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29 results on '"Boyd, Justin D."'

1. Target engagement and immunogenicity of an active immunotherapeutic targeting pathological α-synuclein: a phase 1 placebo-controlled trial

Author

Eijsvogel, Pepijn, Misra, Pinaki, Concha-Marambio, Luis, Boyd, Justin D., Ding, Shuang, Fedor, Lauren, Hsieh, Yueh-Ting, Sun, Yu Shuang, Vroom, Madeline M., Farris, Carly M., Ma, Yihua, de Kam, Marieke L., Radanovic, Igor, Vissers, Maurits F. J. M., Mirski, Dario, Shareghi, Ghazal, Shahnawaz, Mohammad, Singer, Wolfgang, Kremer, Philip, Groeneveld, Geert Jan, Yu, Hui Jing, and Dodart, Jean-Cosme

Published
2024
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2. Optimizing the Cell Painting assay for image-based profiling

Author

Cimini, Beth A., Chandrasekaran, Srinivas Niranj, Kost-Alimova, Maria, Miller, Lisa, Goodale, Amy, Fritchman, Briana, Byrne, Patrick, Garg, Sakshi, Jamali, Nasim, Logan, David J., Concannon, John B., Lardeau, Charles-Hugues, Mouchet, Elizabeth, Singh, Shantanu, Shafqat Abbasi, Hamdah, Aspesi, Jr, Peter, Boyd, Justin D., Gilbert, Tamara, Gnutt, David, Hariharan, Santosh, Hernandez, Desiree, Hormel, Gisela, Juhani, Karolina, Melanson, Michelle, Mervin, Lewis H., Monteverde, Tiziana, Pilling, James E., Skepner, Adam, Swalley, Susanne E., Vrcic, Anita, Weisbart, Erin, Williams, Guy, Yu, Shan, Zapiec, Bolek, and Carpenter, Anne E.

Published
2023
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5. Genomic DISC1 Disruption in hiPSCs Alters Wnt Signaling and Neural Cell Fate

Author

Srikanth, Priya, Han, Karam, Callahan, Dana G, Makovkina, Eugenia, Muratore, Christina R, Lalli, Matthew A, Zhou, Honglin, Boyd, Justin D, Kosik, Kenneth S, Selkoe, Dennis J, and Young-Pearse, Tracy L

Subjects
Biological Sciences, Genetics, Human Genome, Stem Cell Research, Brain Disorders, Neurosciences, Serious Mental Illness, Schizophrenia, Stem Cell Research - Nonembryonic - Non-Human, Biotechnology, Mental Health, 2.1 Biological and endogenous factors, Aetiology, Mental health, Good Health and Well Being, Cells, Cultured, Forkhead Transcription Factors, Genome, Human, Humans, Induced Pluripotent Stem Cells, Nerve Tissue Proteins, Neural Stem Cells, Neurogenesis, Nonsense Mediated mRNA Decay, Protein Isoforms, T-Box Domain Proteins, Translocation, Genetic, Wnt Signaling Pathway, Biochemistry and Cell Biology, Medical Physiology, Biological sciences
Abstract

Genetic and clinical association studies have identified disrupted in schizophrenia 1 (DISC1) as a candidate risk gene for major mental illness. DISC1 is interrupted by a balanced chr(1;11) translocation in a Scottish family in which the translocation predisposes to psychiatric disorders. We investigate the consequences of DISC1 interruption in human neural cells using TALENs or CRISPR-Cas9 to target the DISC1 locus. We show that disruption of DISC1 near the site of the translocation results in decreased DISC1 protein levels because of nonsense-mediated decay of long splice variants. This results in an increased level of canonical Wnt signaling in neural progenitor cells and altered expression of fate markers such as Foxg1 and Tbr2. These gene expression changes are rescued by antagonizing Wnt signaling in a critical developmental window, supporting the hypothesis that DISC1-dependent suppression of basal Wnt signaling influences the distribution of cell types generated during cortical development.

