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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 (show SYT1 ELISA Kits)):soluble NSF attachment protein (show NAPG ELISA Kits) receptor (SNARE (show VTI1B ELISA Kits)) 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 (show DLG4 ELISA Kits) 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 (show KCNK2 ELISA Kits), syntaxin-1A (show STX1A ELISA Kits), and Gai3 exhibit stability and functionality such that isolated proteins can be reconstituted as insulin (show INS ELISA Kits)-secreting porosomes in cell membrane of live cells.
we demonstrate that Syb2 (show VAMP2 ELISA Kits) and SNAP25 mediate the vesicular release of BDNF (show BDNF ELISA Kits) in axons and dendrites of cortical neurons
The extreme C terminus of SNAP25 is a critical region for the GBetaGamma-SNARE (show VTI1B ELISA Kits) interaction.
Data show a significant increase of vesicle-associated membrane protein 2 (VAMP-2 (show VAMP2 ELISA Kits)) mRNA expression, however, the expressions of synaptosome-associated protein of 25 kDa (SNAP-25) and syntaxin 1A (show STX1A ELISA Kits) did not exhibit the changes in hippocampus.
SNAP-25 phosphorylation is regulated in a stress-dependent manner through both central and peripheral mechanisms.
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 (show SH3BP5 ELISA Kits), LMO3 (show LMO3 ELISA Kits), and SNAP25 were expressed in diffuse large B-cell lymphoma cells and associated with clinical features.
show that FOXC1 (show FOXC1 ELISA Kits) regulates the expression of RAB3GAP1 (show RAB3GAP1 ELISA Kits), RAB3GAP2 (show RAB3GAP2 ELISA Kits) and SNAP25
study demonstrated that miR (show MLXIP ELISA Kits)-27a and -b, which are widely expressed in host cells, suppress SNAP25 and TXN2 (show TXN2 ELISA Kits) expression through posttranscriptional gene silencing.
Data suggest that A-syn (show FYN ELISA Kits) (alpha-synuclein) promotes SNARE (show NAPA ELISA Kits)-dependent vesicle docking; phosphatidylserine (PS) removal from t-SNARE (show NAPA ELISA Kits)-bearing vesicles causes A-syn (show FYN ELISA Kits) to inhibit vesicle docking; PS removal from v-SNARE (show VTI1B ELISA Kits)-bearing vesicles promotes vesicle docking; the C-terminal 45 residues of A-syn (show FYN ELISA Kits) are required for promotion of vesicle docking. (Here, t-SNARE (show NAPA ELISA Kits) is SNAP-25; v-SNARE (show VTI1B ELISA Kits) is VAMP2 (show VAMP2 ELISA Kits).)
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 (show FOXC1 ELISA Kits)-C.
Robust association of the rs3746544 SNP and ASD (show ARSD ELISA Kits), 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.
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 (show NAPA ELISA Kits) assembly pathway underlying regulated exocytosis.
microdomains carrying syntaxin1 (show STX1A ELISA Kits)/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 (show NAPA ELISA Kits) proteins VAMP-2 (show VAMP2 ELISA Kits) 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