EDWIN CHAPMAN

Summary

Affiliation: University of Wisconsin
Country: USA

Publications

  1. pmc Synaptotagmins I and II mediate entry of botulinum neurotoxin B into cells
    Min Dong
    Department of Physiology, University of Wisconsin, Madison, Madison, WI 53706, USA
    J Cell Biol 162:1293-303. 2003
  2. pmc Synaptotagmin arrests the SNARE complex before triggering fast, efficient membrane fusion in response to Ca2+
    Michael C Chicka
    Howard Hughes Medical Institute and Department of Physiology, University of Wisconsin, Madison, 1300 University Avenue, SMI 129, Madison, Wisconsin 53706, USA
    Nat Struct Mol Biol 15:827-35. 2008
  3. pmc Analysis of the synaptotagmin family during reconstituted membrane fusion. Uncovering a class of inhibitory isoforms
    Akhil Bhalla
    Howard Hughes Medical Institute, and Department of Physiology, University of Wisconsin, 1300 University Avenue, Madison, WI 53706, USA
    J Biol Chem 283:21799-807. 2008
  4. pmc Synaptotagmin C2B domain regulates Ca2+-triggered fusion in vitro: critical residues revealed by scanning alanine mutagenesis
    Jon D Gaffaney
    Department of Physiology, University of Wisconsin, Madison, Wisconsin 53706, USA
    J Biol Chem 283:31763-75. 2008
  5. pmc Synaptotagmin-IV modulates synaptic function and long-term potentiation by regulating BDNF release
    Camin Dean
    Department of Physiology, University of Wisconsin, Madison, Wisconsin, USA
    Nat Neurosci 12:767-76. 2009
  6. pmc Concurrent binding of complexin and synaptotagmin to liposome-embedded SNARE complexes
    Michael C Chicka
    Department of Physiology and Programs in Cellular and Molecular Biology, University of Wisconsin, 1300 University Avenue, SMI 129, Madison, Wisconsin 53706, USA
    Biochemistry 48:657-9. 2009
  7. pmc Rat and Drosophila synaptotagmin 4 have opposite effects during SNARE-catalyzed membrane fusion
    Zhao Wang
    Department of Physiology, Howard Hughes Medical Institute, University of Wisconsin, Madison, Wisconsin 53706, USA
    J Biol Chem 285:30759-66. 2010
  8. pmc Otoferlin is a calcium sensor that directly regulates SNARE-mediated membrane fusion
    Colin P Johnson
    Howard Hughes Medical Institute, University of Wisconsin, Madison, WI 53706, USA
    J Cell Biol 191:187-97. 2010
  9. pmc Two modes of exocytosis at hippocampal synapses revealed by rate of FM1-43 efflux from individual vesicles
    David A Richards
    Department of Physiology, University of Wisconsin Madison, Madison, WI 53706, USA
    J Cell Biol 168:929-39. 2005
  10. pmc Identification of synaptotagmin effectors via acute inhibition of secretion from cracked PC12 cells
    Ward C Tucker
    Department of Physiology, University of Wisconsin, Madison, WI 53706, USA
    J Cell Biol 162:199-209. 2003

Research Grants

  1. Receptors for clostridial neurotoxins
    EDWIN CHAPMAN; Fiscal Year: 2005
  2. Synaptotagmin in Excitation-Coupling
    EDWIN CHAPMAN; Fiscal Year: 2006
  3. Receptors for clostridial neurotoxins
    EDWIN CHAPMAN; Fiscal Year: 2006
  4. Receptors for clostridial neurotoxins
    EDWIN CHAPMAN; Fiscal Year: 2007
  5. Synaptotagmin C2B Domain as a Ca2+ Sensing Module
    EDWIN CHAPMAN; Fiscal Year: 2007
  6. Synaptotagmin C2B Domain as a Ca2+ Sensing Module
    EDWIN CHAPMAN; Fiscal Year: 2009
  7. Synaptotagmin C2B Domain as a Ca2+ Sensing Module
    Edwin R Chapman; Fiscal Year: 2010
  8. Synaptotagmin in Excitation-Coupling
    EDWIN CHAPMAN; Fiscal Year: 2005
  9. Synaptotagmin C2B Domain as a Ca2+-sensing module
    EDWIN CHAPMAN; Fiscal Year: 2005
  10. Receptors for clostridial neurotoxins
    EDWIN CHAPMAN; Fiscal Year: 2004

Collaborators

  • Meyer Jackson
  • Eric A Johnson
  • Huisheng Liu
  • THOMAS F MARTIN
