A5008631765- Neuroscience and Neuropharmacology Research
- Ion channel regulation and function
- Cellular transport and secretion
- Neuroinflammation and Neurodegeneration Mechanisms
- Mitochondrial Function and Pathology
- Receptor Mechanisms and Signaling
- Hippo pathway signaling and YAP/TAZ
- Photoreceptor and optogenetics research
- Retinal Development and Disorders
- Genetics and Neurodevelopmental Disorders
- Neurobiology and Insect Physiology Research
- Neurogenesis and neuroplasticity mechanisms
- Alzheimer's disease research and treatments
- Axon Guidance and Neuronal Signaling
- Memory and Neural Mechanisms
- Lipid Membrane Structure and Behavior
- Ubiquitin and proteasome pathways
- Neural dynamics and brain function
- Microtubule and mitosis dynamics
- Cell death mechanisms and regulation
- Cardiac electrophysiology and arrhythmias
- Photochromic and Fluorescence Chemistry
- Molecular Sensors and Ion Detection
- Protein Kinase Regulation and GTPase Signaling
- Protein Structure and Dynamics
Massachusetts Institute of Technology
2009-2025
Broad Institute
2020-2025
Stanley Foundation
2023
Stanley Center for Psychiatric Research
2022
Institute of Cognitive and Brain Sciences
2022
University of California, San Francisco
1992-2018
University of Pennsylvania
2017
Gene Therapy Laboratory
2014
Genentech
2011-2014
Howard Hughes Medical Institute
2002-2013
The mechanism by which Ca 2+ mediates gene induction in response to membrane depolarization was investigated. adenosine 3′,5′-monophosphate (cAMP) element-binding protein (CREB) shown function as a -regulated transcription factor and substrate for depolarization-activated -calmodulin-dependent kinases (CaM kinases) I II. CREB residue Ser 133 the major site of phosphorylation CaM vitro after vivo. Mutation impaired ability respond . These results suggest that may transduce electrical signals...
Activation of N-methyl-d-aspartate subtype glutamate receptors (NMDARs) is required for long-term potentiation (LTP) and depression (LTD) excitatory synaptic transmission at hippocampal CA1 synapses, the proposed cellular substrates learning memory. However, little known about how activation NMDARs leads to these two opposing forms plasticity. Using slice preparations, we showed that selectively blocking contain NR2B subunit abolishes induction LTD but not LTP. In contrast, preferential...
Shank is a recently described family of postsynaptic proteins that function as part the NMDA receptor–associated PSD-95 complex (Naisbitt et al., 1999 [this issue Neuron]). Here, we report also bind to Homer. Homer form multivalent complexes proline-rich motifs in group 1 metabotropic glutamate receptors and inositol trisphosphate receptors, thereby coupling these signaling complex. A single Homer-binding site identified Shank, coimmunoprecipitate from brain colocalize at densities....
Selective concentration and anchoring of ionotropic receptors at the synapse is essential for neuronal signaling. Little known about molecules that mediate receptor clustering in CNS. With use yeast two-hybrid system to screen a rat brain cDNA library by vitro binding assays, we have identified an interaction between NMDA subunits 2A 2B (NR2A NR2B) three distinct members PSD-95/SAP90 family membrane-associated putative guanylate kinases. The mediated C terminus first two PDZ (also as GLGF or...