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7. Author Correction: Rare genetic coding variants associated with human longevity and protection against age-related diseases

Author

Lin, Jhih-Rong, Sin-Chan, Patrick, Napolioni, Valerio, Torres, Guillermo G., Mitra, Joydeep, Zhang, Quanwei, Jabalameli, M. Reza, Wang, Zhen, Nguyen, Nha, Gao, Tina, Laudes, Matthias, Görg, Siegfried, Franke, Andre, Nebel, Almut, Greicius, Michael D., Atzmon, Gil, Ye, Kenny, Gorbunova, Vera, Ladiges, Warren C., Shuldiner, Alan R., Niedernhofer, Laura J., Robbins, Paul D., Milman, Sofiya, Suh, Yousin, Vijg, Jan, Barzilai, Nir, and Zhang, Zhengdong D.

Published
2024
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8. Meeting Report: Aging Research and Drug Discovery

Author

Meron, Esther, Thaysen, Maria, Angeli, Suzanne, Antebi, Adam, Barzilai, Nir, Baur, Joseph A, Bekker-Jensen, Simon, Birkisdottir, Maria, Bischof, Evelyne, Bruening, Jens, Brunet, Anne, Buchwalter, Abigail, Cabreiro, Filipe, Cai, Shiqing, Chen, Brian H, Ermolaeva, Maria, Ewald, Collin Y, Ferrucci, Luigi, Florian, Maria Carolina, Fortney, Kristen, Freund, Adam, Georgievskaya, Anastasia, Gladyshev, Vadim N, Glass, David, Golato, Tyler, Gorbunova, Vera, Hoejimakers, Jan, Houtkooper, Riekelt H, Jager, Sibylle, Jaksch, Frank, Janssens, Georges, Jensen, Martin Borch, Kaeberlein, Matt, Karsenty, Gerard, de Keizer, Peter, Kennedy, Brian, Kirkland, James L, Kjaer, Michael, Kroemer, Guido, Lee, Kai-Fu, Lemaitre, Jean-Marc, Liaskos, David, Longo, Valter D, Lu, Yu-Xuan, MacArthur, Michael R, Maier, Andrea B, Manakanatas, Christina, Mitchell, Sarah J, Moskalev, Alexey, Niedernhofer, Laura, Ozerov, Ivan, Partridge, Linda, Passegué, Emmanuelle, Petr, Michael A, Peyer, James, Radenkovic, Dina, Rando, Thomas A, Rattan, Suresh, Riedel, Christian G, Rudolph, Lenhard, Ai, Ruixue, Serrano, Manuel, Schumacher, Björn, Sinclair, David A, Smith, Ryan, Suh, Yousin, Taub, Pam, Trapp, Alexandre, Trendelenburg, Anne-Ulrike, Valenzano, Dario Riccardo, Verburgh, Kris, Verdin, Eric, Vijg, Jan, Westendorp, Rudi GJ, Zonari, Alessandra, Bakula, Daniela, Zhavoronkov, Alex, and Scheibye-Knudsen, Morten

Subjects
Aging, aging, drug discovery, conference, AI, longevity, Biochemistry and Cell Biology, Physiology, Oncology and Carcinogenesis, Developmental Biology
Abstract

Aging is the single largest risk factor for most chronic diseases, and thus possesses large socioeconomic interest to continuously aging societies. Consequently, the field of aging research is expanding alongside a growing focus from the industry and investors in aging research. This year's 8th Annual Aging Research and Drug Discovery (ARDD) meeting was organized as a hybrid meeting from August 30th to September 3rd 2021 with more than 130 attendees participating on-site at the Ceremonial Hall at University of Copenhagen, Denmark, and 1800 engaging online. The conference comprised of presentations from 75 speakers focusing on new research in topics including mechanisms of aging and how these can be modulated as well as the use of AI and new standards of practices within aging research. This year, a longevity workshop was included to build stronger connections with the clinical community.