  • David A Richards
  • Roger Janz
  • Camin Dean
  • Hyun Jung Kim
  • P Wang
  • Rodolfo Llinas
  • Vladimir Parpura
  • Richard Anthony Steinhardt
  • Giulia Baldini
  • N W Andrews
  • Paul T Kelly
  • A Jennifer Morton
  • Wenlei Liu
  • Jihong Bai
  • Ward C Tucker
  • Akhil Bhalla
  • Min Dong
  • Enfu Hui
  • Michael C Chicka
  • William H Tepp
  • Chih Tien Wang
  • Tingting Liu
  • Jun Yao
  • Felix L Yeh
  • Zhao Wang
  • Jon D Gaffaney
  • Tingting Wang
  • J Michael Edwardson
  • James C Weisshaar
  • F Mark Dunning
  • Colin P Johnson
  • Yao Wu
  • Zhenjie Zhang
  • Zhen Zhang
  • Brie E Paddock
  • Midhat H Abdulreda
  • Cecilia Czibener
  • Qing Chai
  • Michael T Madziva
  • Sheldon S Shen
  • Brady J Maher
  • Payne Y Chang
  • Xue Han
  • Evelina Chieregatti
  • Ruslan N Grishanin
  • Bakhrom K Berdiev
  • Yi Wu
  • C A Earles
  • Sung E Kwon
  • Guangyun Lin
  • Elizabeth A Smith
  • Fei Mao
  • Vincent T Moy
  • Noreen E Reist
  • Amelia R Striegel
  • Raymond C Stevens
  • Nathan M Sherer
  • Marc Pypaert
  • Walther Mothes
  • Felix Yeh
  • Steven M Becker
  • Joseph W Arndt
  • Roger L Mackinnon
  • Mutsuyuki Sugimori
  • Biljana Jovov
  • Anjaparavanda P Naren
  • Kyougsook Ann
  • Thomas Weber
  • Roy R L Gerona
  • Catherine M Fuller
  • Vadim A Klenchin
  • Judith A Kowalchyk
  • Dale J Benos
  • Cynthia A Earles
  • Andreas Wyttenbach
  • Sen Fang Sui
  • Shang Rong Ji
  • Yuhong He
  • Michael C Goodnough
  • Belvin Gong
  • Juu Chin Lu
  • J Bai

Detail Information

Publications57

  1. pmc Synaptotagmins I and II mediate entry of botulinum neurotoxin B into cells
    Min Dong
    Department of Physiology, University of Wisconsin, Madison, Madison, WI 53706, USA
    J Cell Biol 162:1293-303. 2003
    ..Finally, we show that syt II fragments, in conjunction with gangliosides, neutralized BoNT/B in intact mice. These findings establish that syts I and II can function as protein receptors for BoNT/B...
  2. pmc Synaptotagmin arrests the SNARE complex before triggering fast, efficient membrane fusion in response to Ca2+
    Michael C Chicka
    Howard Hughes Medical Institute and Department of Physiology, University of Wisconsin, Madison, 1300 University Avenue, SMI 129, Madison, Wisconsin 53706, USA
    Nat Struct Mol Biol 15:827-35. 2008
    ..These findings demonstrate that Ca(2+) converts synaptotagmin from a clamp to a trigger for exocytosis...
  3. pmc Analysis of the synaptotagmin family during reconstituted membrane fusion. Uncovering a class of inhibitory isoforms
    Akhil Bhalla
    Howard Hughes Medical Institute, and Department of Physiology, University of Wisconsin, 1300 University Avenue, Madison, WI 53706, USA
    J Biol Chem 283:21799-807. 2008
    ..Finally, a subset of inhibitory syts down-regulated the ability of syt I to activate fusion, demonstrating that syt isoforms can modulate the function of each other...
  4. pmc Synaptotagmin C2B domain regulates Ca2+-triggered fusion in vitro: critical residues revealed by scanning alanine mutagenesis
    Jon D Gaffaney
    Department of Physiology, University of Wisconsin, Madison, Wisconsin 53706, USA
    J Biol Chem 283:31763-75. 2008
    ..In addition, some mutations uncouple the clamping and stimulatory functions of syt 1, suggesting that these two activities are mediated by distinct structural determinants in C2B...
  5. pmc Synaptotagmin-IV modulates synaptic function and long-term potentiation by regulating BDNF release
    Camin Dean
    Department of Physiology, University of Wisconsin, Madison, Wisconsin, USA
    Nat Neurosci 12:767-76. 2009
    ..Thus, regulation of BDNF secretion by syt-IV emerges as a mechanism for maintaining synaptic strength in a useful range during LTP...