Published
2015

7. JUMP Cell Painting dataset: morphological impact of 136,000 chemical and genetic perturbations

Author

Chandrasekaran, Srinivas Niranj, primary, Ackerman, Jeanelle, additional, Alix, Eric, additional, Ando, D. Michael, additional, Arevalo, John, additional, Bennion, Melissa, additional, Boisseau, Nicolas, additional, Borowa, Adriana, additional, Boyd, Justin D., additional, Brino, Laurent, additional, Byrne, Patrick J., additional, Ceulemans, Hugo, additional, Ch’ng, Carolyn, additional, Cimini, Beth A., additional, Clevert, Djork-Arne, additional, Deflaux, Nicole, additional, Doench, John G, additional, Dorval, Thierry, additional, Doyonnas, Regis, additional, Dragone, Vincenza, additional, Engkvist, Ola, additional, Faloon, Patrick W., additional, Fritchman, Briana, additional, Fuchs, Florian, additional, Garg, Sakshi, additional, Gilbert, Tamara J., additional, Glazer, David, additional, Gnutt, David, additional, Goodale, Amy, additional, Grignard, Jeremy, additional, Guenther, Judith, additional, Han, Yu, additional, Hanifehlou, Zahra, additional, Hariharan, Santosh, additional, Hernandez, Desiree, additional, Horman, Shane R, additional, Hormel, Gisela, additional, Huntley, Michael, additional, Icke, Ilknur, additional, Iida, Makiyo, additional, Jacob, Christina B., additional, Jaensch, Steffen, additional, Khetan, Jawahar, additional, Kost-Alimova, Maria, additional, Krawiec, Tomasz, additional, Kuhn, Daniel, additional, Lardeau, Charles-Hugues, additional, Lembke, Amanda, additional, Lin, Francis, additional, Little, Kevin D., additional, Lofstrom, Kenneth R., additional, Lotfi, Sofia, additional, Logan, David J., additional, Luo, Yi, additional, Madoux, Franck, additional, Marin Zapata, Paula A., additional, Marion, Brittany A., additional, Martin, Glynn, additional, McCarthy, Nicola Jane, additional, Mervin, Lewis, additional, Miller, Lisa, additional, Mohamed, Haseeb, additional, Monteverde, Tiziana, additional, Mouchet, Elizabeth, additional, Nicke, Barbara, additional, Ogier, Arnaud, additional, Ong, Anne-Laure, additional, Osterland, Marc, additional, Otrocka, Magdalena, additional, Peeters, Pieter J., additional, Pilling, James, additional, Prechtl, Stefan, additional, Qian, Chen, additional, Rataj, Krzysztof, additional, Root, David E, additional, Sakata, Sylvie K., additional, Scrace, Simon, additional, Shimizu, Hajime, additional, Simon, David, additional, Sommer, Peter, additional, Spruiell, Craig, additional, Sumia, Iffat, additional, Swalley, Susanne E, additional, Terauchi, Hiroki, additional, Thibaudeau, Amandine, additional, Unruh, Amy, additional, Van de Waeter, Jelle, additional, Van Dyck, Michiel, additional, van Staden, Carlo, additional, Warchoł, Michał, additional, Weisbart, Erin, additional, Weiss, Amélie, additional, Wiest-Daessle, Nicolas, additional, Williams, Guy, additional, Yu, Shan, additional, Zapiec, Bolek, additional, Żyła, Marek, additional, Singh, Shantanu, additional, and Carpenter, Anne E., additional

Published
2023
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10. Optimizing the Cell Painting assay for image-based profiling

Author

Cimini, Beth A., primary, Chandrasekaran, Srinivas Niranj, additional, Kost-Alimova, Maria, additional, Miller, Lisa, additional, Goodale, Amy, additional, Fritchman, Briana, additional, Byrne, Patrick, additional, Garg, Sakshi, additional, Jamali, Nasim, additional, Logan, David J., additional, Concannon, John B., additional, Lardeau, Charles-Hugues, additional, Mouchet, Elizabeth, additional, Singh, Shantanu, additional, Abbasi, Hamdah Shafqat, additional, Aspesi, Peter, additional, Boyd, Justin D., additional, Gilbert, Tamara, additional, Gnutt, David, additional, Hariharan, Santosh, additional, Hernandez, Desiree, additional, Hormel, Gisela, additional, Juhani, Karolina, additional, Melanson, Michelle, additional, Mervin, Lewis, additional, Monteverde, Tiziana, additional, Pilling, James E, additional, Skepner, Adam, additional, Swalley, Susanne E., additional, Vrcic, Anita, additional, Weisbart, Erin, additional, Williams, Guy, additional, Yu, Shan, additional, Zapiec, Bolek, additional, and Carpenter, Anne E., additional