Published
2022

11. Age‐related telomere attrition causes aberrant gene expression in sub‐telomeric regions

Author

Dong, Xiao, Sun, Shixiang, Zhang, Lei, Kim, Seungsoo, Tu, Zhidong, Montagna, Cristina, Maslov, Alexander Y, Suh, Yousin, Wang, Tao, Campisi, Judith, and Vijg, Jan

Subjects
Biological Sciences, Bioinformatics and Computational Biology, Genetics, Aging, Human Genome, 2.1 Biological and endogenous factors, Adult, Aged, Cellular Senescence, Female, Gene Expression, Humans, Male, Middle Aged, Telomere, Young Adult, aging, gene expression, telomere shortening, Medical and Health Sciences, Developmental Biology, Biological sciences, Biomedical and clinical sciences
Abstract

Telomere attrition has been proposed as a biomarker and causal factor in aging. In addition to causing cellular senescence and apoptosis, telomere shortening has been found to affect gene expression in subtelomeric regions. Here, we analyzed the distribution of age-related differentially expressed genes from the GTEx RNA sequencing database of 54 tissue types from 979 human subjects and found significantly more upregulated than downregulated genes in subtelomeric regions as compared to the genome-wide average. Our data demonstrate spatial relationships between telomeres and gene expression in aging.

Published
2021

14. ARDD 2020: from aging mechanisms to interventions

Author

Mkrtchyan, Garik V, Abdelmohsen, Kotb, Andreux, Pénélope, Bagdonaite, Ieva, Barzilai, Nir, Brunak, Søren, Cabreiro, Filipe, de Cabo, Rafael, Campisi, Judith, Cuervo, Ana Maria, Demaria, Marco, Ewald, Collin Y, Fang, Evandro Fei, Faragher, Richard, Ferrucci, Luigi, Freund, Adam, Silva-García, Carlos G, Georgievskaya, Anastasia, Gladyshev, Vadim N, Glass, David J, Gorbunova, Vera, de Grey, Aubrey, He, Wei-Wu, Hoeijmakers, Jan, Hoffmann, Eva, Horvath, Steve, Houtkooper, Riekelt H, Jensen, Majken K, Jensen, Martin Borch, Kane, Alice, Kassem, Moustapha, de Keizer, Peter, Kennedy, Brian, Karsenty, Gerard, Lamming, Dudley W, Lee, Kai-Fu, MacAulay, Nanna, Mamoshina, Polina, Mellon, Jim, Molenaars, Marte, Moskalev, Alexey, Mund, Andreas, Niedernhofer, Laura, Osborne, Brenna, Pak, Heidi H, Parkhitko, Andrey, Raimundo, Nuno, Rando, Thomas A, Rasmussen, Lene Juel, Reis, Carolina, Riedel, Christian G, Franco-Romero, Anais, Schumacher, Björn, Sinclair, David A, Suh, Yousin, Taub, Pam R, Toiber, Debra, Treebak, Jonas T, Valenzano, Dario Riccardo, Verdin, Eric, Vijg, Jan, Young, Sergey, Zhang, Lei, Bakula, Daniela, Zhavoronkov, Alex, and Scheibye-Knudsen, Morten

Subjects
Biochemistry and Cell Biology, Biomedical and Clinical Sciences, Clinical Sciences, Biological Sciences, Aging, Good Health and Well Being, Artificial Intelligence, Biomedical Research, Cellular Senescence, Congresses as Topic, Drug Discovery, Humans, Life Style, Longevity, Pharmaceutical Preparations, aging, interventions, drug discovery, artificial intelligence, Biochemistry and cell biology, Clinical sciences
Abstract

Aging is emerging as a druggable target with growing interest from academia, industry and investors. New technologies such as artificial intelligence and advanced screening techniques, as well as a strong influence from the industry sector may lead to novel discoveries to treat age-related diseases. The present review summarizes presentations from the 7th Annual Aging Research and Drug Discovery (ARDD) meeting, held online on the 1st to 4th of September 2020. The meeting covered topics related to new methodologies to study aging, knowledge about basic mechanisms of longevity, latest interventional strategies to target the aging process as well as discussions about the impact of aging research on society and economy. More than 2000 participants and 65 speakers joined the meeting and we already look forward to an even larger meeting next year. Please mark your calendars for the 8th ARDD meeting that is scheduled for the 31st of August to 3rd of September, 2021, at Columbia University, USA.

