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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
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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
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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
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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
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Human Polyclonal SNAP25 Primary Antibody for IHC, ELISA - ABIN185392
Voeller: Attention-deficit hyperactivity disorder (ADHD). in Journal of child neurology 2004
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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
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 (show SYT1 Antibodies)):soluble NSF attachment protein (show NAPG Antibodies) receptor (SNARE (show VTI1B Antibodies)) 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 Antibodies) 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 Antibodies), syntaxin-1A (show STX1A Antibodies), and Gai3 exhibit stability and functionality such that isolated proteins can be reconstituted as insulin (show INS Antibodies)-secreting porosomes in cell membrane of live cells.
we demonstrate that Syb2 (show VAMP2 Antibodies) and SNAP25 mediate the vesicular release of BDNF (show BDNF Antibodies) in axons and dendrites of cortical neurons
The extreme C terminus of SNAP25 is a critical region for the GBetaGamma-SNARE (show VTI1B Antibodies) 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.
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.
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 Antibodies), LMO3 (show LMO3 Antibodies), and SNAP25 were expressed in diffuse large B-cell lymphoma cells and associated with clinical features.
show that FOXC1 (show FOXC1 Antibodies) regulates the expression of RAB3GAP1 (show RAB3GAP1 Antibodies), RAB3GAP2 (show RAB3GAP2 Antibodies) and SNAP25
study demonstrated that miR (show MLXIP Antibodies)-27a and -b, which are widely expressed in host cells, suppress SNAP25 and TXN2 (show TXN2 Antibodies) expression through posttranscriptional gene silencing.
Data suggest that A-syn (show FYN Antibodies) (alpha-synuclein) promotes SNARE (show NAPA Antibodies)-dependent vesicle docking; phosphatidylserine (PS) removal from t-SNARE (show NAPA Antibodies)-bearing vesicles causes A-syn (show FYN Antibodies) to inhibit vesicle docking; PS removal from v-SNARE (show VTI1B Antibodies)-bearing vesicles promotes vesicle docking; the C-terminal 45 residues of A-syn (show FYN Antibodies) are required for promotion of vesicle docking. (Here, t-SNARE (show NAPA Antibodies) is SNAP-25; v-SNARE (show VTI1B Antibodies) is VAMP2 (show VAMP2 Antibodies).)
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 Antibodies)-C.
Robust association of the rs3746544 SNP and ASD (show ARSD Antibodies), in both allele and haplotype-based analyses, was observed in Iranian population.
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 Antibodies) assembly pathway underlying regulated exocytosis.
microdomains carrying syntaxin1 (show STX1A Antibodies)/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 Antibodies) proteins VAMP-2 (show VAMP2 Antibodies) 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