Manu Sharma

Summary

Affiliation: Stanford University
Country: USA

Publications

  1. 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
  2. doi request reprint 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
  3. 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
  4. 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
  5. doi request reprint 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
  6. 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
  7. pmc Evolution of CASK into a Mg2+-sensitive kinase
    Konark Mukherjee
    Department of Molecular and Cellular Physiology, Stanford University School of Medicine, 1050 Arastradero Road, Palo Alto, CA 94304, USA
    Sci Signal 3:ra33. 2010
  8. 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
  9. ncbi request reprint 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
  10. 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

Publications11

  1. 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...
  2. doi request reprint 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...
  3. 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...
  4. 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
    ....
  5. doi request reprint 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
    ....
  6. 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
    ....
  7. pmc Evolution of CASK into a Mg2+-sensitive kinase
    Konark Mukherjee
    Department of Molecular and Cellular Physiology, Stanford University School of Medicine, 1050 Arastradero Road, Palo Alto, CA 94304, USA
    Sci Signal 3:ra33. 2010
    ..This emergence of Mg(2+) sensitivity (inhibition by Mg(2+)) conferred regulation of CASK activity by divalent cations, in parallel with the evolution of the animal nervous systems...
  8. 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...
  9. ncbi request reprint 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
    ....
  10. 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...
  11. pmc CASK Functions as a Mg2+-independent neurexin kinase
    Konark Mukherjee
    Department of Neuroscience, Howard Hughes Medical Institute, University of Texas Southwestern Medical Center, 6000 Harry Hines Boulevard, Dallas, TX 75390 9111, USA
    Cell 133:328-39. 2008
    ..Moreover, our study suggests that other pseudokinases (10% of the kinome) could also be catalytically active...