  6. pmc Concurrent binding of complexin and synaptotagmin to liposome-embedded SNARE complexes
    Michael C Chicka
    Department of Physiology and Programs in Cellular and Molecular Biology, University of Wisconsin, 1300 University Avenue, SMI 129, Madison, Wisconsin 53706, USA
    Biochemistry 48:657-9. 2009
    ..These data also suggest that during synaptotagmin-regulated vesicle-vesicle fusion, complexin does not function as a fusion clamp that is relieved by Ca(2+)-synaptotagmin...
  7. pmc Rat and Drosophila synaptotagmin 4 have opposite effects during SNARE-catalyzed membrane fusion
    Zhao Wang
    Department of Physiology, Howard Hughes Medical Institute, University of Wisconsin, Madison, Wisconsin 53706, USA
    J Biol Chem 285:30759-66. 2010
    ..In summary, rat SYT4 serves as an inhibitory isoform, whereas fly SYT4 is a bona fide Ca(2+) sensor capable of coupling Ca(2+) to membrane fusion...
  8. pmc Otoferlin is a calcium sensor that directly regulates SNARE-mediated membrane fusion
    Colin P Johnson
    Howard Hughes Medical Institute, University of Wisconsin, Madison, WI 53706, USA
    J Cell Biol 191:187-97. 2010
    ..These results demonstrate for the first time that otoferlin is a calcium sensor that can directly regulate soluble N-ethyl-maleimide sensitive fusion protein attachment protein receptor-mediated membrane fusion reactions...
  9. pmc Two modes of exocytosis at hippocampal synapses revealed by rate of FM1-43 efflux from individual vesicles
    David A Richards
    Department of Physiology, University of Wisconsin Madison, Madison, WI 53706, USA
    J Cell Biol 168:929-39. 2005
    ....
  10. pmc Identification of synaptotagmin effectors via acute inhibition of secretion from cracked PC12 cells
    Ward C Tucker
    Department of Physiology, University of Wisconsin, Madison, WI 53706, USA
    J Cell Biol 162:199-209. 2003
    ..These data suggest that syts trigger fusion via their Ca2+-regulated interactions with t-SNAREs and PIP2, target molecules known to play critical roles in exocytosis...
  11. pmc Mechanism of botulinum neurotoxin B and G entry into hippocampal neurons
    Min Dong
    Howard Hughes Medical Institute, Department of Physiology, University of Wisconsin, Madison, WI 53706, USA
    J Cell Biol 179:1511-22. 2007
    ..These data suggest that gangliosides are the shared coreceptor for BoNT/A, B, and G, supporting a double-receptor model for these three BoNTs for which the protein receptors are known...
  12. pmc The tandem C2 domains of synaptotagmin contain redundant Ca2+ binding sites that cooperate to engage t-SNAREs and trigger exocytosis
    C A Earles
    Department of Physiology, University of Wisconsin, Madison, WI 53706, USA
    J Cell Biol 154:1117-23. 2001
    ..We conclude that synaptotagmin-SNARE interactions regulate membrane fusion and that cooperation between synaptotagmin's C2 domains is crucial to its function...
  13. pmc SV2 mediates entry of tetanus neurotoxin into central neurons
    Felix L Yeh
    Department of Physiology, Howard Hughes Medical Institute, University of Wisconsin, Madison, Wisconsin, USA
    PLoS Pathog 6:e1001207. 2010
    ..In summary, the findings reported here indicate that SV2A and SV2B mediate binding and entry of tetanus neurotoxin into central neurons...
  14. pmc Uncoupling the roles of synaptotagmin I during endo- and exocytosis of synaptic vesicles
    Jun Yao
    Howard Hughes Medical Institute and Department of Neuroscience, University of Wisconsin, Madison, Wisconsin, USA
    Nat Neurosci 15:243-9. 2012
    ..Thus, syt1 functions as a dual Ca(2+) sensor for both endo- and exocytosis, potentially coupling these two components of the vesicle cycle...
  15. ncbi request reprint Synaptotagmin: a Ca(2+) sensor that triggers exocytosis?
    Edwin R Chapman
    Department of Physiology, University of Wisconsin, Madison, Wisconsin 53706, USA
    Nat Rev Mol Cell Biol 3:498-508. 2002
  16. doi request reprint How does synaptotagmin trigger neurotransmitter release?
    Edwin R Chapman
    Howard Hughes Medical Institute and Department of Physiology, University of Wisconsin, Madison, WI 53706, USA
    Annu Rev Biochem 77:615-41. 2008
    ..This work sheds light not only on presynaptic aspects of synaptic transmission, but also on the fundamental problem of membrane fusion, which has remained a puzzle that has yet to be solved in any biological system...
