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anti-Rat (Rattus) SNAP25 Antibodies:
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Chicken Polyclonal SNAP25 Primary Antibody for ICC, IP - ABIN1742235
Young, Franciosi, Spreeuw, Deng, Sanders, Tam, Huang, Singaraja, Zhang, Bissada, Kay, Hayden: Low levels of human HIP14 are sufficient to rescue neuropathological, behavioural, and enzymatic defects due to loss of murine HIP14 in Hip14-/- mice. in PLoS ONE 2012
Show all 9 Pubmed References
Human Polyclonal SNAP25 Primary Antibody for IHC (p), WB - ABIN967060
Gonelle-Gispert, Halban, Niemann, Palmer, Catsicas, Sadoul: SNAP-25a and -25b isoforms are both expressed in insulin-secreting cells and can function in insulin secretion. in The Biochemical journal 1999
Show all 5 Pubmed References
Human Polyclonal SNAP25 Primary Antibody for ICC, IF - ABIN4354886
Cardoso, Ferrari, Garcia, Bregano, Andrade, Nogueira: Immunohistochemical approach to the pathogenesis of clinical cases of bovine Herpesvirus type 5 infections. in Diagnostic pathology 2010
Show all 4 Pubmed References
Human Polyclonal SNAP25 Primary Antibody for IHC (p), IHC - ABIN250341
Mouton-Liger, Sahún, Collin, Lopes Pereira, Masini, Thomas, Paly, Luilier, Même, Jouhault, Bennaï, Beloeil, Bizot, Hérault, Dierssen, Créau: Developmental molecular and functional cerebellar alterations induced by PCP4/PEP19 overexpression: implications for Down syndrome. in Neurobiology of disease 2014
Show all 3 Pubmed References
Chicken Polyclonal SNAP25 Primary Antibody for WB - ABIN550146
Greber, Lubec, Cairns, Fountoulakis: Decreased levels of synaptosomal associated protein 25 in the brain of patients with Down syndrome and Alzheimer's disease. in Electrophoresis 1999
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Human Polyclonal SNAP25 Primary Antibody for IHC (fro), IF (p) - ABIN738111
Wang, Wang, Liu, Zhao, Zhao, He, Qian, Xu, Liu, Liu, Liu, Liu, Zhou, Wang: SNAP25 Ameliorates Sensory Deficit in Rats with Spinal Cord Transection. in Molecular neurobiology 2014
Dog (Canine) Polyclonal SNAP25 Primary Antibody for IHC (p), ELISA - ABIN547437
Voeller: Attention-deficit hyperactivity disorder (ADHD). in Journal of child neurology 2004
Human Monoclonal SNAP25 Primary Antibody for ELISA, WB - ABIN532965
Schulz, Sasaki, Vacquier: Increased association of synaptosome-associated protein of 25 kDa with syntaxin and vesicle-associated membrane protein following acrosomal exocytosis of sea urchin sperm. in The Journal of biological chemistry 1998
Show all 2 Pubmed References
Human Polyclonal SNAP25 Primary Antibody for DB - ABIN1539723
Horváth, Tamás, Sipos, Darula, Bécsi, Nagy, Iván, Erdődi, Lontay: Myosin phosphatase and RhoA-activated kinase modulate neurotransmitter release by regulating SNAP-25 of SNARE complex. in PLoS ONE 2017
Rat (Rattus) Polyclonal SNAP25 Primary Antibody for IHC (p), WB - ABIN3044363
Zhong, Xiang, Hu, Wang, Zeng, Wang, Xia, Wang, Zhang: Synaptosomal-associated protein 25 may be an intervention target for improving sensory and locomotor functions after spinal cord contusion. in Neural regeneration research 2017
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.
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.
Snap-25-null mutant neurons degenerate after 4 days in vitro and contain fewer dense-core vesicles.
a mouse mutant engineered to express normal levels of SNAP-25 but only SNAP-25a shows metabolic disease.
The function of synaptotagmin-1 (syt-1):soluble NSF attachment protein receptor (SNARE) interactions during neurotransmission remains unclear.
