synaptosomal associated protein 25

Summary

Summary: A ubiquitous target SNARE protein that interacts with SYNTAXIN and SYNAPTOBREVIN. It is a core component of the machinery for intracellular MEMBRANE FUSION. The sequence contains 2 SNARE domains, one is the prototype for the Qb-SNARES, and the other is the prototype for the Qc-SNARES.

Top Publications

  1. Sollner T, Bennett M, Whiteheart S, Scheller R, Rothman J. A protein assembly-disassembly pathway in vitro that may correspond to sequential steps of synaptic vesicle docking, activation, and fusion. Cell. 1993;75:409-18 pubmed
    ..The alpha-SNAP-SNARE complex can bind NSF, and NSF-dependent hydrolysis of ATP dissociates the complex, separating syntaxin, SNAP-25, and VAMP. ATP hydrolysis by NSF may provide motion to initiate bilayer fusion. ..
  2. James D, Kowalchyk J, Daily N, Petrie M, Martin T. CAPS drives trans-SNARE complex formation and membrane fusion through syntaxin interactions. Proc Natl Acad Sci U S A. 2009;106:17308-13 pubmed publisher
    ..The results revealed an unexpected activity of a priming protein to accelerate fusion by efficiently promoting trans-SNARE complex formation. CAPS may function in priming by organizing SNARE complexes on the plasma membrane. ..
  3. Selak S, Paternain A, Aller M, Aller I, Picó E, Rivera R, et al. A role for SNAP25 in internalization of kainate receptors and synaptic plasticity. Neuron. 2009;63:357-71 pubmed publisher
    ..As EPSC(KAR) LTD, SNAP25/PICK1/GluK5 interactions are dynamically regulated by PKC. ..
  4. Walter A, Wiederhold K, Bruns D, Fasshauer D, Sørensen J. Synaptobrevin N-terminally bound to syntaxin-SNAP-25 defines the primed vesicle state in regulated exocytosis. J Cell Biol. 2010;188:401-13 pubmed publisher
    ..Our data are consistent with a model in which the N terminus of the SNARE complex assembles during vesicle priming, followed by Ca(2+)-triggered C-terminal assembly and membrane fusion...
  5. Halemani N, Bethani I, Rizzoli S, Lang T. Structure and dynamics of a two-helix SNARE complex in live cells. Traffic. 2010;11:394-404 pubmed publisher
    ..We conclude that a zippered Q(a)Q(b)-SNARE complex represents a short-lived SNARE intermediate in intact cells, most likely providing an initial molecular platform toward membrane fusion. ..
  6. Wiederhold K, Fasshauer D. Is assembly of the SNARE complex enough to fuel membrane fusion?. J Biol Chem. 2009;284:13143-52 pubmed publisher
    ..This strategy revealed that the N-terminal synaptobrevin coil binds reversibly with nanomolar affinity. This suggests that individual, membrane-bridging SNARE complexes can provide much less pulling force than previously claimed. ..
  7. McKee A, Loscher J, O Sullivan N, Chadderton N, Palfi A, Batti L, et al. AAV-mediated chronic over-expression of SNAP-25 in adult rat dorsal hippocampus impairs memory-associated synaptic plasticity. J Neurochem. 2010;112:991-1004 pubmed publisher
    ..Together these studies provide the first evidence that excess SNAP-25 activity, restricted to the adult period, is sufficient to mediate significant deficits in the memory formation process. ..
  8. Domanska M, Kiessling V, Stein A, Fasshauer D, Tamm L. Single vesicle millisecond fusion kinetics reveals number of SNARE complexes optimal for fast SNARE-mediated membrane fusion. J Biol Chem. 2009;284:32158-66 pubmed publisher
    ..This might be interpreted by fusion sites consisting of eight SNARE complexes that each activate in a single rate-limiting step in 8 ms. ..
  9. Gizer I, Ficks C, Waldman I. Candidate gene studies of ADHD: a meta-analytic review. Hum Genet. 2009;126:51-90 pubmed publisher
    ..g., ADHD subtype diagnoses, gender, exposure to environmental risk factors). We conclude with a discussion of these findings in relation to emerging themes relevant to future studies of the genetics of ADHD. ..