  17. ncbi request reprint Fusion pore dynamics are regulated by synaptotagmin*t-SNARE interactions
    Jihong Bai
    Department of Physiology, University of Wisconsin, Madison, WI 53706, USA
    Neuron 41:929-42. 2004
    ..Thus, the final step of Ca2+-triggered exocytosis is regulated, at least in part, by direct contacts between syt and SNAP-25/syntaxin...
  18. ncbi request reprint Different domains of synaptotagmin control the choice between kiss-and-run and full fusion
    Chih Tien Wang
    Department of Physiology, University of Wisconsin Madison, Madison, Wisconsin 53706, USA
    Nature 424:943-7. 2003
    ..Syt thus regulates the choice between full fusion and kiss-and-run, with Ca2+ binding to the C2A and C2B domains playing an important role in this choice...
  19. pmc Role of synaptotagmin in Ca2+-triggered exocytosis
    Ward C Tucker
    Department of Physiology, SMI 129, University of Wisconsin, 1300 University Avenue, Madison, WI 53706, U S A
    Biochem J 366:1-13. 2002
    ..the members of this gene family, with particular emphasis on the question of whether and how synaptotagmin I functions during the final stages of membrane fusion: does it regulate the Ca(2+)-triggered opening and dilation of fusion pores?..
  20. pmc Three distinct kinetic groupings of the synaptotagmin family: candidate sensors for rapid and delayed exocytosis
    Enfu Hui
    Department of Physiology, University of Wisconsin, Madison, WI 53706, USA
    Proc Natl Acad Sci U S A 102:5210-4. 2005
    ..We also compared the temperature dependence of Ca2+.syt.membrane assembly and disassembly reactions by using squid and rat syt I. These results indicate that syts have diverged to release Ca2+ and membranes with distinct kinetics...
  21. ncbi request reprint PIP2 increases the speed of response of synaptotagmin and steers its membrane-penetration activity toward the plasma membrane
    Jihong Bai
    Department of Physiology, University of Wisconsin, Madison, Wisconsin 53706, USA
    Nat Struct Mol Biol 11:36-44. 2004
    ..We propose that syt-PIP2 interactions are involved in exocytosis by facilitating the close apposition of the vesicle and target membrane on rapid time scales in response to Ca2+...
  22. ncbi request reprint Reconstitution of Ca2+-regulated membrane fusion by synaptotagmin and SNAREs
    Ward C Tucker
    Department of Physiology, University of Wisconsin, Madison, WI 53706, USA
    Science 304:435-8. 2004
    ..Stimulation of fusion was abolished by disrupting the Ca2+-binding activity, or by severing the tandem C2 domains, of syt. Thus, syt and SNAREs are likely to represent the minimal protein complement for Ca2+-triggered exocytosis...
  23. ncbi request reprint Mutations in the effector binding loops in the C2A and C2B domains of synaptotagmin I disrupt exocytosis in a nonadditive manner
    Ping Wang
    Department of Physiology, University of Wisconsin, 1300 University Avenue, Madison, WI 53706, USA
    J Biol Chem 278:47030-7. 2003
    ..These findings indicate that the tandem C2 domains of syt cooperate with one another to trigger release via loop-mediated electrostatic interactions with effector molecules...
  24. ncbi request reprint Application of fluorescent probes to study mechanics and dynamics of Ca2+-triggered synaptotagmin C2 domain-membrane interactions
    Jihong Bai
    Department of Physiology, University of Wisconsin, Madison 53706, USA
    Methods Enzymol 360:238-58. 2003
  25. ncbi request reprint The C2 domains of synaptotagmin--partners in exocytosis
    Jihong Bai
    Department of Physiology, University of Wisconsin, 1300 University Avenue, SMI 129, Madison, WI 53706, USA
    Trends Biochem Sci 29:143-51. 2004
    ..Here, we focus on recent structure-function studies that are beginning to provide insights into the mechanism through which the C2 domains of syt trigger exocytosis...
  26. pmc Phosphatidylserine regulation of Ca2+-triggered exocytosis and fusion pores in PC12 cells
    Zhen Zhang
    Molecular and Cellular Pharmacology Graduate Program, University of Wisconsin School of Public Health, Madison, WI 53706, USA
    Mol Biol Cell 20:5086-95. 2009
    ..The possible relevance of these results to Ca(2+)-triggered Syt I binding is discussed along with other possible roles of PS...
  27. ncbi request reprint SV2 is the protein receptor for botulinum neurotoxin A
    Min Dong
    Howard Hughes Medical Institute and Department of Physiology, University of Wisconsin, Madison, WI 53706, USA
    Science 312:592-6. 2006
    ..Finally, mice that lacked an SV2 isoform (SV2B) displayed reduced sensitivity to BoNT/A. Thus, SV2 acts as the protein receptor for BoNT/A...