Published
2020

15. Mitigating age-related somatic mutation burden

Author

Vijg, Jan, Schumacher, Björn, Abakir, Abdulkadir, Antonov, Michael, Bradley, Chris, Cagan, Alex, Church, George, Gladyshev, Vadim N., Gorbunova, Vera, Maslov, Alexander Y., Reik, Wolf, Sharifi, Samim, Suh, Yousin, and Walsh, Kenneth

Published
2023
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18. The shortness of human life constitutes its limit

Author

Milholland, Brandon, Dong, Xiao, and Vijg, Jan

Subjects
Statistics - Applications, Quantitative Biology - Populations and Evolution
Abstract

In this paper, we affirm our earlier findings of evidence for a limit to human lifespan. In particular, we assess the analyses in extreme value theory (EVT) performed by Rootz\'en and Zholud. We find that their criticisms of our work are unfounded and that their analyses are contradicted by several other papers using EVT. Furthermore, we find that even if we completely accept the conclusions about late-life human mortality reached by Rootz\'en and Zholud, their results do not actually contradict the findings presented in our original paper: whether unbounded or not, human lifespan is unlikely to greatly exceed 120 years, and the improbability of longer survival---whether it is exactly zero or merely astronomically small---acts as a de facto limit. In order to eliminate the confusion surrounding the issue, we propose the adoption of the term "limit" to denote the age at which the chance of survival is exactly zero and the term "effective limit" to denote the age at which the change of survival falls below a given threshold. Once this distinction is made, it can be demonstrated that the final result of Rootz\'en and Zholud is essentially a recapitulation of the main conclusion of our paper. Ultimately, much of the controversy surrounding the issue of a limit to human lifespan can be avoided by carefully reading the literature and applying statistics to practical human scales., Comment: 11 pages, 1 figure, 1 table

Published
2018

19. A direct comparison of interphase FISH versus low-coverage single cell sequencing to detect aneuploidy reveals respective strengths and weaknesses.

Author

Andriani, Grasiella A, Maggi, Elaine, Piqué, Daniel, Zimmerman, Samuel E, Lee, Moonsook, Quispe-Tintaya, Wilber, Maslov, Alexander, Campisi, Judith, Vijg, Jan, Mar, Jessica C, and Montagna, Cristina

Subjects
Biochemistry and Cell Biology, Other Physical Sciences
Abstract

Aneuploidy has been reported to occur at remarkably high levels in normal somatic tissues using Fluorescence In Situ Hybridization (FISH). Recently, these reports were contradicted by single-cell low-coverage whole genome sequencing (scL-WGS) analyses, which showed aneuploidy frequencies at least an order of magnitude lower. To explain these seemingly contradictory findings, we used both techniques to analyze artificially generated mock aneuploid cells and cells with natural random aneuploidy. Our data indicate that while FISH tended to over-report aneuploidies, a modified 2-probe approach can accurately detect low levels of aneuploidy. Further, scL-WGS tends to underestimate aneuploidy levels, especially in a polyploid background.

Published
2019

20. Erratum To: A rare human centenarian variant of SIRT6 enhances genome stability and interaction with Lamin A

Author

Simon, Matthew, Yang, Jiping, Gigas, Jonathan, Earley, Eric J, Hillpot, Eric, Zhang, Lei, Zagorulya, Maria, Tombline, Greg, Gilbert, Michael, Yuen, Samantha L, Pope, Alexis, Van Meter, Michael, Emmrich, Stephan, Firsanov, Denis, Athreya, Advait, Biashad, Seyed Ali, Han, Jeehae, Ryu, Seungjin, Tare, Archana, Zhu, Yizhou, Hudgins, Adam, Atzmon, Gil, Barzilai, Nir, Wolfe, Aaron, Moody, Kelsey, Garcia, Benjamin A, Robbins, Paul D, Vijg, Jan, Seluanov, Andrei, Suh, Yousin, and Gorbunova, Vera

Published
2023
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22. A rare human centenarian variant of SIRT6 enhances genome stability and interaction with Lamin A

