambridge Repository
Subjects: 0301 basic medicine, PROTEIN INTERACTION NETWORKS, SUSCEPTIBILITY LOCI, Genotyping Techniques, General Science & Technology, DNA Mutational Analysis, SEQUENCING ASSOCIATION, 030209 endocrinology & metabolism, Genome-wide association study, Biology, Research Support, N.I.H, 03 medical and health sciences, 0302 clinical medicine, Research Support, N.I.H., Extramural, SDG 3 - Good Health and Well-being, MD Multidisciplinary, Genetic predisposition, Journal Article, Humans, Exome, Genetic Predisposition to Disease, GENOME-WIDE ASSOCIATION, Non-U.S. Gov't, Exome sequencing, Alleles, Genetic association, Genetics, RISK, Multidisciplinary, HERITABILITY, Research Support, Non-U.S. Gov't, COMPLEX TRAITS, Extramural, Genetic Variation, Genetic architecture, HUMAN-DISEASE, Europe, 030104 developmental biology, Diabetes Mellitus, Type 2, RARE VARIANTS, Sample Size, LOW-FREQUENCY, Imputation (genetics), Common disease-common variant, Genome-Wide Association Study
Abstract: The genetic architecture of common traits, including the number, frequency, and effect sizes of inherited variants that contribute to individual risk, has been long debated. Genome-wide association studies have identified scores of common variants associated with type 2 diabetes, but in aggregate, these explain only a fraction of the heritability of this disease. Here, to test the hypothesis that lower-frequency variants explain much of the remainder, the GoT2D and T2D-GENES consortia performed whole-genome sequencing in 2,657 European individuals with and without diabetes, and exome sequencing in 12,940 individuals from five ancestry groups. To increase statistical power, we expanded the sample size via genotyping and imputation in a further 111,548 subjects. Variants associated with type 2 diabetes after sequencing were overwhelmingly common and most fell within regions previously identified by genome-wide association studies. Comprehensive enumeration of sequence variation is necessary to identify functional alleles that provide important clues to disease pathophysiology, but large-scale sequencing does not support the idea that lower-frequency variants have a major role in predisposition to type 2 diabetes.
Published: 2016

43. Author Correction: A genomic mutational constraint map using variation in 76,156 human genomes.

Author: Chen, Siwei, Francioli, Laurent C., Goodrich, Julia K., Collins, Ryan L., Kanai, Masahiro, Wang, Qingbo, Alföldi, Jessica, Watts, Nicholas A., Vittal, Christopher, Gauthier, Laura D., Poterba, Timothy, Wilson, Michael W., Tarasova, Yekaterina, Phu, William, Grant, Riley, Yohannes, Mary T., Koenig, Zan, Farjoun, Yossi, Banks, Eric, and Donnelly, Stacey
Published: 2024
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44. p53 polymorphism and risk of cervical cancer

Author: Storey, Alan, Thomas, Miranda, Kalita, Ann, Harwood, Catherine, Gardiol, Daniela, Mantovani, Fiamma, Breuer, Judith, Leigh, Irene M., Matlashewski, Greg, and Banks, Lawrence
Published: 1998

45. Tidal disruption of the Magellanic Clouds by the Milky Way

Author: Putman, M. E., Gibson, B. K., Staveley-Smith, L., Banks, G., Barnes, D. G., Bhatal, R., Disney, M. J., Ekers, R. D., Freeman, K. C., Haynes, R. F., Henning, P., Jerjen, H., Kilborn, V., Koribalski, B., Knezek, P., Malin, D. F., Mould, J. R., Oosterloo, T., Price, R. M., Ryder, S. D., Sadler, E. M., Stewart, I., Stootman, F., Vaile, R. A., Webster, R. L., and Wright, A. E.
Published: 1998

