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892 results on '"Greenberg, Michael E."'

1. Developmental dynamics of RNA translation in the human brain

Author

Duffy, Erin E, Finander, Benjamin, Choi, GiHun, Carter, Ava C, Pritisanac, Iva, Alam, Aqsa, Luria, Victor, Karger, Amir, Phu, William, Sherman, Maxwell A, Assad, Elena G, Pajarillo, Naomi, Khitun, Alexandra, Crouch, Elizabeth E, Ganesh, Sanika, Chen, Jin, Berger, Bonnie, Sestan, Nenad, O’Donnell-Luria, Anne, Huang, Eric J, Griffith, Eric C, Forman-Kay, Julie D, Moses, Alan M, Kalish, Brian T, and Greenberg, Michael E

Subjects
Biological Psychology, Biomedical and Clinical Sciences, Neurosciences, Psychology, Stem Cell Research - Induced Pluripotent Stem Cell - Human, Stem Cell Research - Induced Pluripotent Stem Cell, Stem Cell Research - Nonembryonic - Human, Genetics, Biotechnology, Stem Cell Research, Underpinning research, 1.1 Normal biological development and functioning, Neurological, Adult, Arginine, Brain, Gene Expression Regulation, Glycine, Humans, Protein Biosynthesis, RNA, Messenger, Cognitive Sciences, Neurology & Neurosurgery, Biological psychology
Abstract

The precise regulation of gene expression is fundamental to neurodevelopment, plasticity and cognitive function. Although several studies have profiled transcription in the developing human brain, there is a gap in understanding of accompanying translational regulation. In this study, we performed ribosome profiling on 73 human prenatal and adult cortex samples. We characterized the translational regulation of annotated open reading frames (ORFs) and identified thousands of previously unknown translation events, including small ORFs that give rise to human-specific and/or brain-specific microproteins, many of which we independently verified using proteomics. Ribosome profiling in stem-cell-derived human neuronal cultures corroborated these findings and revealed that several neuronal activity-induced non-coding RNAs encode previously undescribed microproteins. Physicochemical analysis of brain microproteins identified a class of proteins that contain arginine-glycine-glycine (RGG) repeats and, thus, may be regulators of RNA metabolism. This resource expands the known translational landscape of the human brain and illuminates previously unknown brain-specific protein products.

Published
2022

2. Thyroid hormone remodels cortex to coordinate body-wide metabolism and exploration

Author

Hochbaum, Daniel R., Hulshof, Lauren, Urke, Amanda, Wang, Wengang, Dubinsky, Alexandra C., Farnsworth, Hannah C., Hakim, Richard, Lin, Sherry, Kleinberg, Giona, Robertson, Keiramarie, Park, Canaria, Solberg, Alyssa, Yang, Yechan, Baynard, Caroline, Nadaf, Naeem M., Beron, Celia C., Girasole, Allison E., Chantranupong, Lynne, Cortopassi, Marissa D., Prouty, Shannon, Geistlinger, Ludwig, Banks, Alexander S., Scanlan, Thomas S., Datta, Sandeep Robert, Greenberg, Michael E., Boulting, Gabriella L., Macosko, Evan Z., and Sabatini, Bernardo L.

Published
2024
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5. A NPAS4–NuA4 complex couples synaptic activity to DNA repair

Author

Pollina, Elizabeth A., Gilliam, Daniel T., Landau, Andrew T., Lin, Cindy, Pajarillo, Naomi, Davis, Christopher P., Harmin, David A., Yap, Ee-Lynn, Vogel, Ian R., Griffith, Eric C., Nagy, M. Aurel, Ling, Emi, Duffy, Erin E., Sabatini, Bernardo L., Weitz, Charles J., and Greenberg, Michael E.

Published
2023
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8. Correction

Author

Kalish, Brian T., Barkat, Tania R., Diel, Erin E., Zhang, Elizabeth J., Greenberg, Michael E., and Hensch, Takao K.