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
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
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.
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.
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
we demonstrate that Syb2 and SNAP25 mediate the vesicular release of BDNF in axons and dendrites of cortical neurons
The extreme C terminus of SNAP25 is a critical region for the GBetaGamma-SNARE interaction.
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.
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.
SNAP-25 phosphorylation is regulated in a stress-dependent manner through both central and peripheral mechanisms.
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
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
SNAP-25 regulates the organization of the molecular apparatus needed for dendritic spine formation by recruiting and stabilizing p140Cap.
PP2A participates in SNAP-25 dephosphorylation through calcium-dependent and calcium-independent mechanisms but is not involved in GAP-43 dephosphorylation.
Reduced SNAP-25 alters short-term plasticity at developing glutamatergic synapses.
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.
report some evidence supporting the association of SNAP25 to Attention Deficit/Hyperactivity Disorder
Single nucleotide polymorphism in SNAP-25 gene is associated with Attention deficit hyperactivity disorder.
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.
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.
Allelic variation of SNAP25 modulates development and plasticity of the prefrontal-limbic network and a shared genetic vulnerability between Bipolar Disorder and Schizophrenia.
SH3BP5, LMO3, and SNAP25 were expressed in diffuse large B-cell lymphoma cells and associated with clinical features.
show that FOXC1 regulates the expression of RAB3GAP1, RAB3GAP2 and SNAP25
The results of this study suggested that the polymorphisms rs3746544 and rs1051312 may increase the odds of developing ADHD.
study demonstrated that miR-27a and -b, which are widely expressed in host cells, suppress SNAP25 and TXN2 expression through posttranscriptional gene silencing.
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.)
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.
Robust association of the rs3746544 SNP and ASD, in both allele and haplotype-based analyses, was observed in Iranian population.
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.
Our analysis indicated that there is no significant association between none of studied variants in SNAP-25 and ADHD.
These results of this study suggested that SNAP25 and NOS1 genotypes influence ADHD symptoms only in adults with ADHD.
Snap25 rs363050 (G) allele, which results in a reduced expression of Snap25, is associated with altered glycemic parameters in T2DM possibly because of reduced functionality in the exocytotic machinery leading to suboptimal release of insulin.
single nucleotide polymorphisms in either the region of NEUROD6 or SNAP25 were significantly associated with Alzheimer's Disease, in APOE4+ females and APOE4+ males, respectively.
BoNT-A injection, but not Lipotoxin instillation, effectively cleaves SNAP-25 in the suburothelium.
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
dynamic experiments using TIRFM revealed that attenuation of cortical F-actin movement clearly diminishes the mobility of SNAP-25 clusters.
Stable syntaxin/SNAP-25 dimers are a central principle of the SNARE assembly pathway underlying regulated exocytosis.
microdomains carrying syntaxin1/SNAP-25 and different types of calcium channels act as the sites for physiological granule fusion in "in situ" chromaffin cells
These data demonstrate a differential ability of SNAP-25 homlog to support neuronal function.
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
Synaptic vesicle membrane docking and fusion is mediated by SNAREs (soluble N-ethylmaleimide-sensitive factor attachment protein receptors) located on the vesicle membrane (v-SNAREs) and the target membrane (t-SNAREs). The assembled v-SNARE/t-SNARE complex consists of a bundle of four helices, one of which is supplied by v-SNARE and the other three by t-SNARE. For t-SNAREs on the plasma membrane, the protein syntaxin supplies one helix and the protein encoded by this gene contributes the other two. Therefore, this gene product is a presynaptic plasma membrane protein involved in the regulation of neurotransmitter release. Two alternative transcript variants encoding different protein isoforms have been described for this gene.
synaptosomal-associated protein 25
, super protein
, synaptosomal-associated 25 kDa protein
, synaptosomal-associated protein, 25 kDa
, GENA 70
, blind drunk
, resistance to inhibitors of cholinesterase 4 homolog
, synaptosomal associated protein-25
, synaptosomal-associated protein 25 isoform SNAP25B
, synaptosomal-associated 25kD protein