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

251. Myc Requires Distinct E2F Activities to Induce S Phase and Apoptosis

Author

Leone, Gustavo, primary, Sears, Rosalie, additional, Huang, Erich, additional, Rempel, Rachel, additional, Nuckolls, Faison, additional, Park, Chi-Hyun, additional, Giangrande, Paloma, additional, Wu, Lizhao, additional, Saavedra, Harold I, additional, Field, Seth J, additional, Thompson, Margaret A, additional, Yang, Haidi, additional, Fujiwara, Yuko, additional, Greenberg, Michael E, additional, Orkin, Stuart, additional, Smith, Clay, additional, and Nevins, Joseph R, additional

Published
2001
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260. Targeting of nonexpressed genes in embryonic stem cells via homologous recombination

Author

Johnson, Randall S., Sheng, Morgan, Greenberg, Michael E., Kolodner, Richard D., Papaioannou, Virginia E., and Spiegelman, Bruce M.

Subjects
Stem cells -- Research, Genetic transformation -- Research, Genetic recombination -- Research, Science and technology, Research
Abstract

Targeting of Nonexpressed Genes In Embryonic Stem Cells Via Homologous Recombination GENE TARGETING IN ES CELLS HAS been envisioned as a method for studying the effects of specific mutations in [...]

Published
1989

261. MeCP2 Phosphorylation Limits Psychostimulant-Induced Behavioral and Neuronal Plasticity.

Author

Deng, Jie V., Yehong Wan, Xiaoting Wang, Cohen, Sonia, Wetsel, William C., Greenberg, Michael E., Kenny, Paul J., Calakos, Nicole, and West, Anne E.

Subjects
NUCLEUS accumbens, NEUROPLASTICITY, PHOSPHORYLATION, DNA-binding proteins, AMPHETAMINES, POST-translational modification
Abstract

he methyl-DNA binding protein MeCP2 is emerging as an important regulator of drug reinforcement processes. Psychostimulants induce phosphorylation of MeCP2 at Ser421; however, the functional significance of this posttranslational modification for addictive-like behaviors was unknown. Here we show that MeCP2 Ser421Ala knock-in mice display both a reduced threshold for the induction of locomotor sensitization by investigator-administered amphetamine and enhanced behavioral sensitivity to the reinforcing properties of self-administered cocaine. These behavioral differences were accompanied in the knock-in mice by changes in medium spiny neuron intrinsic excitability and nucleus accumbens gene expression typically observed in association with repeated exposure to these drugs. These data show that phosphorylation of MeCP2 at Ser421 functions to limit the circuit plasticities in the nucleus accumbens that underlie addictive-like behaviors. [ABSTRACT FROM AUTHOR]

Published
2014
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262. Exercise Induces Hippocampal BDNF through a PGC-1α/FNDC5 Pathway.

Author

Wrann, Christiane D., White, James P., Salogiannnis, John, Laznik-Bogoslavski, Dina, Wu, Jun, Ma, Di, Lin, Jiandie D., Greenberg, Michael E., and Spiegelman, Bruce M.

Abstract

Summary: Exercise can improve cognitive function and has been linked to the increased expression of brain-derived neurotrophic factor (BDNF). However, the underlying molecular mechanisms driving the elevation of this neurotrophin remain unknown. Here we show that FNDC5, a previously identified muscle protein that is induced in exercise and is cleaved and secreted as irisin, is also elevated by endurance exercise in the hippocampus of mice. Neuronal Fndc5 gene expression is regulated by PGC-1α, and Pgc1a −/− mice show reduced Fndc5 expression in the brain. Forced expression of FNDC5 in primary cortical neurons increases Bdnf expression, whereas RNAi-mediated knockdown of FNDC5 reduces Bdnf. Importantly, peripheral delivery of FNDC5 to the liver via adenoviral vectors, resulting in elevated blood irisin, induces expression of Bdnf and other neuroprotective genes in the hippocampus. Taken together, our findings link endurance exercise and the important metabolic mediators, PGC-1α and FNDC5, with BDNF expression in the brain. [Copyright &y& Elsevier]

Published
2013
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263. The activity-dependent transcription factor NPAS4 regulates domain-specific inhibition.

Author

Bloodgood, Brenda L., Sharma, Nikhil, Browne, Heidi Adlman, Trepman, Alissa Z., and Greenberg, Michael E.

Subjects
TRANSCRIPTION factors, NEURAL circuitry, SYNAPSES, GENETIC regulation, DENDRITES, BRAIN-derived neurotrophic factor, HIPPOCAMPUS (Brain)
Abstract

A heterogeneous population of inhibitory neurons controls the flow of information through a neural circuit. Inhibitory synapses that form on pyramidal neuron dendrites modulate the summation of excitatory synaptic potentials and prevent the generation of dendritic calcium spikes. Precisely timed somatic inhibition limits both the number of action potentials and the time window during which firing can occur. The activity-dependent transcription factor NPAS4 regulates inhibitory synapse number and function in cell culture, but how this transcription factor affects the inhibitory inputs that form on distinct domains of a neuron in vivo was unclear. Here we show that in the mouse hippocampus behaviourally driven expression of NPAS4 coordinatesthe redistribution of inhibitory synapses made onto a CA1 pyramidal neuron, simultaneously increasing inhibitory synapse number on the cell body while decreasing the number of inhibitory synapses on the apical dendrites. This rearrangement of inhibition is mediated in part by the NPAS4 target gene brain derived neurotrophic factor (Bdnf), which specifically regulates somatic, and not dendritic, inhibition. These findings indicate that sensory stimuli, by inducing NPAS4 and its target genes, differentially control spatial features of neuronal inhibition in a way that restricts the output of the neuron while creating a dendritic environment that is permissive for plasticity. [ABSTRACT FROM AUTHOR]

Published
2013
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268. Akt promotes cell survival by phosphorylating and inhibiting a forkhead transcription factor

Author

Brunet, Anne, Bonni, Azad, Zigmond, Michael J., Lin, Michael Z., Juo, Peter, Hu, Linda S., Anderson, Michael J., Arden, Karen C., Blenis, John, and Greenberg, Michael E.

Subjects
Cell death -- Research, Protein kinases -- Research, Cellular control mechanisms -- Research, Phosphorylation -- Research, Biological sciences
Abstract

Previous studies have established that the serine/threonine kinase Akt has the capacity to inactivate the apoptotic process. Aside from this, a recent study found that Akt is also involved with the regulation of FKHRL1 which is a member of the Forkhead family of transcription factors. Serine/threonine kinase Akt is observed to phosphorylate FKHRL1 to bind it with 14-3-3 proteins, thus, keep it within the cytoplasm.

Published
1999

269. A Critical Role for DNA End-Joining Proteins in Both Lymphogenesis and Neurogenesis

Author

Gao, Yijie, primary, Sun, Yi, additional, Frank, Karen M., additional, Dikkes, Pieter, additional, Fujiwara, Yuko, additional, Seidl, Katherine J., additional, Sekiguchi, JoAnn M., additional, Rathbun, Gary A., additional, Swat, Wojciech, additional, Wang, Jiyang, additional, Bronson, Roderick T., additional, Malynn, Barbara A., additional, Bryans, Margaret, additional, Zhu, Chengming, additional, Chaudhuri, Jayanta, additional, Davidson, Laurie, additional, Ferrini, Roger, additional, Stamato, Thomas, additional, Orkin, Stuart H., additional, Greenberg, Michael E., additional, and Alt, Frederick W., additional

Published
1998
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299. 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
Article
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
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