Michael Greenberg

Michael Greenberg, Ph.D.

Nathan Marsh Pusey Professor of Neurobiology, Harvard Medical School
Professor of Neurology, Boston Children's Hospital
Director of the Hock E. Tan and K. Lisa Yang Center for Autism Research, Harvard Medical School

Michael Greenberg, Ph.D. – Faculty Profile

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Title: Nathan Marsh Pusey Professor of Neurobiology, Harvard Medical School; Director of the Hock E. Tan and K. Lisa Yang Center for Autism Research, Harvard Medical School; Professor of Neurology, Boston Children's Hospital.

The Aim

The Greenberg Lab studies how life experiences turn genes on or off to shape learning and brain development. The lab focuses on the molecular mechanisms by which sensory experiences regulate gene expression in the brain.

The Impact

This research has illuminated how the brain rewires itself in response to experience, a process essential for learning, memory, and behavior. Several of the genes and pathways the lab has identified are mutated in autism and other neurodevelopmental disorders, positioning this work as foundational for developing new therapies for these conditions.

A Closer Look

Article: State of Stasis , Harvard Medical School / Harvard Gazette, June 2020. This piece describes how Mike Greenberg and colleagues identified a tiny cluster of hypothalamic neurons that can flip mice into and out of a hibernation‑like state, or torpor, revealing brain circuits that dial down body temperature and metabolism and opening avenues for understanding suspended animation and its medical uses.

Article: Decoding Brain Evolution , Harvard Medical School, December 2021. This article highlights Mike Greenberg’s co‑leadership of the Allen Discovery Center for Human Brain Evolution, which links evolutionary genetic variants to their effects in neurons to explain how human brains acquired uniquely human cognitive and behavioral capacities.

Contact

Email: michael_greenberg@hms.harvard.edu
Lab website: greenberg.hms.harvard.edu

Publications View
Stimulation of protein tyrosine phosphorylation by NMDA receptor activation.
Authors: Authors: Bading H, Greenberg ME.
Science
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CREB: a Ca(2+)-regulated transcription factor phosphorylated by calmodulin-dependent kinases.
Authors: Authors: Sheng M, Thompson MA, Greenberg ME.
Science
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Nur77 is differentially modified in PC12 cells upon membrane depolarization and growth factor treatment.
Authors: Authors: Hazel TG, Misra R, Davis IJ, Greenberg ME, Lau LF.
Mol Cell Biol
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Two distinct destabilizing elements in the c-fos message trigger deadenylation as a first step in rapid mRNA decay.
Authors: Authors: Shyu AB, Belasco JG, Greenberg ME.
Genes Dev
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Growth factor-induced gene expression: the ups and downs of c-fos regulation.
Authors: Authors: Rivera VM, Greenberg ME.
New Biol
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Membrane depolarization and calcium induce c-fos transcription via phosphorylation of transcription factor CREB.
Authors: Authors: Sheng M, McFadden G, Greenberg ME.
Neuron
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The regulation and function of c-fos and other immediate early genes in the nervous system.
Authors: Authors: Sheng M, Greenberg ME.
Neuron
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The inner core of the serum response element mediates both the rapid induction and subsequent repression of c-fos transcription following serum stimulation.
Authors: Authors: Rivera VM, Sheng M, Greenberg ME.
Genes Dev
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Deadenylylation: a mechanism controlling c-fos mRNA decay.
Authors: Authors: Greenberg ME, Shyu AB, Belasco JG.
Enzyme
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Targeting of nonexpressed genes in embryonic stem cells via homologous recombination.
Authors: Authors: Johnson RS, Sheng M, Greenberg ME, Kolodner RD, Papaioannou VE, Spiegelman BM.
Science
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