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anti-Rat (Rattus) SNAP25 Anticorps:
anti-Mouse (Murine) SNAP25 Anticorps:
anti-Human SNAP25 Anticorps:
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Chicken Polyclonal SNAP25 Primary Antibody pour 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. dans PLoS ONE 2012
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Human Polyclonal SNAP25 Primary Antibody pour 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. dans The Biochemical journal 1999
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Human Polyclonal SNAP25 Primary Antibody pour ICC, IF - ABIN4354886
Cardoso, Ferrari, Garcia, Bregano, Andrade, Nogueira: Immunohistochemical approach to the pathogenesis of clinical cases of bovine Herpesvirus type 5 infections. dans Diagnostic pathology 2010
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Human Polyclonal SNAP25 Primary Antibody pour 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. dans Neurobiology of disease 2014
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Human Polyclonal SNAP25 Primary Antibody pour 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. dans Molecular neurobiology 2014
Human Polyclonal SNAP25 Primary Antibody pour IHC, ELISA - ABIN185392
Voeller: Attention-deficit hyperactivity disorder (ADHD). dans Journal of child neurology 2004
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Human Polyclonal SNAP25 Primary Antibody pour 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. dans PLoS ONE 2017
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 (Montrer SYT1 Anticorps)):soluble NSF attachment protein (Montrer NAPG Anticorps) receptor (SNARE (Montrer VTI1B Anticorps)) 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 (Montrer DLG4 Anticorps) 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 (Montrer KCNK2 Anticorps), syntaxin-1A (Montrer STX1A Anticorps), and Gai3 exhibit stability and functionality such that isolated proteins can be reconstituted as insulin (Montrer INS Anticorps)-secreting porosomes in cell membrane of live cells.
we demonstrate that Syb2 (Montrer VAMP2 Anticorps) and SNAP25 mediate the vesicular release of BDNF (Montrer BDNF Anticorps) in axons and dendrites of cortical neurons
The extreme C terminus of SNAP25 is a critical region for the GBetaGamma-SNARE (Montrer VTI1B Anticorps) interaction.
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.
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 (Montrer SH3BP5 Anticorps), LMO3 (Montrer LMO3 Anticorps), and SNAP25 were expressed in diffuse large B-cell lymphoma cells and associated with clinical features.
show that FOXC1 (Montrer FOXC1 Anticorps) regulates the expression of RAB3GAP1 (Montrer RAB3GAP1 Anticorps), RAB3GAP2 (Montrer RAB3GAP2 Anticorps) and SNAP25
study demonstrated that miR (Montrer MLXIP Anticorps)-27a and -b, which are widely expressed in host cells, suppress SNAP25 and TXN2 (Montrer TXN2 Anticorps) expression through posttranscriptional gene silencing.
Data suggest that A-syn (Montrer FYN Anticorps) (alpha-synuclein) promotes SNARE (Montrer NAPA Anticorps)-dependent vesicle docking; phosphatidylserine (PS) removal from t-SNARE (Montrer NAPA Anticorps)-bearing vesicles causes A-syn (Montrer FYN Anticorps) to inhibit vesicle docking; PS removal from v-SNARE (Montrer VTI1B Anticorps)-bearing vesicles promotes vesicle docking; the C-terminal 45 residues of A-syn (Montrer FYN Anticorps) are required for promotion of vesicle docking. (Here, t-SNARE (Montrer NAPA Anticorps) is SNAP-25; v-SNARE (Montrer VTI1B Anticorps) is VAMP2 (Montrer VAMP2 Anticorps).)
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 (Montrer FOXC1 Anticorps)-C.
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 (Montrer NAPA Anticorps) assembly pathway underlying regulated exocytosis.
microdomains carrying syntaxin1 (Montrer STX1A Anticorps)/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 (Montrer NAPA Anticorps) proteins VAMP-2 (Montrer VAMP2 Anticorps) 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