Author

Simon, Matthew, Yang, Jiping, Gigas, Jonathan, Earley, Eric J, Hillpot, Eric, Zhang, Lei, Zagorulya, Maria, Tombline, Greg, Gilbert, Michael, Yuen, Samantha L, Pope, Alexis, Van Meter, Michael, Emmrich, Stephan, Firsanov, Denis, Athreya, Advait, Biashad, Seyed Ali, Han, Jeehae, Ryu, Seungjin, Tare, Archana, Zhu, Yizhou, Hudgins, Adam, Atzmon, Gil, Barzilai, Nir, Wolfe, Aaron, Moody, Kelsey, Garcia, Benjamin A, Thomas, David D, Robbins, Paul D, Vijg, Jan, Seluanov, Andrei, Suh, Yousin, and Gorbunova, Vera

Published
2022
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23. Negative Selection Allows DNA Mismatch Repair-Deficient Mouse Fibroblasts In Vitro to Tolerate High Levels of Somatic Mutations

Author

Zhang, Lei, primary, Lee, Moonsook, additional, Hao, Xiaoxiao, additional, Ehlert, Joseph, additional, Chi, Zhongxuan, additional, Jin, Bo, additional, Maslov, Alexander Y., additional, Barabasi, Albert-Laszlo, additional, Hoeijmakers, Jan H. J., additional, Edelmann, Winfried, additional, Vijg, Jan, additional, and Dong, Xiao, additional

Published
2024
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27. Analysis of individual cells identifies cell‐to‐cell variability following induction of cellular senescence

Author

Wiley, Christopher D, Flynn, James M, Morrissey, Christapher, Lebofsky, Ronald, Shuga, Joe, Dong, Xiao, Unger, Marc A, Vijg, Jan, Melov, Simon, and Campisi, Judith

Subjects
Cancer, Biotechnology, Genetics, Aetiology, 2.1 Biological and endogenous factors, Bleomycin, Cell Cycle Proteins, Cell Line, Cellular Senescence, Cytokines, Fetus, Fibroblasts, Gene Expression Profiling, Gene Expression Regulation, Genetic Variation, Humans, Lung, Microfluidics, Nanotechnology, Polymerase Chain Reaction, Protein Interaction Mapping, Signal Transduction, Single-Cell Analysis, Transcriptome, beta-Galactosidase, aging, cellular senescence, cytokines, single cell, transcriptomics, Biological Sciences, Medical and Health Sciences, Developmental Biology
Abstract

Senescent cells play important roles in both physiological and pathological processes, including cancer and aging. In all cases, however, senescent cells comprise only a small fraction of tissues. Senescent phenotypes have been studied largely in relatively homogeneous populations of cultured cells. In vivo, senescent cells are generally identified by a small number of markers, but whether and how these markers vary among individual cells is unknown. We therefore utilized a combination of single-cell isolation and a nanofluidic PCR platform to determine the contributions of individual cells to the overall gene expression profile of senescent human fibroblast populations. Individual senescent cells were surprisingly heterogeneous in their gene expression signatures. This cell-to-cell variability resulted in a loss of correlation among the expression of several senescence-associated genes. Many genes encoding senescence-associated secretory phenotype (SASP) factors, a major contributor to the effects of senescent cells in vivo, showed marked variability with a subset of highly induced genes accounting for the increases observed at the population level. Inflammatory genes in clustered genomic loci showed a greater correlation with senescence compared to nonclustered loci, suggesting that these genes are coregulated by genomic location. Together, these data offer new insights into how genes are regulated in senescent cells and suggest that single markers are inadequate to identify senescent cells in vivo.

Published
2017

29. Rare genetic coding variants associated with human longevity and protection against age-related diseases

Author

Lin, Jhih-Rong, Sin-Chan, Patrick, Napolioni, Valerio, Torres, Guillermo G., Mitra, Joydeep, Zhang, Quanwei, Jabalameli, M. Reza, Wang, Zhen, Nguyen, Nha, Gao, Tina, Laudes, Matthias, Görg, Siegfried, Franke, Andre, Nebel, Almut, Greicius, Michael D., Atzmon, Gil, Ye, Kenny, Gorbunova, Vera, Ladiges, Warren C., Shuldiner, Alan R., Niedernhofer, Laura J., Robbins, Paul D., Milman, Sofiya, Suh, Yousin, Vijg, Jan, Barzilai, Nir, and Zhang, Zhengdong D.

