Recombinant Mouse Synaptosomal-associated protein 25 (Snap25)

1. We describe a high degree of structural similarity between the CpxII CTD and the SNAP25-SN1 domain (C-terminal half) and show that the CTD peptide lowers the rate of SDS-resistant SNARE complex formation in vitro. Moreover, corresponding CpxII:SNAP25 chimeras do restore complexin's function and even 'superclamp' tonic secretion. PMID: 30044227
2. Our findings provide in vivo functional evidence showing a critical role of SNAP-25 dysfunction on synaptic transmission, which contributes to the developmental of schizophrenia. PMID: 29318050
3. Snap-25-null mutant neurons degenerate after 4 days in vitro and contain fewer dense-core vesicles. PMID: 28404788
4. a mouse mutant engineered to express normal levels of SNAP-25 but only SNAP-25a shows metabolic disease. PMID: 26195742
5. The function of synaptotagmin-1 (syt-1):soluble NSF attachment protein receptor (SNARE) interactions during neurotransmission remains unclear. PMID: 27881774
6. proteins, such as syntaxin-1, Munc18-1, or SNAP-25, modulate alpha-synuclein neuropathy and/or are dysregulated in Alzheimer's disease, understanding this type of neurodegeneration may provide new links between synaptic defects and neurodegeneration in humans PMID: 28348137
7. Study showed that SNAP25 is synthesized in the motor nerve endings and that the level of SNAP25 mRNA affects the activity of exocytosis of the neurotransmitter PMID: 26518545
8. Data demonstrate a role for SNAP-25 in controlling PSD-95 clustering and open the possibility that genetic reductions of the protein levels may contribute to the pathology through an effect on postsynaptic function and plasticity. PMID: 25678324
9. Data suggest that porosome-associated proteins SNAP25, TREK-1, syntaxin-1A, and Gai3 exhibit stability and functionality such that isolated proteins can be reconstituted as insulin-secreting porosomes in cell membrane of live cells. PMID: 26523491
10. Study conducted long-term continuous video-EEG recordings of Snap25S187A/S187A mice and found that all mutant mice followed essentially the same process of epileptogenesis despite some individual differences PMID: 26220374
11. we demonstrate that Syb2 and SNAP25 mediate the vesicular release of BDNF in axons and dendrites of cortical neurons PMID: 25959820
12. The extreme C terminus of SNAP25 is a critical region for the GBetaGamma-SNARE interaction. PMID: 26519224
13. Reduction of SNAP-25 levels in adolescent mice was associated with hyperactivity, cognitive and social impairment and an abnormal EEG, characterized by the occurrence of frequent spikes. PMID: 25629685
14. Data show a significant increase of vesicle-associated membrane protein 2 (VAMP-2) mRNA expression, however, the expressions of synaptosome-associated protein of 25 kDa (SNAP-25) and syntaxin 1A did not exhibit the changes in hippocampus. PMID: 24488208
15. SNAP-25 phosphorylation is regulated in a stress-dependent manner through both central and peripheral mechanisms. PMID: 24374286
16. Results indicate that reduction of SNAP-25 expression is associated to generation of epileptiform discharges and cognitive dysfunctions, which can be effectively treated by antiepileptic drugs PMID: 23064108
17. direct interaction between TRIM9 and the Netrin-1 receptor DCC as well as a Netrin-1-sensitive interaction between TRIM9 and the SNARE component SNAP25. The interaction with SNAP25 negatively regulates SNARE-mediated exocytosis and axon PMID: 24778312
18. SNAP-25 regulates the organization of the molecular apparatus needed for dendritic spine formation by recruiting and stabilizing p140Cap. PMID: 23868368
19. PP2A participates in SNAP-25 dephosphorylation through calcium-dependent and calcium-independent mechanisms but is not involved in GAP-43 dephosphorylation. PMID: 23376809
20. Reduced SNAP-25 alters short-term plasticity at developing glutamatergic synapses. PMID: 23732542
21. Snapin, a SNAP-25 (synaptosomal-associated protein-25) interacting protein, interacts with LRRK2. PMID: 23949442
22. the substitution of Ala for Ser187 in SNAP-25 induces the immaturity of the dentate granule cells phenotype. PMID: 23497716
23. Data show the presence of the cleaved SNAP-25 (cl-SNAP-25) from the peripheral endings to the spinal cord, suggesting a retrograde transport of botulinum neurotoxin A (BoNT/A). PMID: 23110146
24. Cpsf2,Ppil2, and SNAP-25 are the most promising targets for the NSm protein of the virus during an infection. PMID: 22838834
25. Coimmunoprecipitation experiments between SNAP25 and VLGR1 show a physical interaction of these two proteins in organ of Corti and brain. PMID: 23035094