46. Nicotinamide N-methyltransferase knockdown protects against diet-induced obesity

Author: Yana Cen, Fengying Gong, Brett P. Monia, John M. Asara, Joseph T. Rodgers, Lin Zhang, Odile D. Peroni, Anthony A. Sauve, Daniel Kraus, Ya Chin Wang, Qin Yang, Thomas Pulinilkunnil, Sanjay Bhanot, Pere Puigserver, Alexander S. Banks, Dong Kong, Eija Pirinen, Leena Alhonen, and Barbara B. Kahn
Subjects: Male, Niacinamide, S-Adenosylmethionine, medicine.medical_specialty, Adipose Tissue, White, Spermine, Nicotinamide N-methyltransferase, Biology, Ornithine Decarboxylase, Article, Ornithine decarboxylase, Mice, chemistry.chemical_compound, Sirtuin 1, Thinness, Acetyltransferases, Internal medicine, Glucose Intolerance, Adipocytes, Nicotinamide N-Methyltransferase, medicine, Animals, Obesity, Oxidoreductases Acting on CH-NH Group Donors, Glucose Transporter Type 4, Multidisciplinary, Nicotinamide, NAD, Diet, Fatty Liver, Mice, Inbred C57BL, Endocrinology, Adipose Tissue, Diabetes Mellitus, Type 2, Liver, chemistry, Gene Knockdown Techniques, biology.protein, NAD+ kinase, Insulin Resistance, Energy Metabolism, Polyamine, Polyamine oxidase, GLUT4
Abstract: In obesity and type 2 diabetes, Glut4 glucose transporter expression is decreased selectively in adipocytes1. Adipose-specific knockout or overexpression of Glut4 alters systemic insulin sensitivity2. Here we show, using DNA array analyses, that nicotinamide N-methyltransferase (Nnmt) is the most strongly reciprocally regulated gene when comparing gene expression in white adipose tissue (WAT) from adipose-specific Glut4-knockout or adipose-specific Glut4-overexpressing mice with their respective controls. NNMT methylates nicotinamide (vitamin B3) using S-adenosylmethionine (SAM) as a methyl donor3,4. Nicotinamide is a precursor of NAD+, an important cofactor linking cellular redox states with energy metabolism5. SAM provides propylamine for polyamine biosynthesis and donates a methyl group for histone methylation6. Polyamine flux including synthesis, catabolism and excretion, is controlled by the rate-limiting enzymes ornithine decarboxylase (ODC) and spermidine–spermine N1-acetyltransferase (SSAT; encoded by Sat1) and by polyamine oxidase (PAO), and has a major role in energy metabolism7,8. We report that NNMT expression is increased in WAT and liver of obese and diabetic mice. Nnmt knockdown in WAT and liver protects against diet-induced obesity by augmenting cellular energy expenditure. NNMT inhibition increases adipose SAM and NAD+ levels and upregulates ODC and SSAT activity as well as expression, owing to the effects of NNMT on histone H3 lysine 4 methylation in adipose tissue. Direct evidence for increased polyamine flux resulting from NNMT inhibition includes elevated urinary excretion and adipocyte secretion of diacetylspermine, a product of polyamine metabolism. NNMT inhibition in adipocytes increases oxygen consumption in an ODC-, SSAT- and PAO-dependent manner. Thus, NNMT is a novel regulator of histone methylation, polyamine flux and NAD+-dependent SIRT1 signalling, and is a unique and attractive target for treating obesity and type 2 diabetes.
Published: 2014

47. De novo mutations in schizophrenia implicate synaptic networks

Author: Hywel Williams, Jessica S. Johnson, Panos Roussos, Milind Mahajan, Vihra Milanova, Kimberly Chambert, Douglas Barker, David J. Kavanagh, Sarah Dwyer, Isla Humphreys, Michael Conlon O'Donovan, Steven A. McCarroll, Menachem Fromer, George Kirov, Peter Holmans, Elliott Rees, Andrew Pocklington, Shaun Purcell, Seth G. N. Grant, Pamela Sklar, Samuel A. Rose, Eric Banks, Jennifer L. Moran, Priit Palta, Eilis Hannon, Michael John Owen, Douglas M. Ruderfer, Lyudmila Georgieva, Padhraig Gormley, Aarno Palotie, Edward M. Scolnick, and Noa Carrera
Subjects: Mutation rate, Models, Neurological, Nerve Tissue Proteins, Biology, medicine.disease_cause, Receptors, N-Methyl-D-Aspartate, Article, Substrate Specificity, Fragile X Mental Retardation Protein, 03 medical and health sciences, 0302 clinical medicine, Mutation Rate, Postsynaptic potential, Intellectual Disability, Neural Pathways, medicine, Humans, Exome, RNA, Messenger, Copy-number variation, Gene, 030304 developmental biology, Genetics, 0303 health sciences, Mutation, Multidisciplinary, Arc (protein), Phenotype, Cytoskeletal Proteins, Child Development Disorders, Pervasive, Synapses, Schizophrenia, Nerve Net, 030217 neurology & neurosurgery
Abstract: Inherited alleles account for most of the genetic risk for schizophrenia. However, new (de novo) mutations, in the form of large chromosomal copy number changes, occur in a small fraction of cases and disproportionally disrupt genes encoding postsynaptic proteins. Here we show that small de novo mutations, affecting one or a few nucleotides, are overrepresented among glutamatergic postsynaptic proteins comprising activity-regulated cytoskeleton-associated protein (ARC) and N-methyl-d-aspartate receptor (NMDAR) complexes. Mutations are additionally enriched in proteins that interact with these complexes to modulate synaptic strength, namely proteins regulating actin filament dynamics and those whose messenger RNAs are targets of fragile X mental retardation protein (FMRP). Genes affected by mutations in schizophrenia overlap those mutated in autism and intellectual disability, as do mutation-enriched synaptic pathways. Aligning our findings with a parallel case-control study, we demonstrate reproducible insights into aetiological mechanisms for schizophrenia and reveal pathophysiology shared with other neurodevelopmental disorders.
Published: 2014
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48. The perception of heading during eye movements

Author: Royden, Constance S, Banks, Martin S, and Crowell, James A
Subjects: Behavioral Sciences
Abstract: Warren and Hannon (1988, 1990), while studying the perception of heading during eye movements, concluded that people do not require extraretinal information to judge heading with eye/head movements present. Here, heading judgments are examined at higher, more typical eye movement velocities than the extremely slow tracking eye movements used by Warren and Hannon. It is found that people require extraretinal information about eye position to perceive heading accurately under many viewing conditions.
Published: 1992
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49. Mapping and characterization of structural variation in 17,795 human genomes.

