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STX1A encodes a member of the syntaxin superfamily. Additionally we are shipping Syntaxin 1A (Brain) Kits (15) and Syntaxin 1A (Brain) Proteins (15) and many more products for this protein.
Showing 10 out of 152 products:
Human Polyclonal STX1A Primary Antibody for FACS, IHC (p) - ABIN955037
Hamdan, Piton, Gauthier, Lortie, Dubeau, Dobrzeniecka, Spiegelman, Noreau, Pellerin, Côté, Henrion, Fombonne, Mottron, Marineau, Drapeau, Lafrenière, Lacaille, Rouleau, Michaud: De novo STXBP1 mutations in mental retardation and nonsyndromic epilepsy. in Annals of neurology 2009
Show all 6 references for ABIN955037
Cow (Bovine) Monoclonal STX1A Primary Antibody for IHC (p), IP - ABIN492371
Margolskee: Molecular mechanisms of bitter and sweet taste transduction. in The Journal of biological chemistry 2002
Show all 5 references for ABIN492371
Human Polyclonal STX1A Primary Antibody for IF, IHC - ABIN1532785
Zhang, Maksymowych, Simpson: Cloning and sequence analysis of a cDNA encoding human syntaxin 1A, a polypeptide essential for exocytosis. in Gene 1995
Cow (Bovine) Polyclonal STX1A Primary Antibody for EIA, WB - ABIN374595
Kang, Leung, Manning-Fox, Xia, Xie, Sheu, Tsushima, Light, Gaisano: Syntaxin-1A inhibits cardiac KATP channels by its actions on nucleotide binding folds 1 and 2 of sulfonylurea receptor 2A. in The Journal of biological chemistry 2004
Human Polyclonal STX1A Primary Antibody for IF, ELISA - ABIN1531756
Hillier, Graves, Fulton, Fulton, Pepin, Minx, Wagner-McPherson, Layman, Wylie, Sekhon, Becker, Fewell, Delehaunty, Miner, Nash, Kremitzki, Oddy, Du, Sun, Bradshaw-Cordum, Ali, Carter, Cordes, Harris et al.: Generation and annotation of the DNA sequences of human chromosomes 2 and 4. ... in Nature 2005
The authors found two syntaxin1A mutations that confer opposite general anesthesia phenotypes
Data suggest that Ca(2 (show CA2 Antibodies)+)-CaM (show CALM Antibodies) regulation of V100 may control SNARE (show NAPA Antibodies) complex assembly for a subset of synaptic vesicles that sustain spontaneous release.
these results indicate that SNAP-25 (show SNAP25 Antibodies)-R206 and syntaxin (show STX4 Antibodies)-D253 play a major role in neuroexocytosis and support a radial assembly of several SNARE (show NAPA Antibodies) complexes interacting via the ionic couple formed by these two residues.
Syntaxin1A domain formation is induced by phosphoinositide-3,4,5-triphosphate; this clustering is dependent on positively charged residues in the juxtamembrane domain.
The Syx1A dependent trafficking of Grk (show GRK4 Antibodies) protein is required for efficient EGFR (show EGFR Antibodies) signaling during dorsal-ventral patterning.
analysis of epistatic interactions related to mutation of Syx1A
Syntaxin 1A molecules share a conserved threonine in C-terminal +7 layer near transmembrane domain. Mutation of threonine to isoleucine results in a structural change that resembles those found in syntaxins ascribed to the constitutive secretory pathway
Mislocalization of syntaxin-1 was found in pluripotent stem cells from epileptic encephalopathy patient.
Blockade of the SNARE (show NAPA Antibodies) protein syntaxin 1 inhibits glioblastoma tumor growth.
SNARE (show NAPA Antibodies) complex genes and their interactions may play a significant role in susceptibility and working memory of ADHD.