More Information

Publications62

  1. Cognato G, Agostinho P, Hockemeyer J, Muller C, Souza D, Cunha R. Caffeine and an adenosine A(2A) receptor antagonist prevent memory impairment and synaptotoxicity in adult rats triggered by a convulsive episode in early life. J Neurochem. 2010;112:453-62 pubmed publisher
    ..These results show that a single convulsive episode in early life causes a delayed memory deficit in adulthood accompanied by a glutamatergic synaptotoxicity that was prevented by caffeine or adenosine A(2A)R antagonists. ..
  2. Abdulreda M, Bhalla A, Rico F, Berggren P, Chapman E, Moy V. Pulling force generated by interacting SNAREs facilitates membrane hemifusion. Integr Biol (Camb). 2009;1:301-10 pubmed publisher
  3. Gonçalves J, Baptista S, Martins T, Milhazes N, Borges F, Ribeiro C, et al. Methamphetamine-induced neuroinflammation and neuronal dysfunction in the mice hippocampus: preventive effect of indomethacin. Eur J Neurosci. 2010;31:315-26 pubmed publisher
    ..In conclusion, we demonstrated that METH triggers an inflammatory process and leads to neuronal dysfunction in the hippocampus, which can be prevented by an anti-inflammatory treatment. ..
  4. Sakon J, WENINGER K. Detecting the conformation of individual proteins in live cells. Nat Methods. 2010;7:203-5 pubmed publisher
    ..Individual proteins rapidly incorporated into folded complexes at the cell membrane, demonstrating the potential of this method to reveal dynamic interactions within cells. ..
  5. Liu Y, Ye Z, Yang H, Zhou L, Fan D, He S, et al. Disturbances of soluble N-ethylmaleimide-sensitive factor attachment proteins in hippocampal synaptosomes contribute to cognitive impairment after repetitive formaldehyde inhalation in male rats. Neuroscience. 2010;169:1248-54 pubmed publisher
  6. Cohen D, Segal M. Homeostatic presynaptic suppression of neuronal network bursts. J Neurophysiol. 2009;101:2077-88 pubmed publisher
    ..Thus a long-lasting increase in activity downregulates neurotransmitter release to prevent over-excitation of the network and, consequently, blocks the generation of network bursts. ..
  7. Beasley C, Dwork A, Rosoklija G, Mann J, Mancevski B, Jakovski Z, et al. Metabolic abnormalities in fronto-striatal-thalamic white matter tracts in schizophrenia. Schizophr Res. 2009;109:159-66 pubmed publisher
    ..Observed changes in lactate and alanine levels indicate metabolic abnormalities within the ALIC in schizophrenia. ..
  8. Hu X, Ji S, Li Y, Fan C, Cai H, Yang J, et al. Acrosome formation-associated factor is involved in fertilization. Fertil Steril. 2010;93:1482-92 pubmed publisher
    ..To investigate the effects of a novel acrosome formation-associated factor (Afaf) on fertilization by its regulation of acrosomal exocytosis and endosomal trafficking...
  9. Masuyer G, Thiyagarajan N, James P, Marks P, Chaddock J, Acharya K. Crystal structure of a catalytically active, non-toxic endopeptidase derivative of Clostridium botulinum toxin A. Biochem Biophys Res Commun. 2009;381:50-3 pubmed publisher
  10. Condliffe S, Corradini I, Pozzi D, Verderio C, Matteoli M. Endogenous SNAP-25 regulates native voltage-gated calcium channels in glutamatergic neurons. J Biol Chem. 2010;285:24968-76 pubmed publisher
    ..Overall, this study demonstrates that endogenous SNAP-25 negatively regulates native VGCCs in glutamatergic neurons which could have important implications for neurological diseases associated with altered SNAP-25 expression. ..
  11. Guan L, Wang B, Chen Y, Yang L, Li J, Qian Q, et al. A high-density single-nucleotide polymorphism screen of 23 candidate genes in attention deficit hyperactivity disorder: suggesting multiple susceptibility genes among Chinese Han population. Mol Psychiatry. 2009;14:546-54 pubmed publisher
    ..05. This study has identified several genes as promising susceptibility loci for ADHD. Replication efforts and further investigations remain necessary to provide definite proof of association. ..