Published
2022
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15. Generating Neurons from Stem Cells

Author

Androutsellis-Theotokis, Andreas, primary, Murase, Sachiko, additional, Boyd, Justin D., additional, Park, Deric M., additional, Hoeppner, Daniel J., additional, Ravin, Rea, additional, and McKay, Ronald D.G., additional

Published
2008
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20. Prolonged Treatment with Propofol Transiently Impairs Proliferation but Not Survival of Rat Neural Progenitor Cells In Vitro

Author

Palanisamy, Arvind, Friese, Matthew B., Cotran, Emily, Möller, Ludde, Boyd, Justin D., Crosby, Gregory, Culley, Deborah J., Palanisamy, Arvind, Friese, Matthew B., Cotran, Emily, Möller, Ludde, Boyd, Justin D., Crosby, Gregory, and Culley, Deborah J.

Abstract

Neurocognitive dysfunction is common in survivors of intensive care. Prolonged sedation has been implicated but the mechanisms are unclear. Neurogenesis continues into adulthood and is implicated in learning. The neural progenitor cells (NPC) that drive neurogenesis have receptors for the major classes of sedatives used clinically, suggesting that interruption of neurogenesis may partly contribute to cognitive decline in ICU survivors. Using an in vitro system, we tested the hypothesis that prolonged exposure to propofol concentration- and duration-dependently kills or markedly decreases the proliferation of NPCs. NPCs isolated from embryonic day 14 Sprague-Dawley rat pups were exposed to 0, 2.5, or 5.0 mu g/ mL of propofol, concentrations consistent with deep clinical anesthesia, for either 4 or 24 hours. Cells were assayed for cell death and proliferation either immediately following propofol exposure or 24 hours later. NPC death and apoptosis were measured by propidium iodine staining and cleaved caspase-3 immunocytochemistry, respectively, while proliferation was measured by EdU incorporation. Staurosporine (1 mu M for 6h) was used as a positive control for cell death. Cells were analyzed with unbiased high-throughput immunocytochemistry. There was no cell death at either concentration of propofol or duration of exposure. Neither concentration of propofol impaired NPC proliferation when exposure lasted 4 h, but when exposure lasted 24 h, propofol had an anti-proliferative effect at both concentrations (P < 0.0001, propofol vs. control). However, this effect was transient; proliferation returned to baseline 24 h after discontinuation of propofol (P = 0.37, propofol vs. control). The transient but reversible suppression of NPC proliferation, absence of cytotoxicity, and negligible effect on the neural stem cell pool pool suggest that propofol, even in concentrations used for clinical anesthesia, has limited impact on neural progenitor cell biology.

Published
2016
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23. The CD33 Alzheimer's disease locus: Correcting the functional consequences of the risk allele using small molecules

Author

Ryan, Katie J., primary, Boyd, Justin D., additional, Laversenne, Vanessa, additional, Chan, Gail, additional, Winn, Phoebe, additional, Frangieh, Michael, additional, Cimpean, Maria, additional, Mchenry, Alison, additional, Chibnik, Lori B., additional, Glicksman, Marcie A., additional, Dejager, Philip L., additional, and Bradshaw, Elizabeth M., additional

Published
2014
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26. Angiogenic Factors Stimulate Growth of Adult Neural Stem Cells

Author

Androutsellis-Theotokis, Andreas, primary, Rueger, Maria A., additional, Park, Deric M., additional, Boyd, Justin D., additional, Padmanabhan, Raji, additional, Campanati, Loraine, additional, Stewart, Craig V., additional, LeFranc, Yann, additional, Plenz, Dietmar, additional, Walbridge, Stuart, additional, Lonser, Russell R., additional, and McKay, Ronald D. G., additional

Published
2010
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27. Generating Neurons from Stem Cells.

Author

Walker, John M., Weiner, Leslie P., Androutsellis-Theotokis, Andreas, Murase, Sachiko, Boyd, Justin D., Park, Deric M., Hoeppner, Daniel J., Ravin, Rea, and McKay, Ronald D.G.