We described clinical, genetic, and functional data from 17 families with a diagnosis of benign familial neonatal epilepsy caused by KCNQ2 (show KCNQ2 Antibodies) or KCNQ3 (show KCNQ3 Antibodies) mutations and we showed that some mutations lead to a reduction of Q2 channel regulation by syntaxin-1A.
no associaton with idiopathic generalized epilepsy was found regarding Intron 7 rs1569061 of Syntaxin 1A gene, MnlI rs3746544 and DdeI rs1051312 polymorphisms of SNAP-25 (show SNAP25 Antibodies) gene compared with healthy subjects
The clinical relevance of STX1A variants in CF
PIP2 affects islet beta-cell KATP channels not only by its actions on Kir6.2 but also by sequestering Syn-1A to modulate Syn-1A availability and its interactions with SUR1 on PM.
Prefusion structure of syntaxin-1A suggests pathway for folding into neuronal trans-SNARE (show NAPA Antibodies) complex fusion intermediate.
N-peptide and LE mutation have no effect on the global conformation of the Munc18a-Syx1a complex.
the p (show CAPS Antibodies)referential binding of CAPS1 to open syntaxin-1 can contribute to the stabilization of the open state of syntaxi (show UNC13A Antibodies)n-1 during its transition from "closed" state to the SNARE complex formation.
Data suggest that porosome-associated proteins SNAP25 (show SNAP25 Antibodies), TREK-1 (show KCNK2 Antibodies), syntaxin-1A, 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.
syntaxin 1 and vesicle-associated membrane protein 1 (show VAMP1 Antibodies) are more suitable targets to abolish functional soluble N-ethylmaleimide-sensitive factor attachment protein receptor (show VTI1B Antibodies) complexes
Data show a significant increase of vesicle-associated membrane protein 2 (VAMP-2 (show VAMP2 Antibodies)) mRNA expression, however, the expressions of synaptosome-associated protein of 25 kDa (SNAP-25 (show SNAP25 Antibodies)) and syntaxin 1A did not exhibit the changes in hippocampus.
Although STX1A and STX1B (show STX1B Antibodies) share a basic function as neuronal t-SNAREs, STX1B (show STX1B Antibodies) but not STX1A is necessary for the regulation of spontaneous and evoked synaptic vesicle exocytosis in fast transmission.
we found that STX1A and STX1B (show STX1B Antibodies) play distinct roles in neuronal survival using
point mutation in syntaxin-1A causes abnormal regulation of neuronal plasticity and vesicle recycling and that the affected syntaxin-1A/CaMKII (show CAMK2G Antibodies) interaction is essential for normal brain and synaptic functions in vivo.
overall release efficiency of affected hippocampal neurons was severely impaired by reducing levels of Stx1, as demonstrated by a smaller readily releasable pool size, slower refilling rate of primed vesicles, and lower release probability.
CAPS1 (show CAPS Antibodies) binds to the full-length of cytoplasmic syntaxin-1 with preference to its "open" conformation, whereas Munc13-1 (show UNC13A Antibodies) binds to the first 80 N-terminal residues of syntaxin-1.
The N-terminal syntaxin-1 domains mediate different functions in synaptic vesicle fusion, probably via formation of distinct Munc18/SNARE (show VTI1B Antibodies)-protein complexes.
Direct interaction between syntaxin 1A and the Kv2.1 (show KCNB1 Antibodies) C-terminus is required for efficient insulin (show INS Antibodies) exocytosis and glucose-stimulated insulin (show INS Antibodies) secretion.
Syntaxin 1A drives fusion of large dense-core neurosecretory granules into a planar lipid bilayer
microdomains carrying syntaxin1/SNAP-25 (show SNAP25 Antibodies) and different types of calcium channels act as the sites for physiological granule fusion in "in situ" chromaffin cells
This gene encodes a member of the syntaxin superfamily. Syntaxins are nervous system-specific proteins implicated in the docking of synaptic vesicles with the presynaptic plasma membrane. Syntaxins possess a single C-terminal transmembrane domain, a SNARE
, syntaxin 1
, syntaxin 1A
, syntx 1
, syntaxin 1A (brain)
, neuron-specific antigen HPC-1
, synaptotagmin-associated 35 kDa protein
, syntaxin 1A (brain)-like
, syntaxin 1 a