Author: Abel, Haley J., Larson, David E., Regier, Allison A., Chiang, Colby, Das, Indraniel, Kanchi, Krishna L., Layer, Ryan M., Neale, Benjamin M., Salerno, William J., Reeves, Catherine, Buyske, Steven, NHGRI Centers for Common Disease Genomics, Abecasis, Goncalo R., Appelbaum, Elizabeth, Baker, Julie, Banks, Eric, Bernier, Raphael A., Bloom, Toby, Boehnke, Michael, and Boerwinkle, Eric
Abstract: A key goal of whole-genome sequencing for studies of human genetics is to interrogate all forms of variation, including single-nucleotide variants, small insertion or deletion (indel) variants and structural variants. However, tools and resources for the study of structural variants have lagged behind those for smaller variants. Here we used a scalable pipeline1 to map and characterize structural variants in 17,795 deeply sequenced human genomes. We publicly release site-frequency data to create the largest, to our knowledge, whole-genome-sequencing-based structural variant resource so far. On average, individuals carry 2.9 rare structural variants that alter coding regions; these variants affect the dosage or structure of 4.2 genes and account for 4.0–11.2% of rare high-impact coding alleles. Using a computational model, we estimate that structural variants account for 17.2% of rare alleles genome-wide, with predicted deleterious effects that are equivalent to loss-of-function coding alleles; approximately 90% of such structural variants are noncoding deletions (mean 19.1 per genome). We report 158,991 ultra-rare structural variants and show that 2% of individuals carry ultra-rare megabase-scale structural variants, nearly half of which are balanced or complex rearrangements. Finally, we infer the dosage sensitivity of genes and noncoding elements, and reveal trends that relate to element class and conservation. This work will help to guide the analysis and interpretation of structural variants in the era of whole-genome sequencing. Structural variants in more than 17,000 human genomes are mapped and characterized using whole-genome sequencing, showing how this type of variation contributes to rare deleterious coding and noncoding alleles. [ABSTRACT FROM AUTHOR]
Published: 2020
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50. Transcript expression-aware annotation improves rare variant interpretation.

Author: Cummings, Beryl B., Karczewski, Konrad J., Kosmicki, Jack A., Seaby, Eleanor G., Watts, Nicholas A., Singer-Berk, Moriel, Mudge, Jonathan M., Karjalainen, Juha, Satterstrom, F. Kyle, O'Donnell-Luria, Anne H., Poterba, Timothy, Seed, Cotton, Solomonson, Matthew, Alföldi, Jessica, Genome Aggregation Database Production Team, Armean, Irina M., Banks, Eric, Bergelson, Louis, Cibulskis, Kristian, and Collins, Ryan L.
Abstract: The acceleration of DNA sequencing in samples from patients and population studies has resulted in extensive catalogues of human genetic variation, but the interpretation of rare genetic variants remains problematic. A notable example of this challenge is the existence of disruptive variants in dosage-sensitive disease genes, even in apparently healthy individuals. Here, by manual curation of putative loss-of-function (pLoF) variants in haploinsufficient disease genes in the Genome Aggregation Database (gnomAD)1, we show that one explanation for this paradox involves alternative splicing of mRNA, which allows exons of a gene to be expressed at varying levels across different cell types. Currently, no existing annotation tool systematically incorporates information about exon expression into the interpretation of variants. We develop a transcript-level annotation metric known as the 'proportion expressed across transcripts', which quantifies isoform expression for variants. We calculate this metric using 11,706 tissue samples from the Genotype Tissue Expression (GTEx) project2 and show that it can differentiate between weakly and highly evolutionarily conserved exons, a proxy for functional importance. We demonstrate that expression-based annotation selectively filters 22.8% of falsely annotated pLoF variants found in haploinsufficient disease genes in gnomAD, while removing less than 4% of high-confidence pathogenic variants in the same genes. Finally, we apply our expression filter to the analysis of de novo variants in patients with autism spectrum disorder and intellectual disability or developmental disorders to show that pLoF variants in weakly expressed regions have similar effect sizes to those of synonymous variants, whereas pLoF variants in highly expressed exons are most strongly enriched among cases. Our annotation is fast, flexible and generalizable, making it possible for any variant file to be annotated with any isoform expression dataset, and will be valuable for the genetic diagnosis of rare diseases, the analysis of rare variant burden in complex disorders, and the curation and prioritization of variants in recall-by-genotype studies. A novel variant annotation metric that quantifies the level of expression of genetic variants across tissues is validated in the Genome Aggregation Database (gnomAD) and is shown to improve rare variant interpretation. [ABSTRACT FROM AUTHOR]
Published: 2020
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