  28. pmc Productive hemifusion intermediates in fast vesicle fusion driven by neuronal SNAREs
    Tingting Liu
    Department of Chemistry, University of Wisconsin Madison, Madison, Wisconsin, USA
    Biophys J 94:1303-14. 2008
    ..This suggests similar underlying molecular pathways for protein-free and neuronal SNARE-driven fusion. Removal of phosphatidylserine from the v-SNARE vesicle has no effect on docking or fusion...
  29. pmc C2A activates a cryptic Ca(2+)-triggered membrane penetration activity within the C2B domain of synaptotagmin I
    Jihong Bai
    Department of Physiology, University of Wisconsin, Madison, WI 53706, USA
    Proc Natl Acad Sci U S A 99:1665-70. 2002
    ..A number of proteins contain more than one C2 domain; the findings reported here suggest these domains may harbor cryptic activities that are not detected when they are studied in isolation...
  30. ncbi request reprint Fusion pores and fusion machines in Ca2+-triggered exocytosis
    Meyer B Jackson
    Howard Hughes Medical Institute, 2Department of Physiology, University of Wisconsin, Madison, Wisconsin 53706, USA
    Annu Rev Biophys Biomol Struct 35:135-60. 2006
    ..We summarize present knowledge of fusion machines and fusion pores studied in vitro, in neurons, and in neuroendocrine cells, and synthesize this knowledge into some specific and detailed hypotheses for exocytosis...
  31. ncbi request reprint Transmembrane segments of syntaxin line the fusion pore of Ca2+-triggered exocytosis
    Xue Han
    Department of Physiology, University of Wisconsin, 1300 University Avenue, Madison, WI 53706, USA
    Science 304:289-92. 2004
    ..The residues that influenced fusion-pore flux lay along one face of an alpha-helical model. Thus, the fusion pore is formed at least in part by a circular arrangement of 5 to 8 Syx transmembrane segments in the plasma membrane...
  32. pmc Synaptotagmin IV: a multifunctional regulator of peptidergic nerve terminals
    Zhenjie Zhang
    Department of Physiology, University of Wisconsin School of Medicine and Public Health, 1300 University Avenue, Madison, Wisconsin 53706, USA
    Nat Neurosci 12:163-71. 2009
    ..Given the neuroendocrine functions of the posterior pituitary, changes in Syt IV levels could be involved in endocrine transitions involving alterations in the release of the neuropeptides oxytocin and vasopressin...
  33. pmc Glycosylated SV2A and SV2B mediate the entry of botulinum neurotoxin E into neurons
    Min Dong
    Howard Hughes Medical Institute and Department of Physiology, University of Wisconsin, Madison, WI 53706, USA
    Mol Biol Cell 19:5226-37. 2008
    ..Together, the data reported here demonstrate that glycosylated SV2A and SV2B act in conjunction with gangliosides to mediate the entry of BoNT/E into neurons...
  34. ncbi request reprint CAPS acts at a prefusion step in dense-core vesicle exocytosis as a PIP2 binding protein
    Ruslan N Grishanin
    Department of Biochemistry, University of Wisconsin, Madison, Wisconsin 53706, USA
    Neuron 43:551-62. 2004
    ..Regulation of PIP2 levels and CAPS-1 activity would control the secretion of neuropeptides and monoaminergic transmitters...
  35. ncbi request reprint Ca(2+)-synaptotagmin directly regulates t-SNARE function during reconstituted membrane fusion
    Akhil Bhalla
    Howard Hughes Medical Institute, University of Wisconsin, 1300 University Avenue, SMI 129, Madison, Wisconsin, USA
    Nat Struct Mol Biol 13:323-30. 2006
    ..Ca(2+)-syt drove assembly of SNAP-25 onto membrane-embedded syntaxin, providing direct evidence that Ca(2+)-syt alters t-SNARE structure...
  36. pmc Synaptotagmin-Ca2+ triggers two sequential steps in regulated exocytosis in rat PC12 cells: fusion pore opening and fusion pore dilation
    Chih Tien Wang
    Department of Physiology, University of Wisconsin, Madison, 53706, USA
    J Physiol 570:295-307. 2006
    ..The C2A and C2B domains of Syt I have different actions during these steps, and these actions may be linked to their distinctive effector interactions...
  37. pmc Autapses and networks of hippocampal neurons exhibit distinct synaptic transmission phenotypes in the absence of synaptotagmin I
    Huisheng Liu
    Howard Hughes Medical Institute and Department of Physiology, University of Wisconsin, Madison, Wisconsin 53706, USA
    J Neurosci 29:7395-403. 2009
    ..Thus, aspects of synaptic transmission differ between autaptic and dissociated cultures, and the synaptic transmission phenotype, resulting from loss of syt-I, is dictated by the connectivity of neurons...