  12. Conti A, Maas J, Muglia L, Dave B, Vogt S, Tran T, et al. Distinct regional and subcellular localization of adenylyl cyclases type 1 and 8 in mouse brain. Neuroscience. 2007;146:713-29 pubmed
    ..Together, these data provide insight into the functional roles of AC1 and AC8 in mice as reflected by their distinct localization in cellular and subcellular compartments. ..
  13. Coghill D, Banaschewski T. The genetics of attention-deficit/hyperactivity disorder. Expert Rev Neurother. 2009;9:1547-65 pubmed publisher
    ..Gene-environment interactions, which are as yet relatively understudied, are likely to be of importance in fully understanding the role of genes in ADHD and will be discussed. ..
  14. Serra S, Cuenca Le n E, Llobet A, Rubio Moscardo F, Plata C, Carre o O, et al. A mutation in the first intracellular loop of CACNA1A prevents P/Q channel modulation by SNARE proteins and lowers exocytosis. Proc Natl Acad Sci U S A. 2010;107:1672-7 pubmed publisher
  15. Nuss J, Ruthel G, Tressler L, Wanner L, Torres Melendez E, Hale M, et al. Development of cell-based assays to measure botulinum neurotoxin serotype A activity using cleavage-sensitive antibodies. J Biomol Screen. 2010;15:42-51 pubmed publisher
    ..Importantly, these assays provided novel methods for evaluating BoNT/A activity in cellular models of intoxication and allowed for the high-throughput evaluation of experimental compounds. ..
  16. Mima J, Wickner W. Phosphoinositides and SNARE chaperones synergistically assemble and remodel SNARE complexes for membrane fusion. Proc Natl Acad Sci U S A. 2009;106:16191-6 pubmed publisher
    ..This ternary synergy of phosphoinositides and 2 SNARE chaperone systems is required for rapid fusion. ..
  17. McMahon H, Sudhof T. Synaptic core complex of synaptobrevin, syntaxin, and SNAP25 forms high affinity alpha-SNAP binding site. J Biol Chem. 1995;270:2213-7 pubmed
    ..Thus, alpha-SNAP probably functions in a late step of the membrane fusion reaction after the formation of the synaptobrevin-syntaxin-SNAP25 core complex. ..
  18. Chen S, Tari P, She K, Haas K. Neurexin-neuroligin cell adhesion complexes contribute to synaptotropic dendritogenesis via growth stabilization mechanisms in vivo. Neuron. 2010;67:967-83 pubmed publisher
  19. Gnanasekar M, Suleman F, Ramaswamy K, Caldwell J. Identification of sex hormone binding globulin-interacting proteins in the brain using phage display screening. Int J Mol Med. 2009;24:421-6 pubmed
    ..Of the twenty binding proteins analyzed, three were found to be membrane-associated proteins: synaptosomal associated protein 25 (SNAP25), Thy-1 cell surface antigen and zonadhesin...
  20. Yamboliev I, Smyth L, Durnin L, Dai Y, Mutafova Yambolieva V. Storage and secretion of beta-NAD, ATP and dopamine in NGF-differentiated rat pheochromocytoma PC12 cells. Eur J Neurosci. 2009;30:756-68 pubmed publisher
    ..However, the three substances appear to have different preferential sites of release upon membrane depolarization including sites associated with SNAP-25 and sites not associated with SNAP-25. ..
  21. Wang Y, Cunningham D, Tempel B, Rubel E. Compartment-specific regulation of plasma membrane calcium ATPase type 2 in the chick auditory brainstem. J Comp Neurol. 2009;514:624-40 pubmed publisher
    ..This provides a potential mechanism by which deprivation can change calcium transport that, in turn, may be important for rapid, compartment-specific dendritic remodeling. ..
  22. Weber J, Reim K, Sørensen J. Opposing functions of two sub-domains of the SNARE-complex in neurotransmission. EMBO J. 2010;29:2477-90 pubmed publisher
    ..In addition, the N-terminal deletion delays vesicle priming after a high-frequency train. We propose that the stability of N-terminal two-thirds of the SNARE-bundle has a function for vesicle priming and limiting spontaneous release. ..