Published
2020

11. Kinesin superfamily protein Kif26b links Wnt5a-Ror signaling to the control of cell and tissue behaviors in vertebrates.

Author

Susman, Michael W, Karuna, Edith P, Kunz, Ryan C, Gujral, Taranjit S, Cantú, Andrea V, Choi, Shannon S, Jong, Brigette Y, Okada, Kyoko, Scales, Michael K, Hum, Jennie, Hu, Linda S, Kirschner, Marc W, Nishinakamura, Ryuichi, Yamada, Soichiro, Laird, Diana J, Jao, Li-En, Gygi, Steven P, Greenberg, Michael E, and Ho, Hsin-Yi Henry

Subjects
Cell Line, Animals, Mice, Inbred C57BL, Humans, Mice, Kinesin, Proteomics, Signal Transduction, Gene Expression Regulation, Developmental, Morphogenesis, Embryonic Development, beta Catenin, Receptor Tyrosine Kinase-like Orphan Receptors, HEK293 Cells, Wnt Signaling Pathway, Wnt-5a Protein, Kif26b, Ror, developmental biology, mouse, noncanonical Wnt signaling, regulated proteolysis, signal transduction, stem cells, tissue morphogenesis, Regenerative Medicine, Stem Cell Research, 1.1 Normal biological development and functioning, Biochemistry and Cell Biology
Abstract

Wnt5a-Ror signaling constitutes a developmental pathway crucial for embryonic tissue morphogenesis, reproduction and adult tissue regeneration, yet the molecular mechanisms by which the Wnt5a-Ror pathway mediates these processes are largely unknown. Using a proteomic screen, we identify the kinesin superfamily protein Kif26b as a downstream target of the Wnt5a-Ror pathway. Wnt5a-Ror, through a process independent of the canonical Wnt/β-catenin-dependent pathway, regulates the cellular stability of Kif26b by inducing its degradation via the ubiquitin-proteasome system. Through this mechanism, Kif26b modulates the migratory behavior of cultured mesenchymal cells in a Wnt5a-dependent manner. Genetic perturbation of Kif26b function in vivo caused embryonic axis malformations and depletion of primordial germ cells in the developing gonad, two phenotypes characteristic of disrupted Wnt5a-Ror signaling. These findings indicate that Kif26b links Wnt5a-Ror signaling to the control of morphogenetic cell and tissue behaviors in vertebrates and reveal a new role for regulated proteolysis in noncanonical Wnt5a-Ror signal transduction.

Published
2017

15. Unidirectional Eph/ephrin signaling creates a cortical actomyosin differential to drive cell segregation.

Author

O'Neill, Audrey K, Kindberg, Abigail A, Niethamer, Terren K, Larson, Andrew R, Ho, Hsin-Yi Henry, Greenberg, Michael E, and Bush, Jeffrey O

Subjects
Neuroepithelial Cells, Animals, Humans, Mice, Actins, Receptors, Eph Family, Ephrin-B1, Actomyosin, Green Fluorescent Proteins, Cell Count, Signal Transduction, Cell Differentiation, Models, Biological, Embryo, Mammalian, rho-Associated Kinases, HEK293 Cells, Receptors, Eph Family, Models, Biological, Embryo, Mammalian, Developmental Biology, Biological Sciences, Medical and Health Sciences
Abstract

Cell segregation is the process by which cells self-organize to establish developmental boundaries, an essential step in tissue formation. Cell segregation is a common outcome of Eph/ephrin signaling, but the mechanisms remain unclear. In craniofrontonasal syndrome, X-linked mosaicism for ephrin-B1 expression has been hypothesized to lead to aberrant Eph/ephrin-mediated cell segregation. Here, we use mouse genetics to exploit mosaicism to study cell segregation in the mammalian embryo and integrate live-cell imaging to examine the underlying cellular and molecular mechanisms. Our data demonstrate that dramatic ephrin-B1-mediated cell segregation occurs in the early neuroepithelium. In contrast to the paradigm that repulsive bidirectional signaling drives cell segregation, unidirectional EphB kinase signaling leads to cell sorting by the Rho kinase-dependent generation of a cortical actin differential between ephrin-B1- and EphB-expressing cells. These results define mechanisms of Eph/ephrin-mediated cell segregation, implicating unidirectional regulation of cortical actomyosin contractility as a key effector of this fundamental process.