  38. pmc Synaptotagmin isoforms couple distinct ranges of Ca2+, Ba2+, and Sr2+ concentration to SNARE-mediated membrane fusion
    Akhil Bhalla
    Department of Physiology, University of Wisconsin, Madison, WI 53706, USA
    Mol Biol Cell 16:4755-64. 2005
    ..Our data demonstrate that different syt isoforms are specialized to sense different ranges of divalent cations and that PS is an essential effector of Ca2+.syt action...
  39. pmc Biophysical characterization of styryl dye-membrane interactions
    Yao Wu
    Howard Hughes Medical Institute, University of Wisconsin, Madison, Wisconsin, USA
    Biophys J 97:101-9. 2009
    ..The data reported here aid interpretation of dye-release kinetics from single synaptic vesicles, and indicate that these probes dissociate from membranes on more rapid timescales than previously appreciated...
  40. pmc Synaptotagmin VII is targeted to secretory organelles in PC12 cells, where it functions as a high-affinity calcium sensor
    Ping Wang
    Department of Physiology, University of Wisconsin, 1300 University Ave, SMI 129, Madison, WI 53706, USA
    Mol Cell Biol 25:8693-702. 2005
    ..These data support the hypothesis that the complement of syt's expressed by a cell, in conjunction with their metal affinity, determines the divalent cation sensitivity of exocytosis...
  41. pmc Ca2+-triggered simultaneous membrane penetration of the tandem C2-domains of synaptotagmin I
    Enfu Hui
    Howard Hughes Medical Institute and Department of Physiology, University of Wisconsin School of Medicine, Madison, Wisconsin 53706, USA
    Biophys J 91:1767-77. 2006
    ..Tethering C2B to a mutant version of C2A that does not bind Ca2+ or membranes significantly increases the stability of Ca2+.C2B.membrane complexes, confirming that C2A affects the membrane-binding properties of the adjacent C2B domain...
  42. pmc Lipid mixing and content release in single-vesicle, SNARE-driven fusion assay with 1-5 ms resolution
    Tingting Wang
    Department of Chemistry, University of Wisconsin, Madison, Wisconsin, USA
    Biophys J 96:4122-31. 2009
    ..This may be related to in vivo observations suggesting that membrane lysis often competes with membrane fusion...
  43. pmc SNARE-driven, 25-millisecond vesicle fusion in vitro
    Tingting Liu
    Departments of Chemistry and Physiology, University of Wisconsin Madison, Madison, WI 53706, USA
    Biophys J 89:2458-72. 2005
    ..At present, in vitro fusion driven by SNARE complexes alone remains approximately 40 times slower than the fastest, submillisecond presynaptic vesicle population response...
  44. ncbi request reprint Expression of mutant huntingtin blocks exocytosis in PC12 cells by depletion of complexin II
    J Michael Edwardson
    Department of Pharmacology, Tennis Court Road, Cambridge CB2 1PD, United Kingdom
    J Biol Chem 278:30849-53. 2003
    ..Complexin II depletion in the brain may account for some of the abnormalities in neurotransmission associated with HD...
  45. pmc Ca2+-dependent, phospholipid-binding residues of synaptotagmin are critical for excitation-secretion coupling in vivo
    Brie E Paddock
    Department of Biomedical Sciences, Molecular, Cellular, and Integrative Neuroscience Program, Colorado State University, Fort Collins, Colorado 80523 1617, USA
    J Neurosci 28:7458-66. 2008
    ..Our model for synaptotagmin's direct role in coupling Ca(2+) binding to vesicle fusion incorporates this finding with results from multiple in vitro and in vivo studies...
  46. pmc SNAP-23 functions in docking/fusion of granules at low Ca2+
    Evelina Chieregatti
    Department of Anatomy and Cell Biology, Columbia University, College of Physicians and Surgeons, New York, New York 10032, USA
    Mol Biol Cell 15:1918-30. 2004
    ..Thus, the relative expression levels of SNAP-25 and SNAP-23 might control the mode (regulated vs. basal) of granule release by forming docking complexes at different Ca(2+) thresholds...
  47. ncbi request reprint Activation of postsynaptic Ca(2+) stores modulates glutamate receptor cycling in hippocampal neurons
    Brady J Maher
    Department of Molecular Biosciences, 4006 Haworth Hall, The University of Kansas, Lawrence, KS 66045 2106, USA
    J Neurophysiol 93:178-88. 2005
    ..These results suggest that IP(3)R-mediated Ca(2+) release can enhance AMPAR EPSC amplitudes through mechanisms that involve AMPAR-PDZ interactions and/or synaptotagmin-SNARE-mediated receptor trafficking...