  23. Canas P, Duarte J, Rodrigues R, Köfalvi A, Cunha R. Modification upon aging of the density of presynaptic modulation systems in the hippocampus. Neurobiol Aging. 2009;30:1877-84 pubmed publisher
    ..Thus aging causes an imbalance of excitatory versus inhibitory nerve terminal markers and causes a predominant decrease of inhibitory rather than facilitatory presynaptic modulation systems. ..
  24. Gomes C, Simões P, Canas P, Quiroz C, Sebastião A, Ferré S, et al. GDNF control of the glutamatergic cortico-striatal pathway requires tonic activation of adenosine A receptors. J Neurochem. 2009;108:1208-19 pubmed publisher
    ..The results provide the first functional and morphological evidence that GDNF controls cortico-striatal glutamatergic pathways in a manner largely dependent on the co-activation of adenosine A(2A) receptors. ..
  25. Corradini I, Verderio C, Sala M, Wilson M, Matteoli M. SNAP-25 in neuropsychiatric disorders. Ann N Y Acad Sci. 2009;1152:93-9 pubmed publisher
    ..Recent genetic studies of human populations and of some mouse models implicate alterations in SNAP-25 gene structure, expression, and/or function in contributing directly to these distinct neuropsychiatric and neurological disorders. ..
  26. Greaves J, Prescott G, Gorleku O, Chamberlain L. Regulation of SNAP-25 trafficking and function by palmitoylation. Biochem Soc Trans. 2010;38:163-6 pubmed publisher
    ..In this review, we discuss the mechanisms of SNAP-25 palmitoylation and how this modification regulates the intracellular trafficking and exocytotic function of this essential protein. ..
  27. Lee M, Zhu Y, Sun Z, Rhee H, Jeromin A, Roder J, et al. Accumulation of synaptosomal-associated protein of 25 kDa (SNAP-25) and other proteins associated with the secretory pathway in GH4C1 cells upon treatment with estradiol, insulin, and epidermal growth factor. Endocrinology. 2000;141:3485-92 pubmed
    ..Hormone treatment of GH4C1 cells therefore induces accumulation of specific proteins in all parts of the secretory pathway and causes morphological changes in addition to accumulating secretory granules. ..
  28. Sato M, Mori Y, Matsui T, Aoki R, Oya M, Yanagihara Y, et al. Role of the polybasic sequence in the Doc2alpha C2B domain in dense-core vesicle exocytosis in PC12 cells. J Neurochem. 2010;114:171-81 pubmed publisher
    ..These results indicate that the polybasic sequence in the C2B domain functions as a binding site for syntaxin-1a/SNAP-25 heterodimer and controls the number of 'readily releasable' vesicles in neuroendocrine cells. ..
  29. Froehlich T, McGough J, Stein M. Progress and promise of attention-deficit hyperactivity disorder pharmacogenetics. CNS Drugs. 2010;24:99-117 pubmed publisher
  30. Pires Alves M, Ho M, Aberle K, Janda K, Wilson B. Tandem fluorescent proteins as enhanced FRET-based substrates for botulinum neurotoxin activity. Toxicon. 2009;53:392-9 pubmed publisher
  31. Mazelova J, Ransom N, Astuto Gribble L, Wilson M, Deretic D. Syntaxin 3 and SNAP-25 pairing, regulated by omega-3 docosahexaenoic acid, controls the delivery of rhodopsin for the biogenesis of cilia-derived sensory organelles, the rod outer segments. J Cell Sci. 2009;122:2003-13 pubmed publisher
    ..We show further that DHA, an essential polyunsaturated fatty acid of the ROS, increases pairing of syntaxin 3 and SNAP-25 to regulate expansion of the ciliary membrane and ROS biogenesis. ..
  32. Chen S, Barbieri J. Engineering botulinum neurotoxin to extend therapeutic intervention. Proc Natl Acad Sci U S A. 2009;106:9180-4 pubmed publisher
    ..These studies show the feasibility of genetically modifying LCs to target a nonneuronal SNARE protein that extends therapeutic potential for treatment of human hypersecretion diseases. ..
