Browse our anti-SNAP25 (SNAP25) Antibodies

Mouse (Murine) Synaptosomal-Associated Protein, 25kDa (SNAP25) interaction partners

1. overexpression of miR-1 in the heart attenuated SV exocytosis in the hippocampus by posttranscriptionally regulating SNAP-25 through the transportation of exosomes

2. These results suggest that SN25 in developing SACs dampens the spatiotemporal properties of retinal waves and limits visual circuit refinement by phosphorylation at T138. Therefore, SN25 in SACs plays a profound role in regulating visual circuit refinement.

3. Mutant mice lacking the phosphorylation of SNAP-25 serine-187 exhibited reduced neurotransmitter release and enhanced presynaptic short-term plasticity.

4. Single-molecule optical tweezers were used to measure the assembly energy and kinetics of SNARE complexes containing single mutations I67T/N in SNAP-25B, which disrupt neurotransmitter release and have been implicated in neurological disorders. Both mutations lead to unfolding of the C-terminal region in the t-SNARE complex.

5. Study identified Gbeta1 and Gbeta2 as the interacting partners of both SNAP-25 isoforms in mouse hippocampus, but Gbeta2 was less efficiently captured by SNAP-25a. These results implicate that the two SNAP-25 isoforms could differently mediate protein interactions outside the ternary SNARE core complex and thereby contribute to modulate neurotransmission.

6. SNAP25 is necessary for accurate regulation of Ca2+-dynamics and insulin secretion in pancreatic beta cells.

7. 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.

8. 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.

9. Snap-25-null mutant neurons degenerate after 4 days in vitro and contain fewer dense-core vesicles.

10. a mouse mutant engineered to express normal levels of SNAP-25 but only SNAP-25a shows metabolic disease.

11. The function of synaptotagmin-1 (syt-1):soluble NSF attachment protein receptor (SNARE) interactions during neurotransmission remains unclear.

12. 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

13. 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

14. 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.

15. 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.

16. 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

17. we demonstrate that Syb2 and SNAP25 mediate the vesicular release of BDNF in axons and dendrites of cortical neurons

18. The extreme C terminus of SNAP25 is a critical region for the GBetaGamma-SNARE interaction.

19. 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.

20. 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.

Human Synaptosomal-Associated Protein, 25kDa (SNAP25) interaction partners

1. We interpret these data to propose that increasing the duration or extent of oltage-gated calcium channels activation prolongs the opportunity for low-efficiency fusion by fusogenic complexes incorporating Botulinum neurotoxins /A-cleaved SNAP-25.

2. Compared with SNAP-25 polymorphism rs3746544 G-allele carriers, TT homozygous, which confers a high risk for Attention deficit/hyperactivity disorder (ADHD), exhibited significantly decreased local and long-range functional connectivity density (FCD) in the anterior cingulate cortex and dorsal lateral prefrontal cortex. Moreover, both higher local and long-range FCD could predict better working memory capacity.

3. Strong deregulation of SNAP25 and STX1B has been found at both mRNA and protein levels suggesting impaired synaptic function through SNAP25 reduction as a possible cause of calcium elevation and glutamate excitotoxicity in amyotrophic lateral sclerosis.

4. NUPR1 regulates the late stages of autolysosome processing through the induction of the SNARE protein SNAP25

5. apolipoprotein E epsilon4 may affect CSF SNAP levels in mild cognitive impairment patients

6. Specific alleles of the SNAP25 (a synaptosome protein coding gene) were found to be significantly associated with Attention-Deficit Hyperactivity Disorder in more than 70% of the studies.

7. Comparing clinical features of reported patients with SNAP25 mutations, the current patients demonstrated apparently milder clinical features with normal intelligence, and no magnetic resonance imaging abnormality or facial dysmorphism. Our results expand the clinical spectrum of SNAP25 mutations.

8. report some evidence supporting the association of SNAP25 to Attention Deficit/Hyperactivity Disorder

9. Single nucleotide polymorphism in SNAP-25 gene is associated with Attention deficit hyperactivity disorder.

10. nine ADHD candidate single nucleotide polymorphisms (SNPs) in seven genes were tested for association with PD in 5333 cases and 12,019 healthy controls. No significant association was observed.

11. Findings indicate that lower SNAP-25 in ventromedial caudate in schizophrenia is primarily due to less SNAP-25A, and that the remaining SNAP-25 is associated with greater protein-protein interaction with syntaxin. The absence of a link to recent treatment effects in the human samples, or to administration of antipsychotic drugs in rats suggests the findings are illness- and not treatment-related.

12. Allelic variation of SNAP25 modulates development and plasticity of the prefrontal-limbic network and a shared genetic vulnerability between Bipolar Disorder and Schizophrenia.

13. SH3BP5, LMO3, and SNAP25 were expressed in diffuse large B-cell lymphoma cells and associated with clinical features.

14. show that FOXC1 regulates the expression of RAB3GAP1, RAB3GAP2 and SNAP25

15. The results of this study suggested that the polymorphisms rs3746544 and rs1051312 may increase the odds of developing ADHD.

16. study demonstrated that miR-27a and -b, which are widely expressed in host cells, suppress SNAP25 and TXN2 expression through posttranscriptional gene silencing.

17. Data suggest that A-syn (alpha-synuclein) promotes SNARE-dependent vesicle docking; phosphatidylserine (PS) removal from t-SNARE-bearing vesicles causes A-syn to inhibit vesicle docking; PS removal from v-SNARE-bearing vesicles promotes vesicle docking; the C-terminal 45 residues of A-syn are required for promotion of vesicle docking. (Here, t-SNARE is SNAP-25; v-SNARE is VAMP2.)

18. our data indicate that the expression of SNAP25 is crucial for dendrite formation and is associated with the effects of targeted chemotherapy. The detection of SNAP25 expression in MB cells may thus be essential for the chemotherapeutic application of Ara-C.

19. Robust association of the rs3746544 SNP and ASD, in both allele and haplotype-based analyses, was observed in Iranian population.

20. Our results will provide novel evidence to reveal the possible role of SNAP-25 in B[a]P-induced neurotoxicity and may be helpful for searching the potential strategy for the prevention measures against B[a]P neurotoxicity.

Cow (Bovine) Synaptosomal-Associated Protein, 25kDa (SNAP25) interaction partners

1. In individual chromaffin cells, we tracked conformational changes in SNAP25 by total internal reflection fluorescence resonance energy transfer (FRET) microscopy while exocytotic catecholamine release from single vesicles was simultaneously recorded

2. dynamic experiments using TIRFM revealed that attenuation of cortical F-actin movement clearly diminishes the mobility of SNAP-25 clusters.

3. Stable syntaxin/SNAP-25 dimers are a central principle of the SNARE assembly pathway underlying regulated exocytosis.

4. microdomains carrying syntaxin1/SNAP-25 and different types of calcium channels act as the sites for physiological granule fusion in "in situ" chromaffin cells

Rhesus Monkey Synaptosomal-Associated Protein, 25kDa (SNAP25) interaction partners

1. These data demonstrate a differential ability of SNAP-25 homlog to support neuronal function.

Zebrafish Synaptosomal-Associated Protein, 25kDa (SNAP25) interaction partners

1. data indicate that SNARE proteins VAMP-2 and SNAP-25 play an essential role in daughter blastomere apposition, possibly via the delivery of components that promote the cell-to-cell adhesion required for the successful completion of cytokinesis