  48. pmc Effects of synaptotagmin reveal two distinct mechanisms of agonist-stimulated internalization of the M4 muscarinic acetylcholine receptor
    Michael T Madziva
    Department of Pharmacology, University of Cambridge, Cambridge CB2 1PD
    Br J Pharmacol 144:761-71. 2005
    ..PIP2 might play a role as an intermediary in the formation of this complex...
  49. ncbi request reprint Molecular regulation of membrane resealing in 3T3 fibroblasts
    Sheldon S Shen
    Department of Genetics, Development, and Cell Biology, Iowa State University, Ames, Iowa 50011, USA
    J Biol Chem 280:1652-60. 2005
    ..The pattern of inhibition by synaptotagmin C2 fragments that we observed cannot be used to specify a vesicle compartment, such as lysosomes, in membrane repair...
  50. pmc Visualization of synaptotagmin I oligomers assembled onto lipid monolayers
    Yi Wu
    Department of Biological Sciences and Biotechnology, State Key Laboratory of Biomembranes, Tsinghua University, Beijing 100084, People s Republic of China
    Proc Natl Acad Sci U S A 100:2082-7. 2003
    ..Ca(2+)-mediated rearrangements between syt subunits may regulate the opening or dilation kinetics of fusion pores or may play a role in endocytosis after fusion...
  51. pmc Single molecule mechanical probing of the SNARE protein interactions
    W Liu
    Department of Physics, University of California, Riverside, California 92521, USA
    Biophys J 91:744-58. 2006
    ..When SNAP25B is present in the complex, it creates a local interaction at the 0 (ionic) layer by cuffing Sx1A and Sb2. Force loading rate studies indicate that the ternary complex interaction is more stable than the Sx1A-Sb2 interaction...
  52. pmc Ca2+ and synaptotagmin VII-dependent delivery of lysosomal membrane to nascent phagosomes
    Cecilia Czibener
    Section of Microbial Pathogenesis, Yale University School of Medicine, New Haven, CT 06510, USA
    J Cell Biol 174:997-1007. 2006
    ..Thus, Syt VII regulates the Ca2+-dependent mobilization of lysosomes as a supplemental source of membrane during phagocytosis...
  53. ncbi request reprint Structural basis of cell surface receptor recognition by botulinum neurotoxin B
    Qing Chai
    Department of Molecular Biology, The Scripps Research Institute, 10550 N Torrey Pines Road, La Jolla, California 92037, USA
    Nature 444:1096-100. 2006
    ..The results provide structural insights into how BoNTs recognize protein receptors and reveal a promising target for blocking toxin-receptor recognition...
  54. ncbi request reprint ENaC subunit-subunit interactions and inhibition by syntaxin 1A
    Bakhrom K Berdiev
    Univ of Alabama at Birmingham, 1918 University Blvd, MCLM 704, Birmingham, AL 35294 0005, USA
    Am J Physiol Renal Physiol 286:F1100-6. 2004
    ..Our findings provide evidence for a direct physical interaction between ENaC and syntaxin 1A and suggest involvement of ENaC's cytoplasmic domains in functional modulation of ENaC activity by syntaxin 1A...
  55. pmc Atomic force microscope spectroscopy reveals a hemifusion intermediate during soluble N-ethylmaleimide-sensitive factor-attachment protein receptors-mediated membrane fusion
    Midhat H Abdulreda
    University of Miami Miller School of Medicine, Physiology and Biophysics Department, Miami, Florida 33136, USA
    Biophys J 94:648-55. 2008
    ....
  56. pmc Botulinum toxin type B micromechanosensor
    W Liu
    Department of Physics, University of California, Riverside, CA 92521, USA
    Proc Natl Acad Sci U S A 100:13621-5. 2003
    ..The technique is of broad interest and will find uses outside toxicology...

Research Grants23

  1. Receptors for clostridial neurotoxins
    EDWIN CHAPMAN; Fiscal Year: 2005
    ..The studies proposed here will provide new insights into the molecular mechanism of action of the BoNTs, and may provide a novel means to prevent poisoning by these substances. ..
  2. Synaptotagmin in Excitation-Coupling
    EDWIN CHAPMAN; Fiscal Year: 2006
    ..Finally, defining this mechanism should ultimately provide targets for treatment of diseases in which synaptic transmission is impaired. ..
  3. Receptors for clostridial neurotoxins
    EDWIN CHAPMAN; Fiscal Year: 2006
    ..The studies proposed here will provide new insights into the molecular mechanism of action of the BoNTs, and may provide a novel means to prevent poisoning by these substances. ..