  33. Schames J, Dov Prero Y, Schames D, Schames M, Gabriel W, Reed R. Uncontrollable distant effects of botulinum neurotoxin injections. J Calif Dent Assoc. 2009;37:44-5 pubmed
    ..These uncontrollable distant effects of "off-label" botulinum neurotoxin injections, at the very least, must be thoroughly disclosed to patients. ..
  34. Clapp T, Medler K, Damak S, Margolskee R, Kinnamon S. Mouse taste cells with G protein-coupled taste receptors lack voltage-gated calcium channels and SNAP-25. BMC Biol. 2006;4:7 pubmed
    ..The taste receptor cells responsible for the transduction of bitter, sweet, and umami stimuli are unlikely to communicate with nerve fibers by using conventional chemical synapses. ..
  35. Lawrence G, Aoki K, Dolly J. Excitatory cholinergic and purinergic signaling in bladder are equally susceptible to botulinum neurotoxin a consistent with co-release of transmitters from efferent fibers. J Pharmacol Exp Ther. 2010;334:1080-6 pubmed publisher
    ..Because purinergic receptors are known mediators of sensory afferent excitation, inhibition of efferent ATP release by BoNT/A could also help to ameliorate acute pain and urgency sensation reported by some recipients. ..
  36. Li Q, Wong J, Lu G, Antonio G, Yeung D, Ng T, et al. Gene expression of synaptosomal-associated protein 25 (SNAP-25) in the prefrontal cortex of the spontaneously hypertensive rat (SHR). Biochim Biophys Acta. 2009;1792:766-76 pubmed publisher
    ..We also measured the expression of synaptosomal-associated protein 25 (SNAP-25) in SHR in PFC. The results showed decreased expression of SNAP-25 mRNA in the PFC of SHR; this defect disappeared after repeated injection of D-AMP. ..
  37. Ardais A, Viola G, Costa M, Nunes F, Behr G, Klamt F, et al. Acute treatment with diphenyl diselenide inhibits glutamate uptake into rat hippocampal slices and modifies glutamate transporters, SNAP-25, and GFAP immunocontent. Toxicol Sci. 2010;113:434-43 pubmed publisher
  38. Darios F, Ruipérez V, Lopez I, Villanueva J, Gutierrez L, Davletov B. Alpha-synuclein sequesters arachidonic acid to modulate SNARE-mediated exocytosis. EMBO Rep. 2010;11:528-33 pubmed publisher
    ..Alpha-synuclein sequesters arachidonic acid and thereby blocks the activation of SNAREs. Our data provide mechanistic insights into the action of alpha-synuclein in the modulation of neurotransmission. ..
  39. Ghiani C, Starcevic M, Rodriguez Fernandez I, Nazarian R, Cheli V, Chan L, et al. The dysbindin-containing complex (BLOC-1) in brain: developmental regulation, interaction with SNARE proteins and role in neurite outgrowth. Mol Psychiatry. 2010;15:115, 204-15 pubmed publisher
  40. Zhang H, Zhu Y, Chang H, Chen J. [Association between SNAP-25 gene polymorphism and attention deficit hyperactivity disorder]. Zhonghua Er Ke Za Zhi. 2008;46:564-9 pubmed
    ..05). No association was found between SNAP-25 polymorphisms and ADHD. There was a possible association between rs362549 SNP polymorphism and ADHD subtypes, but the findings require replication before drawing a definitive conclusion. ..
  41. Grumelli C, Corradini I, Matteoli M, Verderio C. Intrinsic calcium dynamics control botulinum toxin A susceptibility in distinct neuronal populations. Cell Calcium. 2010;47:419-24 pubmed publisher
    ..These data indicate that intrinsic calcium dynamics control botulinum A susceptibility in distinct neuronal populations. ..
  42. Wu Q, Rui Q, He K, Shen L, Wang D. UNC-64 and RIC-4, the plasma membrane-associated SNAREs syntaxin and SNAP-25, regulate fat storage in nematode Caenorhabditis elegans. Neurosci Bull. 2010;26:104-16 pubmed publisher
    ..The plasma membrane-associated SNAREs syntaxin/unc-64 and SNAP-25/ric-4 function in parallel in regulating fat storage in C. elegans, probably through the ARC105/mdt-15- and SREBP/sbp-1-mediated signaling pathways. ..