Published
2016

16. Neurons that regulate mouse torpor

Author

Hrvatin, Sinisa, Sun, Senmiao, Wilcox, Oren F., Yao, Hanqi, Lavin-Peter, Aurora J., Cicconet, Marcelo, Assad, Elena G., Palmer, Michaela E., Aronson, Sage, Banks, Alexander S., Griffith, Eric C., and Greenberg, Michael E.

Published
2020
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18. Using Whole-Exome Sequencing to Identify Inherited Causes of Autism

Author

Yu, Timothy W, Chahrour, Maria H, Coulter, Michael E, Jiralerspong, Sarn, Okamura-Ikeda, Kazuko, Ataman, Bulent, Schmitz-Abe, Klaus, Harmin, David A, Adli, Mazhar, Malik, Athar N, D’Gama, Alissa M, Lim, Elaine T, Sanders, Stephan J, Mochida, Ganesh H, Partlow, Jennifer N, Sunu, Christine M, Felie, Jillian M, Rodriguez, Jacqueline, Nasir, Ramzi H, Ware, Janice, Joseph, Robert M, Hill, R Sean, Kwan, Benjamin Y, Al-Saffar, Muna, Mukaddes, Nahit M, Hashmi, Asif, Balkhy, Soher, Gascon, Generoso G, Hisama, Fuki M, LeClair, Elaine, Poduri, Annapurna, Oner, Ozgur, Al-Saad, Samira, Al-Awadi, Sadika A, Bastaki, Laila, Ben-Omran, Tawfeg, Teebi, Ahmad S, Al-Gazali, Lihadh, Eapen, Valsamma, Stevens, Christine R, Rappaport, Leonard, Gabriel, Stacey B, Markianos, Kyriacos, State, Matthew W, Greenberg, Michael E, Taniguchi, Hisaaki, Braverman, Nancy E, Morrow, Eric M, and Walsh, Christopher A

Subjects
Biological Psychology, Biomedical and Clinical Sciences, Neurosciences, Psychology, Human Genome, Brain Disorders, Genetic Testing, Genetics, Clinical Research, Intellectual and Developmental Disabilities (IDD), Mental Health, Autism, Pediatric, 2.1 Biological and endogenous factors, Aetiology, Adolescent, Animals, Autistic Disorder, Cells, Cultured, Child, Child, Preschool, Cohort Studies, Exome, Female, Genome-Wide Association Study, Humans, Male, Pedigree, Rats, Sequence Analysis, DNA, Young Adult, Cognitive Sciences, Neurology & Neurosurgery, Biological psychology
Abstract

Despite significant heritability of autism spectrum disorders (ASDs), their extreme genetic heterogeneity has proven challenging for gene discovery. Studies of primarily simplex families have implicated de novo copy number changes and point mutations, but are not optimally designed to identify inherited risk alleles. We apply whole-exome sequencing (WES) to ASD families enriched for inherited causes due to consanguinity and find familial ASD associated with biallelic mutations in disease genes (AMT, PEX7, SYNE1, VPS13B, PAH, and POMGNT1). At least some of these genes show biallelic mutations in nonconsanguineous families as well. These mutations are often only partially disabling or present atypically, with patients lacking diagnostic features of the Mendelian disorders with which these genes are classically associated. Our study shows the utility of WES for identifying specific genetic conditions not clinically suspected and the importance of partial loss of gene function in ASDs.