  4. Receptors for clostridial neurotoxins
    EDWIN CHAPMAN; Fiscal Year: 2007
    ..The studies proposed here will provide new insights into the molecular mechanism of action of the BoNTs, and may provide a novel means to prevent poisoning by these substances. ..
  5. Synaptotagmin C2B Domain as a Ca2+ Sensing Module
    EDWIN CHAPMAN; Fiscal Year: 2007
    ..This will aid efforts to alter communication between neurons in disease states where synaptic transmission is impaired. ..
  6. Synaptotagmin C2B Domain as a Ca2+ Sensing Module
    EDWIN CHAPMAN; Fiscal Year: 2009
    ..This will aid efforts to alter communication between neurons in disease states where synaptic transmission is impaired. ..
  7. Synaptotagmin C2B Domain as a Ca2+ Sensing Module
    Edwin R Chapman; Fiscal Year: 2010
    ..This will aid efforts to alter communication between neurons in disease states where synaptic transmission is impaired. ..
  8. Synaptotagmin in Excitation-Coupling
    EDWIN CHAPMAN; Fiscal Year: 2005
    ..Finally, defining this mechanism should ultimately provide targets for treatment of diseases in which synaptic transmission is impaired. ..
  9. Synaptotagmin C2B Domain as a Ca2+-sensing module
    EDWIN CHAPMAN; Fiscal Year: 2005
    ..Thus, a better understanding of the release process will provide insights into novel modes of synaptic plasticity and should ultimately provide targets for the treatment of diseases in which synaptic transmission is impaired. ..
  10. Receptors for clostridial neurotoxins
    EDWIN CHAPMAN; Fiscal Year: 2004
    ..The studies proposed here will provide new insights into the molecular mechanism of action of the BoNTs, and may provide a novel means to prevent poisoning by these substances. ..
  11. SYNAPTOTAGMIN IN EXCITATION/SECRETION COUPLING
    EDWIN CHAPMAN; Fiscal Year: 1999
    ..Finally, defining this mechanism should ultimately provide targets for treatment of diseases in which synaptic transmission is impaired. ..
  12. SYNAPTOTAGMIN IN EXCITATION/SECRETION COUPLING
    EDWIN CHAPMAN; Fiscal Year: 2000
    ..Finally, defining this mechanism should ultimately provide targets for treatment of diseases in which synaptic transmission is impaired. ..
  13. SYNAPTOTAGMIN IN EXCITATION/SECRETION COUPLING
    EDWIN CHAPMAN; Fiscal Year: 2001
    ..Finally, defining this mechanism should ultimately provide targets for treatment of diseases in which synaptic transmission is impaired. ..
  14. Synaptotagmin C2B Domain as a Ca2+-sensing module
    EDWIN CHAPMAN; Fiscal Year: 2002
    ..Thus, a better understanding of the release process will provide insights into novel modes of synaptic plasticity and should ultimately provide targets for the treatment of diseases in which synaptic transmission is impaired. ..
  15. SYNAPTOTAGMIN IN EXCITATION/SECRETION COUPLING
    EDWIN CHAPMAN; Fiscal Year: 2002
    ..Finally, defining this mechanism should ultimately provide targets for treatment of diseases in which synaptic transmission is impaired. ..
  16. Synaptotagmin in Excitation-Coupling
    EDWIN CHAPMAN; Fiscal Year: 2003
    ..Finally, defining this mechanism should ultimately provide targets for treatment of diseases in which synaptic transmission is impaired. ..
  17. Synaptotagmin C2B Domain as a Ca2+-sensing module
    EDWIN CHAPMAN; Fiscal Year: 2003
    ..Thus, a better understanding of the release process will provide insights into novel modes of synaptic plasticity and should ultimately provide targets for the treatment of diseases in which synaptic transmission is impaired. ..
  18. Synaptotagmin C2B Domain as a Ca2+-sensing module
    EDWIN CHAPMAN; Fiscal Year: 2004
    ..Thus, a better understanding of the release process will provide insights into novel modes of synaptic plasticity and should ultimately provide targets for the treatment of diseases in which synaptic transmission is impaired. ..
  19. Synaptotagmin in Excitation-Coupling
    EDWIN CHAPMAN; Fiscal Year: 2004
    ..Finally, defining this mechanism should ultimately provide targets for treatment of diseases in which synaptic transmission is impaired. ..
  20. Synaptotagmin C2B Domain as a Ca2+ Sensing Module
    EDWIN CHAPMAN; Fiscal Year: 2009
    ..This will aid efforts to alter communication between neurons in disease states where synaptic transmission is impaired. ..