  43. Fanous A, Zhao Z, van den Oord E, Maher B, Thiselton D, Bergen S, et al. Association study of SNAP25 and schizophrenia in Irish family and case-control samples. Am J Med Genet B Neuropsychiatr Genet. 2010;153B:663-674 pubmed publisher
    ..Although we failed to replicate this in an independent sample, this gene should be further tested in other samples. ..
  44. Kovacs Nagy R, Hu J, Ronai Z, Sasvari Szekely M. SNAP-25: a novel candidate gene in psychiatric genetics. Neuropsychopharmacol Hung. 2009;11:89-94 pubmed
    ..If the putative miR SNPs are shown to have a function in vivo their implication in further psychogenetic association studies will have a higher impact. ..
  45. Vikman J, Svensson H, Huang Y, Kang Y, Andersson S, Gaisano H, et al. Truncation of SNAP-25 reduces the stimulatory action of cAMP on rapid exocytosis in insulin-secreting cells. Am J Physiol Endocrinol Metab. 2009;297:E452-61 pubmed publisher
    ..Thus we hypothesize that SNAP-25 is a necessary partner in the complex mediating cAMP-enhanced rapid exocytosis in insulin-secreting cells. ..
  46. Miller V, Lawrence D, Coccaro G, Mondal T, Andrews K, Dreiem A, et al. Sex effects of interleukin-6 deficiency on neuroinflammation in aged C57Bl/6 mice. Brain Res. 2010;1318:11-22 pubmed publisher
    ..We suggest that IL-6 is important for promoting myelin synthesis in aged females, and that drugs which inhibit the synthesis of IL-6 in males may inadvertently affect fatty acid metabolism and augment aging-related neuroinflammation. ..
  47. Honma S, Taki K, Lei S, Niwa H, Wakisaka S. Immunohistochemical localization of SNARE proteins in dental pulp and periodontal ligament of the rat incisor. Anat Rec (Hoboken). 2010;293:1070-80 pubmed publisher
    ..Because those proteins participate in docking and exocytosis of synapse vesicles in the central nervous system, they might also contribute to vesicle exocytosis at receptive fields where apparent synapses are not present. ..
  48. Zhang Y, Kolli T, Hivley R, Jaber L, Zhao F, Yan J, et al. Characterization of the expression pattern of adrenergic receptors in rat taste buds. Neuroscience. 2010;169:1421-37 pubmed publisher
  49. Yu F, Sun L, Machaca K. Orai1 internalization and STIM1 clustering inhibition modulate SOCE inactivation during meiosis. Proc Natl Acad Sci U S A. 2009;106:17401-6 pubmed publisher
    ..Although STIM1 is phosphorylated during meiosis, phosphomimetic and alanine substitution mutations do not modulate STIM1 clustering, arguing that phosphorylation does not mediate STIM1 clustering inhibition during meiosis. ..
  50. Gao X, Su L, Zhao A, Luo X, Xia K. [Association of 14 polymorphisms in the five candidate genes and attention deficit hyperactivity disorder]. Zhongguo Dang Dai Er Ke Za Zhi. 2009;11:617-22 pubmed
    ..The specific combination of three sites of SNP in SNAP-25 gene and DRDI gene is found and shows an association with ADHD in 12 polymorphisms of the five candidate genes on glutamatergic/dopaminergic pathway. ..
  51. Bailey J, Lahiri D. A novel effect of rivastigmine on pre-synaptic proteins and neuronal viability in a neurodegeneration model of fetal rat primary cortical cultures and its implication in Alzheimer's disease. J Neurochem. 2010;112:843-53 pubmed publisher
  52. Shen J, Rathore S, Khandan L, Rothman J. SNARE bundle and syntaxin N-peptide constitute a minimal complement for Munc18-1 activation of membrane fusion. J Cell Biol. 2010;190:55-63 pubmed publisher
    ..Thus, the SNARE four-helix bundle and syntaxin N-peptide constitute a minimal complement for Munc18-1 activation of fusion. ..
  53. Oliver P, Davies K. Interaction between environmental and genetic factors modulates schizophrenic endophenotypes in the Snap-25 mouse mutant blind-drunk. Hum Mol Genet. 2009;18:4576-89 pubmed publisher