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Some Autism spectrum disorder patients had haploidy of STX1A gene and lower STX1A gene expression.
Analysing protein mobility, cluster size and accessibility to myc-epitopes the authors show that forces acting on the transmembrane segment produce loose clusters, while cytoplasmic protein interactions mediate a tightly packed state.
Our results suggest that, as in the CNS, CADM1 interactions drive exocytic site assembly and promote actin network formation. These results support the broader hypothesis that the effects of cell-cell contact on beta-cell maturation and function are mediated by the same extracellular protein interactions that drive the formation of the presynaptic exocytic machinery. These interactions may be therapeutic targets for re...
A significant interactive two-locus model of STX1A_rs4363087|VAMP2_rs2278637 (presynaptic genes) was observed among SVC variants in all epilepsy cases.
Mislocalization of syntaxin-1 was found in pluripotent stem cells from epileptic encephalopathy patient.
Blockade of the SNARE protein syntaxin 1 inhibits glioblastoma tumor growth.
SNARE 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 or KCNQ3 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 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 complex fusion intermediate.
N-peptide and LE mutation have no effect on the global conformation of the Munc18a-Syx1a complex.
the preferential binding of CAPS1 to open syntaxin-1 can contribute to the stabilization of the open state of syntaxin-1 during its transition from "closed" state to the SNARE complex formation.
The histone modification marks were significantly increased in bipolar disorder and major depression and this effect was correlated with significant increases in Syn1a gene expression.
syntaxin 1 and SNAP-25 cooperate as SNARE proteins to support neuron survival.
In dementia with Lewy bodies patients there were lower levels of syntaxin in visual cortex compared to controls.
Platelets deficient in Munc18b from a Familial Hemophagocytic Lymphohistiocytosis type 5 had secretion defect.
Exocytotic dysfunctions in schizophrenia are probably related to an imbalance of the interaction between munc18-1a and SNARE (mainly syntaxin-1A) complex.
Direct interaction between syntaxin 1A and the Kv2.1 C-terminus is required for efficient insulin exocytosis and glucose-stimulated insulin secretion.
Syntaxin 1A drives fusion of large dense-core neurosecretory granules into a planar lipid bilayer
microdomains carrying syntaxin1/SNAP-25 and different types of calcium channels act as the sites for physiological granule fusion in "in situ" chromaffin cells
The role of syntaxin 1A in GLP1 release from intestinal cells as a response to external stimuli is reported.
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
Therefore, our work provides insights into differential functions of Stx1 in neuronal maintenance and neurotransmission, with the latter explored further into its functions in vesicle docking and fusion.
Syn-1A actions on newcomer SGs were partly mediated by Syn-1A interactions with newcomer SG VAMP8
The results of this study suggested that STX1A plays an important role in social behavior through regulation of the OXTergic neural system.
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.
syntaxin 1 and vesicle-associated membrane protein 1 are more suitable targets to abolish functional soluble N-ethylmaleimide-sensitive factor attachment protein receptor complexes
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.
Although STX1A and STX1B share a basic function as neuronal t-SNAREs, STX1B but not STX1A is necessary for the regulation of spontaneous and evoked synaptic vesicle exocytosis in fast transmission.
we found that STX1A and STX1B 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 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 binds to the full-length of cytoplasmic syntaxin-1 with preference to its "open" conformation, whereas Munc13-1 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-protein complexes.
Nesca directly binds KIF5B, kinesin light-chain and syntaxin-1
Sytaxin 1A may be involved in rearrangement of synaptic connections between neurons in the spinal dorsal horn induced by peripheral nerve injury.
Lack of STX1A could induce dysfunction of the HPA axis, and the deficit may result in abnormal behavioural properties, such as unusual responses to stress stimuli.
HPC-1/syntaxin 1A regulates catecholaminergic systems via exocytosis of dense-core synaptic vesicles. Deletion of HPC-1/syntaxin 1A causes impairment of long term potentiation induction.
Syntaxin-1A inhibits KATP channels by interacting with specific conserved motifs within sulfonylurea receptor 2A.
The data demonstrate that polyphosphoinositide favors syntaxin1A trapping, and show that SNARE complex disassembly leads to syntaxin1A dissociation from presynaptic nanoclusters.
The authors found two syntaxin1A mutations that confer opposite general anesthesia phenotypes
Data suggest that Ca(2+)-CaM regulation of V100 may control SNARE complex assembly for a subset of synaptic vesicles that sustain spontaneous release.
these results indicate that SNAP-25-R206 and syntaxin-D253 play a major role in neuroexocytosis and support a radial assembly of several SNARE 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 protein is required for efficient EGFR 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
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
neuron-specific antigen HPC-1
, synaptotagmin-associated 35 kDa protein
, syntaxin 1A (brain)-like
, syntaxin 1A (brain)
, syntaxin 1 a
, syntaxin 1
, syntaxin 1A
, syntx 1