Published
2013

20. A chemical genetic approach reveals distinct EphB signaling mechanisms during brain development.

Author

Soskis, Michael J, Ho, Hsin-Yi Henry, Bloodgood, Brenda L, Robichaux, Michael A, Malik, Athar N, Ataman, Bulent, Rubin, Alex A, Zieg, Janine, Zhang, Chao, Shokat, Kevan M, Sharma, Nikhil, Cowan, Christopher W, and Greenberg, Michael E

Subjects
Brain, Cells, Cultured, Animals, Mice, Inbred C57BL, Mice, Transgenic, Humans, Mice, Rats, Receptors, Eph Family, Organ Culture Techniques, Protein Engineering, Signal Transduction, Brain Chemistry, Amino Acid Sequence, Pregnancy, Molecular Sequence Data, Female, Gene Knock-In Techniques, Mice, 129 Strain, HEK293 Cells, Cells, Cultured, Inbred C57BL, Transgenic, Receptors, Eph Family, Strain, Neurology & Neurosurgery, Neurosciences, Psychology, Cognitive Sciences
Abstract

EphB receptor tyrosine kinases control multiple steps in nervous system development. However, it remains unclear whether EphBs regulate these different developmental processes directly or indirectly. In addition, given that EphBs signal through multiple mechanisms, it has been challenging to define which signaling functions of EphBs regulate particular developmental events. To address these issues, we engineered triple knock-in mice in which the kinase activity of three neuronally expressed EphBs can be rapidly, reversibly and specifically blocked. We found that the tyrosine kinase activity of EphBs was required for axon guidance in vivo. In contrast, EphB-mediated synaptogenesis occurred normally when the kinase activity of EphBs was inhibited, suggesting that EphBs mediate synapse development by an EphB tyrosine kinase-independent mechanism. Taken together, our data indicate that EphBs control axon guidance and synaptogenesis by distinct mechanisms and provide a new mouse model for dissecting EphB function in development and disease.

Published
2012

24. Stress-Dependent Regulation of FOXO Transcription Factors by the SIRT1 Deacetylase

Author

Brunet, Anne, Sweeney, Lora B., Sturgill, J. Fitzhugh, Chua, Katrin F., Greer, Paul L., Lin, Yingxi, Tran, Hien, Ross, Sarah E., Mostoslavsky, Raul, Cohen, Haim Y., Hu, Linda S., Cheng, Hwei-Ling, Jedrychowski, Mark P., Gygi, Steven P., Sinclair, David A., Alt, Frederick W., and Greenberg, Michael E.

Published
2004

25. Thyroid hormone rewires cortical circuits to coordinate body-wide metabolism and exploratory drive

Author

Hochbaum, Daniel R., primary, Dubinsky, Alexandra C., additional, Farnsworth, Hannah C., additional, Hulshof, Lauren, additional, Kleinberg, Giona, additional, Urke, Amanda, additional, Wang, Wengang, additional, Hakim, Richard, additional, Robertson, Keira, additional, Park, Canaria, additional, Solberg, Alyssa, additional, Yang, Yechan, additional, Baynard, Caroline, additional, Nadaf, Naeem M., additional, Beron, Celia C., additional, Girasole, Allison E., additional, Chantranupong, Lynne, additional, Cortopassi, Marissa, additional, Prouty, Shannon, additional, Geistlinger, Ludwig, additional, Banks, Alexander, additional, Scanlan, Thomas, additional, Greenberg, Michael E., additional, Boulting, Gabriella L., additional, Macosko, Evan Z., additional, and Sabatini, Bernardo L., additional

Published
2023
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26. Activity-Induced MeCP2 Phosphorylation Regulates Retinogeniculate Synapse Refinement

Author

Tzeng, Christopher P., primary, Whitwam, Tess, additional, Boxer, Lisa D., additional, Li, Emmy, additional, Silberfeld, Andrew, additional, Trowbridge, Sara, additional, Mei, Kevin, additional, Lin, Cindy, additional, Shamah, Rebecca, additional, Griffith, Eric C., additional, Renthal, William, additional, Chen, Chinfei, additional, and Greenberg, Michael E., additional

Published
2023
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28. Bad-Deficient Mice Develop Diffuse Large B Cell Lymphoma

Author

Ranger, Ann M., Zha, Jiping, Harada, Hisashi, Datta, Sandeep Robert, Danial, Nika N., Gilmore, Andrew P., Kutok, Jeffery L., Le Beau, Michelle M., Greenberg, Michael E., and Korsmeyer, Stanley J.