Published
2021
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31. The central role of DNA damage in the ageing process

Author

Schumacher, Björn, Pothof, Joris, Vijg, Jan, and Hoeijmakers, Jan H. J.

Subjects
Aging -- Genetic aspects, DNA damage -- Physiological aspects, Environmental issues, Science and technology, Zoology and wildlife conservation
Abstract

Ageing is a complex, multifaceted process leading to widespread functional decline that affects every organ and tissue, but it remains unknown whether ageing has a unifying causal mechanism or is grounded in multiple sources. Phenotypically, the ageing process is associated with a wide variety of features at the molecular, cellular and physiological level--for example, genomic and epigenomic alterations, loss of proteostasis, declining overall cellular and subcellular function and deregulation of signalling systems. However, the relative importance, mechanistic interrelationships and hierarchical order of these features of ageing have not been clarified. Here we synthesize accumulating evidence that DNA damage affects most, if not all, aspects of the ageing phenotype, making it a potentially unifying cause of ageing. Targeting DNA damage and its mechanistic links with the ageing phenotype will provide a logical rationale for developing unified interventions to counteract age-related dysfunction and disease. This Review examines the evidence showing that DNA damage is associated with ageing phenotypes, suggesting that it may have a central role as the cause of ageing., Author(s): Björn Schumacher [sup.1] [sup.2] , Joris Pothof [sup.3] , Jan Vijg [sup.4] [sup.5] , Jan H. J. Hoeijmakers [sup.1] [sup.2] [sup.3] [sup.6] Author Affiliations: (1) Institute for Genome Stability [...]

Published
2021
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34. Whole Chromosome Instability induces senescence and promotes SASP.

Author

Andriani, Grasiella Angelina, Almeida, Vinnycius Pereira, Faggioli, Francesca, Mauro, Maurizio, Tsai, Wanxia Li, Santambrogio, Laura, Maslov, Alexander, Gadina, Massimo, Campisi, Judith, Vijg, Jan, and Montagna, Cristina

Subjects
Cells, Cultured, Humans, DNA Damage, Chromosomal Instability, Protein-Serine-Threonine Kinases, Cell Cycle Proteins, Chromosomal Proteins, Non-Histone, In Situ Hybridization, Fluorescence, Apoptosis, Cell Proliferation, Phenotype, Gene Knockdown Techniques, Cellular Senescence, Biochemistry and Cell Biology, Other Physical Sciences
Abstract

Age-related accumulation of ploidy changes is associated with decreased expression of genes controlling chromosome segregation and cohesin functions. To determine the consequences of whole chromosome instability (W-CIN) we down-regulated the spindle assembly checkpoint component BUB1 and the mitotic cohesin SMC1A, and used four-color-interphase-FISH coupled with BrdU incorporation and analyses of senescence features to reveal the fate of W-CIN cells. We observed significant correlations between levels of not-diploid cells and senescence-associated features (SAFs). W-CIN induced DNA double strand breaks and elevated oxidative stress, but caused low apoptosis. SAFs of W-CIN cells were remarkably similar to those induced by replicative senescence but occurred in only 13 days versus 4 months. Cultures enriched with not-diploid cells acquired a senescence-associated secretory phenotype (SASP) characterized by IL1B, CXCL8, CCL2, TNF, CCL27 and other pro-inflammatory factors including a novel SASP component CLEC11A. These findings suggest that W-CIN triggers premature senescence, presumably to prevent the propagation of cells with an abnormal DNA content. Cells deviating from diploidy have the ability to communicate with their microenvironment by secretion of an array of signaling factors. Our results suggest that aneuploid cells that accumulate during aging in some mammalian tissues potentially contribute to age-related pathologies and inflammation through SASP secretion.