26. recently ingested chemical signals in the oral cavity during weaning increase the accumulation of SNAP25 in the gustatory and somatosensory cortices and promote neural plasticity during the development of the gustatory and somatosensory nervous systems. PMID: 22641083
27. Maternal lead exposure decreased the expression of SNAP-25 and negatively affected the learning and memory of the offspring. PMID: 21126476
28. The results of this study suggested that increased hippocampal SNAP-25 and Munc18-1 which seemingly result from decreased serum THs might involve the age-related impairment of spatial learning and memory. PMID: 22261019
29. Using unbiased, systematic proteomics to identify cysteine string protein alpha (CSPalpha) client proteins, study shows that SNAP-25 and the endocytic GTPase dynamin 1 are key clients of the Hsc70-CSPalpha chaperone complex. PMID: 22500636
30. The results of this study suggested that the isoform expression and total level of SNAP-25 affect both [Ca(2+)](res) dynamics and the ability of releasable vesicles to enter into a facilitated state. PMID: 22119397
31. findings suggest that the neurodegeneration in CSPalpha KO mice is primarily produced by defective SNAP-25 function, which causes neurodegeneration by impairing SNARE-complex assembly PMID: 22187053
32. AC6-mediated inhibition of neurite outgrowth was reversed by the overexpression of Snap25 or a Snapin mutant that could not be phosphorylated. PMID: 21986494
33. These results indicate that the three SNAP-25 family proteins display a differential distribution in the brain as well as in neuronal cells, and possibly play distinct roles. PMID: 21280044
34. Data show that deletion of CSPalpha produces an abnormal SNAP-25 conformer that inhibits SNARE-complex formation, and is subject to ubiquitylation and proteasomal degradation. PMID: 21151134
35. endogenous SNAP-25 regulates native voltage-gated calcium channels in glutamatergic neurons PMID: 20522554
36. used cultured autaptic hippocampal neurons from Snap-25 null mice rescued with mutants challenging the C-terminal, N-terminal and middle domains of the SNARE-bundle to dissect out the involvement of these domains in neurotransmission. PMID: 20562829
37. Synaptobrevin N-terminally bound to syntaxin-SNAP-25 defines the primed vesicle state in regulated exocytosis. PMID: 20142423
38. Environmental and genetic factors contribute to schizophrenic endophenotypes in a Snap-25 knockout mouse model. PMID: 19729413
39. SNARE protein SNAP-25 is the target of protein kinase C (PKC) phosphorylation critical to PKC-dependent incorporation of synaptic NMDA receptors. PMID: 20053906
40. spinal motor neurons up-regulate SNAP-25 to preserve vital neuromuscular function PMID: 11829411
41. Ca2+ modulates dynamic docking of granules to the plasma membrane and this process is due to a Ca2+-dependent interaction between SNAP-25 and synaptotagmin PMID: 12047557
42. SNAP25 is negatively regulated by thyroid hormones in the mouse adrenal gland PMID: 12438134
43. The removal of 9 C-terminal residues from SNAP-25 by BoNT/A leads to persistence of the inhibitory product due to the formation of a nonproductive SNARE complex(es) at release sites. PMID: 12727443
44. Without SNAP-25, vesicle docking persisted, but primed vesicle pools were empty and fast calcium-triggered release abolished. Single vesicular fusion events showed normal characteristics, except for a shorter duration of the fusion pore. PMID: 12859899
45. the relative expression levels of SNAP-25 and SNAP-23 might control the mode of granule release by forming docking complexes at different Ca(2+) thresholds PMID: 14742706
46. We conclude that increased expression of SNAP-25 is associated with NEFA-induced impairment of insulin secretion in mouse islets. PMID: 15063781
47. These observations support the hypothesis that SNAP25 is a plasma membrane factor that is responsible for sequential exocytosis. PMID: 15117968
48. Potentiated thalamic low voltage-acttivated currents that precede the appearance of slow wave discharges were noted in absence epilepsy model Coloboma SNAP-25 deficient mice PMID: 15175394
49. SNAP25 showed a significant decrease in mRNA expression, which likely caused the impairment in acid secretion from parietal cells in Foxl1-deficient mice. PMID: 15240114
50. chronic morphine treatment inhibits phosphorylation of SNAP-25 at Ser187 and leads to a down-regulation of SNARE complex formation PMID: 15277518

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KEGG: mmu:20614

STRING: 10090.ENSMUSP00000028727

UniGene: Mm.45953