Published
2003

35. Calcium Regulation of Neuronal Gene Expression

Author

West, Anne E., Chen, Wen G., Dalva, Matthew B., Dolmetsch, Ricardo E., Kornhauser, Jon M., Shaywitz, Adam J., Takasu, Mari A., Tao, Xu, and Greenberg, Michael E.

Published
2001

45. Efficacy of a trivalent influenza vaccine against seasonal strains and against 2009 pandemic H1N1: A randomized, placebo-controlled trial

Author

Mcbride, William J.H., Abhayaratna, Walter P., Barr, Ian, Booy, Robert, Carapetis, Jonathan, Carson, Simon, De Looze, Ferdinandus, Ellis-Pegler, Rod, Heron, Leon, Karrasch, Jeff, Marshall, Helen, Mcvernon, Jodie, Nolan, Terry, Rawlinson, William, Reid, Jim, Richmond, Peter, Shakib, Sepehr, Basser, Russell L., Hartel, Gunter F., Lai, Michael H., Rockman, Steven, and Greenberg, Michael E.

Published
2016
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46. Activity-induced MeCP2 phosphorylation regulates retinogeniculate synapse refinement.

Author

Tzeng, Christopher P., Whitwam, Tess, Boxer, Lisa D., Li, Emmy, Silberfeld, Andrew, Trowbridge, Sara, Mei, Kevin, Lin, Cindy, Shamah, Rebecca, Griffith, Eric C., Renthal, William, Chinfei Chen, and Greenberg, Michael E.

Subjects
SYNAPSES, NEURAL circuitry, RETT syndrome, PHOSPHORYLATION, PUERPERIUM
Abstract

Mutations in MECP2 give rise to Rett syndrome (RTT), an X-linked neurodevelopmental disorder that results in broad cognitive impairments in females. While the exact etiology of RTT symptoms remains unknown, one possible explanation for its clinical presentation is that loss of MECP2 causes miswiring of neural circuits due to defects in the brain's capacity to respond to changes in neuronal activity and sensory experience. Here, we show that MeCP2 is phosphorylated at four residues in the mouse brain (S86, S274, T308, and S421) in response to neuronal activity, and we generate a quadruple knock-in (QKI) mouse line in which all four activity-dependent sites are mutated to alanines to prevent phosphorylation. QKI mice do not display overt RTT phenotypes or detectable gene expression changes in two brain regions. However, electrophysiological recordings from the retinogeniculate synapse of QKI mice reveal that while synapse elimination is initially normal at P14, it is significantly compromised at P20. Notably, this phenotype is distinct from the synapse refinement defect previously reported for Mecp2 null mice, where synapses initially refine but then regress after the third postnatal week. We thus propose a model in which activity-induced phosphorylation of MeCP2 is critical for the proper timing of retinogeniculate synapse maturation specifically during the early postnatal period. [ABSTRACT FROM AUTHOR]

Published
2023
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49. Mouse Brain Organization Revealed through Direct Genome-Scale TF Expression Analysis

Author

Gray, Paul A., Fu, Hui, Luo, Ping, Zhao, Qing, Yu, Jing, Ferrari, Annette, Tenzen, Toyoaki, Yuk, Dong-in, Tsung, Eric F., Cai, Zhaohui, Alberta, John A., Cheng, Le-ping, Liu, Yang, Stenman, Jan M., Valerius, M. Todd, Billings, Nathan, Kim, Haesun A., Greenberg, Michael E., McMahon, Andrew P., Rowitch, David H., Stiles, Charles D., and Ma, Qiufu

Published
2004

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