Genomes and Genes
THOMAS C contact SUDHOF
Affiliation: Stanford University
- Synaptic vesicle exocytosisThomas C Sudhof
Department of Molecular and Cellular Physiology, and Howard Hughes Medical Institute, Stanford University Medical School, Stanford, California 94305, USA
Cold Spring Harb Perspect Biol 3:. 2011..The synaptic membrane-fusion machinery is controlled by synaptotagmin, and additionally regulated by a presynaptic protein matrix (the "active zone") that includes Munc13 and RIM proteins as central components...
- Generation of induced neuronal cells by the single reprogramming factor ASCL1Soham Chanda
Institute for Stem Cell Biology and Regenerative Medicine and Department of Pathology, Stanford University, Stanford, CA 94305, USA Department of Molecular and Cellular Physiology and Howard Hughes Medical Institute, Stanford University, Stanford, CA 94305, USA
Stem Cell Reports 3:282-96. 2014..Surprisingly, ASCL1-induced iN cells were predominantly excitatory, demonstrating that ASCL1 is permissive but alone not deterministic for the inhibitory neuronal lineage. ..
- Munc18-1 binding to the neuronal SNARE complex controls synaptic vesicle primingFerenc Deak
Howard Hughes Medical Institute, Department of Neuroscience, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA
J Cell Biol 184:751-64. 2009....
- Synaptotagmin-1 functions as a Ca2+ sensor for spontaneous releaseJun Xu
Department of Molecular and Cellular Physiology, Stanford University, Palo Alto, California, USA
Nat Neurosci 12:759-66. 2009..These data suggest that Syt1 controls both evoked and spontaneous release at a synapse as a simultaneous Ca2+-dependent activator and clamp of exocytosis...
- Neurotransmitter release: the last millisecond in the life of a synaptic vesicleThomas C Sudhof
Department of Molecular and Cellular Physiology, and Howard Hughes Medical Institute, Lorry Lokey SIM1 Building, 265 Campus Drive, Stanford University School of Medicine, Stanford, CA 94305, USA Electronic address
Neuron 80:675-90. 2013..This architecture allows direct flow of Ca(2+) ions from Ca(2+) channels to synaptotagmin, which then triggers fusion, thus mediating tight millisecond coupling of an action potential to neurotransmitter release. ..
- The presynaptic active zoneThomas C Sudhof
Department of Molecular and Cellular Physiology, and Howard Hughes Medical Institute, Stanford University School of Medicine, Stanford, CA 94304 5453, USA
Neuron 75:11-25. 2012..Moreover, this complex mediates short- and long-term plasticity in response to bursts of action potentials, thus critically contributing to the computational power of a synapse...
- Calcium control of neurotransmitter releaseThomas C Sudhof
Department of Molecular and Cellular Physiology, Howard Hughes Medical Institute, Stanford University School of Medicine, Stanford, California 94305, USA
Cold Spring Harb Perspect Biol 4:a011353. 2012....
- Neuroligins and neurexins link synaptic function to cognitive diseaseThomas C Sudhof
Neuroscience Institute, Department of Molecular and Cellular Physiology, Stanford University, 1050 Arastradero Road B249, Palo Alto, California 94304, USA
Nature 455:903-11. 2008..In humans, alterations in genes encoding neurexins or neuroligins have recently been implicated in autism and other cognitive diseases, linking synaptic cell adhesion to cognition and its disorders...
- Membrane fusion: grappling with SNARE and SM proteinsThomas C Sudhof
Department of Cellular and Molecular Physiology, Stanford University, Palo Alto, CA 94304, USA
Science 323:474-7. 2009....
- SYNUCLEIN FUNCTIONS: ROLE IN PARKINSON'S DISEASETHOMAS SUDHOF; Fiscal Year: 2003..We anticipate that these experiments will establish a molecular understanding of synuclein functions in the brain and provide insight into the role of an alpha synuclein in Parkinson's disease. ..
- A systematic test of the relation of ASD heterogeneity to synaptic functionTHOMAS C contact SUDHOF; Fiscal Year: 2010..This project will address these issues by studying the changes in neuron-to-neuron communication caused by the genes associated with autism. ..
- APP, Alzheimer's Disease, and Synaptic FunctionTHOMAS SUDHOF; Fiscal Year: 2008..Together these studies will contribute to our understanding of APP function and Abeta toxicity in AD, and may suggest new avenues for interfering with the pathogenesis of AD. ..