Manu Sharma

Summary

Affiliation: Stanford University
Country: USA

Publications

  1. doi Proteasome inhibition alleviates SNARE-dependent neurodegeneration
    Manu Sharma
    Department of Molecular and Cellular Physiology, and Howard Hughes Medical Institute, Stanford University, Stanford, CA 94305 5453, USA
    Sci Transl Med 4:147ra113. 2012
  2. pmc Alpha-synuclein promotes SNARE-complex assembly in vivo and in vitro
    Jacqueline Burré
    Department of Molecular and Cellular Physiology, and Howard Hughes Medical Institute, Stanford University, 1050 Arastradero Road, Palo Alto, CA 94304 5543, USA
    Science 329:1663-7. 2010
  3. pmc Autism-linked neuroligin-3 R451C mutation differentially alters hippocampal and cortical synaptic function
    Mark Etherton
    Department of Molecular and Cellular Physiology, Stanford University Medical School, Stanford, CA 94305, USA
    Proc Natl Acad Sci U S A 108:13764-9. 2011
  4. pmc CSPα knockout causes neurodegeneration by impairing SNAP-25 function
    Manu Sharma
    Department of Molecular and Cellular Physiology, Howard Hughes Medical Institute, Stanford University, Stanford, CA, USA
    EMBO J 31:829-41. 2012
  5. pmc Systematic mutagenesis of α-synuclein reveals distinct sequence requirements for physiological and pathological activities
    Jacqueline Burré
    Department of Molecular and Cellular Physiology, Stanford University, Stanford, California 94305 5453, USA
    J Neurosci 32:15227-42. 2012
  6. doi CSPα promotes SNARE-complex assembly by chaperoning SNAP-25 during synaptic activity
    Manu Sharma
    Department of Molecular and Cellular Physiology, Stanford University, SIM1, 265 Campus Drive, Palo Alto, CA 94304 5453, USA
    Nat Cell Biol 13:30-9. 2011
  7. pmc An autism-associated point mutation in the neuroligin cytoplasmic tail selectively impairs AMPA receptor-mediated synaptic transmission in hippocampus
    Mark R Etherton
    Department of Molecular and Cellular Physiology, Stanford University, Palo Alto, CA, USA
    EMBO J 30:2908-19. 2011
  8. ncbi Microsecond Dissection of Neurotransmitter Release: SNARE-Complex Assembly Dictates Speed and Ca(2+) Sensitivity
    Claudio Acuna
    Department of Molecular and Cellular Physiology and Howard Hughes Medical Institute, Stanford University, 265 Campus Drive, Stanford, CA 94305 5453, USA Electronic address
    Neuron 82:1088-100. 2014
  9. pmc Native α-synuclein induces clustering of synaptic-vesicle mimics via binding to phospholipids and synaptobrevin-2/VAMP2
    Jiajie Diao
    Department of Molecular and Cellular Physiology, Stanford University, Stanford, United States Department of Structural Biology, Stanford University, Stanford, United States Departments of Photon Sciences, and Neurology and Neurological Sciences, Stanford University, Stanford, United States Howard Hughes Medical Institute, Stanford University, Stanford, United States
    elife 2:e00592. 2013

Collaborators

Detail Information

Publications9

  1. doi Proteasome inhibition alleviates SNARE-dependent neurodegeneration
    Manu Sharma
    Department of Molecular and Cellular Physiology, and Howard Hughes Medical Institute, Stanford University, Stanford, CA 94305 5453, USA
    Sci Transl Med 4:147ra113. 2012
    ....
  2. pmc Alpha-synuclein promotes SNARE-complex assembly in vivo and in vitro
    Jacqueline Burré
    Department of Molecular and Cellular Physiology, and Howard Hughes Medical Institute, Stanford University, 1050 Arastradero Road, Palo Alto, CA 94304 5543, USA
    Science 329:1663-7. 2010
    ..Thus, synucleins may function to sustain normal SNARE-complex assembly in a presynaptic terminal during aging...
  3. pmc Autism-linked neuroligin-3 R451C mutation differentially alters hippocampal and cortical synaptic function
    Mark Etherton
    Department of Molecular and Cellular Physiology, Stanford University Medical School, Stanford, CA 94305, USA
    Proc Natl Acad Sci U S A 108:13764-9. 2011
    ....
  4. pmc CSPα knockout causes neurodegeneration by impairing SNAP-25 function
    Manu Sharma
    Department of Molecular and Cellular Physiology, Howard Hughes Medical Institute, Stanford University, Stanford, CA, USA
    EMBO J 31:829-41. 2012
    ..Our findings suggest that the neurodegeneration in CSPα KO mice is primarily produced by defective SNAP-25 function, which causes neurodegeneration by impairing SNARE-complex assembly...
  5. pmc Systematic mutagenesis of α-synuclein reveals distinct sequence requirements for physiological and pathological activities
    Jacqueline Burré
    Department of Molecular and Cellular Physiology, Stanford University, Stanford, California 94305 5453, USA
    J Neurosci 32:15227-42. 2012
    ....
  6. doi CSPα promotes SNARE-complex assembly by chaperoning SNAP-25 during synaptic activity
    Manu Sharma
    Department of Molecular and Cellular Physiology, Stanford University, SIM1, 265 Campus Drive, Palo Alto, CA 94304 5453, USA
    Nat Cell Biol 13:30-9. 2011
    ..Thus, SNAP-25 function is maintained during rapid SNARE cycles by equilibrium between CSPα-dependent chaperoning and ubiquitin-dependent degradation, revealing unique protein quality-control machinery within the presynaptic compartment...
  7. pmc An autism-associated point mutation in the neuroligin cytoplasmic tail selectively impairs AMPA receptor-mediated synaptic transmission in hippocampus
    Mark R Etherton
    Department of Molecular and Cellular Physiology, Stanford University, Palo Alto, CA, USA
    EMBO J 30:2908-19. 2011
    ..Our results suggest that the cytoplasmic tail of neuroligin-3 has a central role in synaptic transmission by modulating the recruitment of AMPA receptors to postsynaptic sites at excitatory synapses...
  8. ncbi Microsecond Dissection of Neurotransmitter Release: SNARE-Complex Assembly Dictates Speed and Ca(2+) Sensitivity
    Claudio Acuna
    Department of Molecular and Cellular Physiology and Howard Hughes Medical Institute, Stanford University, 265 Campus Drive, Stanford, CA 94305 5453, USA Electronic address
    Neuron 82:1088-100. 2014
    ....
  9. pmc Native α-synuclein induces clustering of synaptic-vesicle mimics via binding to phospholipids and synaptobrevin-2/VAMP2
    Jiajie Diao
    Department of Molecular and Cellular Physiology, Stanford University, Stanford, United States Department of Structural Biology, Stanford University, Stanford, United States Departments of Photon Sciences, and Neurology and Neurological Sciences, Stanford University, Stanford, United States Howard Hughes Medical Institute, Stanford University, Stanford, United States
    elife 2:e00592. 2013
    ..Synuclein may therefore lead to accumulation of synaptic vesicles at the active zone, providing a 'buffer' of synaptic vesicles, without affecting neurotransmitter release itself. DOI:http://dx.doi.org/10.7554/eLife.00592.001...