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

2. 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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3. 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.

Published
2022
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5. Correction

Author

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

Published
2020

11. 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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17. 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

19. 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

26. 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

27. 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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37. 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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39. Evolution of Osteocrin as an activity-regulated factor in the primate brain

Author

Ataman, Bulent, Boulting, Gabriella L., Harmin, David A., Yang, Marty G., Baker-Salisbury, Mollie, Yap, Ee-Lynn, Malik, Athar N., Mei, Kevin, Rubin, Alex A., Spiegel, Ivo, Durresi, Ershela, Sharma, Nikhil, Hu, Linda S., Pletikos, Mihovil, Griffith, Eric C., Partlow, Jennifer N., Stevens, Christine R., Adli, Mazhar, Chahrour, Maria, Sestan, Nenad, Walsh, Christopher A., Berezovskii, Vladimir K., Livingstone, Margaret S., and Greenberg, Michael E.

Subjects
Primates -- Physiological aspects, Fetal brain -- Research, Transcription (Genetics) -- Methods, Brain research, Environmental issues, Science and technology, Zoology and wildlife conservation
Abstract

Sensory stimuli drive the maturation and function of the mammalian nervous system in part through the activation of gene expression networks that regulate synapse development and plasticity. These networks have primarily been studied in mice, and it is not known whether there are species- or clade-specific activity-regulated genes that control features of brain development and function. Here we use transcriptional profiling of human fetal brain cultures to identify an activity-dependent secreted factor, Osteocrin (OSTN), that is induced by membrane depolarization of human but not mouse neurons. We find that OSTN has been repurposed in primates through the evolutionary acquisition of DNA regulatory elements that bind the activity-regulated transcription factor MEF2. In addition, we demonstrate that OSTN is expressed in primate neocortex and restricts activity-dependent dendritic growth in human neurons. These findings suggest that, in response to sensory input, OSTN regulates features of neuronal structure and function that are unique to primates., Author(s): Bulent Ataman [1]; Gabriella L. Boulting [1]; David A. Harmin [1]; Marty G. Yang [1]; Mollie Baker-Salisbury [1]; Ee-Lynn Yap [1]; Athar N. Malik [1]; Kevin Mei [1]; Alex [...]

Published
2016
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41. 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

44. Disruption of DNA-methylation-dependent long gene repression in Rett syndrome

Author

Gabel, Harrison W., Kinde, Benyam, Stroud, Hume, Gilbert, Caitlin S., Harmin, David A., Kastan, Nathaniel R., Hemberg, Martin, Ebert, Daniel H., and Greenberg, Michael E.

Subjects
Gene expression -- Health aspects, Methylation -- Health aspects, Rett syndrome -- Genetic aspects, Environmental issues, Science and technology, Zoology and wildlife conservation
Abstract

Disruption of the MECP2 gene leads to Rett syndrome (RTT), a severe neurological disorder with features of autism (1). MECP2 encodes a methyl-DNA-binding protein (2) that has been proposed to function as a transcriptional repressor, but despite numerous mouse studies examining neuronal gene expression in Mecp2 mutants, no clear model has emerged for how MeCP2 protein regulates transcription (3-9). Here we identify a genome-wide length-dependent increase in gene expression in MeCP2 mutant mouse models and human RTT brains. We present evidence that MeCP2 represses gene expression by binding to methylated CA sites within long genes, and that in neurons lacking MeCP2, decreasing the expression of long genes attenuates RTT-associated cellular deficits. In addition, we find that long genes as a population are enriched for neuronal functions and selectively expressed in the brain. These findings suggest that mutations in MeCP2 may cause neurological dysfunction by specifically disrupting long gene expression in the brain., To identify common features of genes whose expression is misregulated in RTT, we surveyed gene expression data sets from studies of Mecp2 mutant mice, asking if genes that are misregulated [...]

Published
2015

47. Identifying Autism Loci and Genes by Tracing Recent Shared Ancestry

Author

Morrow, Eric M., Yoo, Seung-Yun, Flavell, Steven W., Kim, Tae-Kyung, Lin, Yingxi, Hill, Robert Sean, Mukaddes, Nahit M., Balkhy, Soher, Gascon, Generoso, Hashmi, Asif, Al-Saad, Samira, Ware, Janice, Joseph, Robert M., Greenblatt, Rachel, Gleason, Danielle, Ertelt, Julia A., Apse, Kira A., Bodell, Adria, Partlow, Jennifer N., Barry, Brenda, Yao, Hui, Markianos, Kyriacos, Ferland, Russell J., Greenberg, Michael E., and Walsh, Christopher A.

Published
2008
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