Abstract

Recent work shows that major developmental and clinical processes such as central nervous system regeneration and carcinogenesis involve stem cells (SCs) in the brain. In spite of this importance, the requirements of these SCs and their differentiated offspring (neurons, astrocytes, and oligodendrocytes) for survival and proper function are little understood. In vivo, the SCs themselves interact with their environment. This "SC niche" may be complex because it likely includes cells of the vascular and immune systems. The ability to maintain (1) and differentiate (1 -4) central nervous system (CNS) SCs in tissue culture where they can be pharmacologically or genetically (5) manipulated provides a powerful starting point for understanding their behavior. We present detailed information on the methods that permit CNS SCs to differentiate into functional neurons in tissue culture. Important aspects of the culture systems include (1) homogeneity, so that the input and output of a manipulation is known to involve the SC itself; (2) growth in monolayer to visualize and study individual SCs and their offspring; and (3) the use of fully defined culture components to exclude unknown factors from the culture. These conditions support the differentiation of functional, electrically active neurons. These methods allow cell growth and differentiation from normal adult and diseased tissue derived from both animal models and clinical samples. Ultimate validation of such a system comes from accurate prediction of in vivo effects, and the methods we present for CNS SC culture have also successfully predicted regenerative responses in the injured adult nervous system. [ABSTRACT FROM AUTHOR]

Published
2008
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28. Genomic DISC1Disruption in hiPSCs Alters Wnt Signaling and Neural Cell Fate

Author

Srikanth, Priya, Han, Karam, Callahan, Dana G., Makovkina, Eugenia, Muratore, Christina R., Lalli, Matthew A., Zhou, Honglin, Boyd, Justin D., Kosik, Kenneth S., Selkoe, Dennis J., and Young-Pearse, Tracy L.

Abstract

Genetic and clinical association studies have identified disrupted in schizophrenia 1 (DISC1) as a candidate risk gene for major mental illness. DISC1is interrupted by a balanced chr(1;11) translocation in a Scottish family in which the translocation predisposes to psychiatric disorders. We investigate the consequences of DISC1interruption in human neural cells using TALENs or CRISPR-Cas9 to target the DISC1locus. We show that disruption of DISC1near the site of the translocation results in decreased DISC1 protein levels because of nonsense-mediated decay of long splice variants. This results in an increased level of canonical Wnt signaling in neural progenitor cells and altered expression of fate markers such as Foxg1 and Tbr2. These gene expression changes are rescued by antagonizing Wnt signaling in a critical developmental window, supporting the hypothesis that DISC1-dependent suppression of basal Wnt signaling influences the distribution of cell types generated during cortical development.

Published
2015
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29. A New Means To Identify Type 3 Secreted Effectors: Functionally Interchangeable Class IB Chaperones Recognize a Conserved Sequence

Author

Schmitz, Alexa M., Jahufar, Fathima F., Boyd, Justin D., Cho, Min Y., Costa, Sonia, Glicksman, Marcie Ann, and Lesser, Cammie

Abstract

Many Gram-negative bacteria utilize specialized secretion systems to inject proteins (effectors) directly into host cells. Little is known regarding how bacteria ensure that only small subsets of the thousands of proteins they encode are recognized as substrates of the secretion systems, limiting their identification through bioinformatic analyses. Many of these proteins require chaperones to direct their secretion. Here, using the newly described protein interaction platform assay, we demonstrate that type 3 secretion system class IB chaperones from one bacterium directly bind their own effectors as well as those from other species. In addition, we observe that expression of class IB homologs from seven species, including pathogens and endosymbionts, mediate the translocation of effectors from Shigella directly into host cells, demonstrating that class IB chaperones are often functionally interchangeable. Notably, class IB chaperones bind numerous effectors. However, as previously proposed, they are not promiscuous; rather they recognize a defined sequence that we designate the conserved chaperone-binding domain (CCBD) sequence [(LMIF)\(_{1}\)XXX(IV)\(_{5}\)XX(IV)\(_{8}\)X(N)\(_{10}\)]. This sequence is the first defined amino acid sequence to be identified for any interspecies bacterial secretion system, i.e., a system that delivers proteins directly into eukaryotic cells. This sequence provides a new means to identify substrates of type III secretion systems. Indeed, using a pattern search algorithm for the CCBD sequence, we have identified the first two probable effectors from an endosymbiont, Sodalis glossinidius.

Published
2012
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