Published
2016

38. SIRT6 Is Responsible for More Efficient DNA Double-Strand Break Repair in Long-Lived Species

Author

Tian, Xiao, Firsanov, Denis, Zhang, Zhihui, Cheng, Yang, Luo, Lingfeng, Tombline, Gregory, Tan, Ruiyue, Simon, Matthew, Henderson, Steven, Steffan, Janine, Goldfarb, Audrey, Tam, Jonathan, Zheng, Kitty, Cornwell, Adam, Johnson, Adam, Yang, Jiang-Nan, Mao, Zhiyong, Manta, Bruno, Dang, Weiwei, Zhang, Zhengdong, Vijg, Jan, Wolfe, Aaron, Moody, Kelsey, Kennedy, Brian K., Bohmann, Dirk, Gladyshev, Vadim N., Seluanov, Andrei, and Gorbunova, Vera

Published
2019
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42. Single-cell analysis of somatic mutation burden in mammary epithelial cells of pathogenic BRCA1/2 mutation carriers

Author

Sun, Shixiang, Brazhnik, Kristina, Lee, Moonsook, Maslov, Alexander Y., Zhang, Yi, Huang, Zhenqiu, Klugman, Susan, Park, Ben H., Vijg, Jan, and Montagna, Cristina

Subjects
Oncology, Experimental, Somatic cells -- Genetic aspects, Epithelial cells -- Genetic aspects, Breast cancer -- Genetic aspects -- Development and progression -- Risk factors, Cancer -- Research, BRCA mutations -- Research, Health care industry
Abstract

Inherited germline mutations in the breast cancer gene 1 (BRCA1) or BRCA2 genes (herein BRCA1/2) greatly increase the risk of breast and ovarian cancer, presumably by elevating somatic mutational errors as a consequence of deficient DNA repair. However, this has never been directly demonstrated by a comprehensive analysis of the somatic mutational landscape of primary, noncancer, mammary epithelial cells of women diagnosed with pathogenic BRCA1/2 germline mutations. Here, we used an accurate, single-cell whole-genome sequencing approach to first show that telomerized primary mammary epithelial cells heterozygous for a highly penetrant BRCA1 variant displayed a robustly elevated mutation frequency as compared with their isogenic control cells. We then demonstrated a small but statistically significant increase in mutation frequency in mammary epithelial cells isolated from the breast of BRCA1/2 mutation carriers as compared with those obtained from age-matched controls with no genetically increased risk for breast cancer., Introduction Breast cancer is the most common cancer in women worldwide (1). Up to 10% of breast cancer is due to genetic predisposition (2), with inherited mutations in breast cancer [...]

Published
2022
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43. Impact papers on aging in 2009

Author

Blagosklonny, Mikhail V, Campisi, Judy, Sinclair, David A, Bartke, Andrzej, Blasco, Maria A, Bonner, William M, Bohr, Vilhelm A, Jr, Robert M Brosh, Brunet, Anne, DePinho, Ronald A, Donehower, Lawrence A, Finch, Caleb E, Finkel, Toren, Gorospe, Myriam, Gudkov, Andrei V, Hall, Michael N, Hekimi, Siegfried, Helfand, Stephen L, Karlseder, Jan, Kenyon, Cynthia, Kroemer, Guido, Longo, Valter, Nussenzweig, Andre, Osiewacz, Heinz D, Peeper, Daniel S, Rando, Thomas A, Rudolph, K Lenhard, Sassone-Corsi, Paolo, Serrano, Manuel, Sharpless, Norman E, Skulachev, Vladimir P, Tilly, Jonathan L, Tower, John, Verdin, Eric, and Vijg, Jan

Subjects
Biochemistry and Cell Biology, Biological Sciences, Genetics, Aging, 1.1 Normal biological development and functioning, Underpinning research, Good Health and Well Being, Adult Stem Cells, Animals, Autophagy, Caloric Restriction, Cellular Reprogramming, Circadian Rhythm, DNA Damage, Humans, Mitochondria, Neoplasms, Oxidative Stress, RNA Processing, Post-Transcriptional, Telomere, aging, senescence, signal transduction, genes for longevity, Biochemistry and cell biology, Clinical sciences
Abstract

The Editorial Board of Aging reviews research papers published in 2009, which they believe have or will have significant impact on aging research. Among many others, the topics include genes that accelerate aging or in contrast promote longevity in model organisms, DNA damage responses and telomeres, molecular mechanisms of life span extension by calorie restriction and pharmacological interventions into aging. The emerging message in 2009 is that aging is not random but determined by a genetically-regulated longevity network and can be decelerated both genetically and pharmacologically.

Published
2010

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