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Genetic interaction experiments demonstrate Syx4, Syt4, and Nlg1 regulate synaptic growth and plasticity through both shared and parallel signaling pathways.
these results indicate that the activation of beta-ARs induces secretory granules and cell membrane fusion via the interaction of VAMP-2 and syntaxin-4 in a PKA- and F-actin-dependent manner in human submandibular gland. Up-regulated beta-ARs might participate in altering protein secretion in transplanted submandibular gland by promoting the interaction of VAMP-2 with syntaxin-4.
Confocal immunofluorescence microscopy revealed a colocalization of syntaxin 4 with a MVB-specific marker, exosomes and hepatitis C virus (HCV) core, which suggests a fraction of syntaxin 4 is associated with exosomes loaded with HCV. Altogether, it is assumed that syntaxin 4 is a novel essential cellular factor for the release of HCV.
The authors found that activation of dendritic cells by bacterial lipopolysaccharide leads to increased Forster resonance energy transfer-fluorescence of fluorescently labeled syntaxin 4 with VAMP3 specifically at the plasma membrane, indicating increased SNARE complex formation, whereas FRET with other tested SNAREs was unaltered.
Data suggest MUNC18C is required for STX4-mediated invadopodium formation and tumor invasion of extracellular matrix; N-terminal STX4 fragment binds to MUNC18C and inhibits interactions of STX4 with synaptosome-associated protein 23 (SNAP23) and vesicle-associated membrane protein 2 (VAMP2). Fibrosarcoma/adenocarcinoma cell lines were used in these studies. (MUNC18C = syntaxin binding protein MUNC18C; STX4 = syntaxin 4)
The analysis revealed three candidate genes GSK3B, PTPN1, STX4 that are differentially expressed in study subjects. GSK3B was highly significant in Ps-T2D (P=0.00018, FR=-26.6), followed by Ps (P=0.0028, FR=-14.5) and T2D groups (P=0.032, FR=-5.9). PTPN1 showed significant association only with PS-T2D (P=0.00027, FR=-8.5). STX4 showed significant association with both Ps (P=0.0002, FR=-20) and Ps-T2D (P=0.0016, FR=-11.2).
When the expression of STX4 mRNA was inhibited with short or small interfering, or silencing, RNA in macrophages, the survival of Brucella melitensis was significantly reduced.
Syntaxin-4 has a role in mediating exocytosis of pre-docked and newcomer insulin granules underlying biphasic glucose-stimulated insulin secretion in human pancreatic beta cells
Increased level of SNAP23-Syntaxin4-VAMP7 interaction correlates with decreased Syntaxin4 phosphorylation and trafficking of MT1-MMP to invadopodia during cellular invasion.
upregulation of Syntaxin 4 is sufficient to significantly improve insulin secretory function to human type 2 diabetes islets retaining low levels of residual function
STX4 is implicated in the antibody secretion.
Syntaxin-4 plays a vital role in exocytosis of IgE from plasma cells. Knock-down of syntaxin-4, but not VAMP3 dramatically reduced IgE secretion from U266 plasma cells causing it to accumulate in the cell.
These results revealed, for the first time, the extracellular role of syntaxin4 and shed light on the division of the extracellular effects exerted by epimorphin and syntaxin4 on keratinocyte cornification.
siRNA knockdown (KD) of syntaxins 3 and 4 in HeLa cells reduced cell surface expression of alpha5beta1 and alpha3beta1 integrins
Syntaxin 4 activation and insulin release in the absence of the glucose stimulus, consistent with nitrosative stress and dysfunctional exocytosis
Stx4 is an essential postsynaptic component for synaptic plasticity in hippocampal neurons.
Syntaxin 4 is required for acid sphingomyelinase activity and apoptotic function.
dysferlin and syntaxin-4 similarly transit a common endosomal pathway in skeletal muscle cells.
Stx4 defines an exocytic zone that directs membrane fusion for postsynaptic plasticity, revealing a novel specialization for local membrane traffic in dendritic spines.
Syntaxin 4 and Synip (syntaxin 4 interacting protein) regulate insulin secretion in the pancreatic beta HC-9 cells
syntaxin 4 is involved in the intracellular transport of MT1-MMP toward the plasma membrane
Remarkably, betaTG-Stx4 mice resisted the loss of beta-cell mass and the glucose intolerance that multiple low doses of streptozotocin (STZ) induce. Under standard conditions, glucose tolerance was enhanced and mice maintained normal fasting glycemia and insulinemia. Conversely, Stx4 heterozygous knockout mice succumbed rapidly to STZ-induced glucose intolerance compared with their wild-type littermates.
Spontaneous membrane translocation of syntaxin-4 is critical for maintenance of embryonic stem cell pluripotency.
Stx4a plays a critical role in bone matrix production by osteoblasts.
Syntaxin-4 not only bound to laminin but also latched onto the glycosaminoglycan side chains of syndecan-1, a laminin receptor that mediates epithelial morphogenesis. Thus, temporal extracellular extrusion of syntaxin-4 emerged as a novel regulatory element for laminin-induced mammary epithelial cell behaviors.
Syn4 transgenic mice with high level expression of Syn4 had a significant extension of lifespan (33% increase in median) and showed increased peripheral insulin sensitivity, even at ages where controls exhibited age-related insulin resistance.
Non-directional stimulation with extracellular syntaxin-4 induces a dramatic morphological change in teratocarcinoma F9 cells and in several endodermal markers, both of which effects are reminiscent of the cells treated with all-trans retinoic acid.
Delivery of GLUT4 to the plasma membrane is mediated by formation of functional SNARE complexes containing syntaxin4, SNAP23, and VAMP2.
data support a mechanistic model for gelsolin's role in insulin exocytosis: gelsolin clamps unsolicited soluble N-ethylmaleimide-sensitive factor attachment receptor-regulated exocytosis through association with Syn4 which is relieved upon stimulus-induced calcium influx to activate gelsolin to facilitate insulin exocytosis
regulated during macrophage activation to function in membrane traffic and cytokine secretion
functions as the necessary t-SNARE protein responsible for correct fusion of the GLUT8-containing vesicle with the plasma membrane in the mouse blastocyst
Interacts with tomosyn and plays a role in insulin-stimulated GLUT4 translocation.
female Syn4 transgenic mice exhibited an increased rate of glucose clearance during glucose tolerance tests that was repressible by the administration of tetracycline
Data show that Munc18c binds to monomeric syntaxin4 and the N-terminal 29 amino acids of syntaxin4 are necessary for this interaction.
One mechanism accounting for the PDGF induction of Glut4 translocation is the suppression of the Munc18c negative regulation of Syntaxin 4 function.
analysis of a new underlying mechanism by which F-actin negatively regulates exocytosis via binding and blocking Syntaxin 4 accessibility
tyrosine phosphorylation of Munc18c induces a switch in binding specificity from syntaxin 4 to Doc2beta
CENPF and syntaxin 4 colocalize with components of plasma membrane recycling: SNAP-25 and VAMP2. Depletion of endogenous CENPF disrupts GLUT4 trafficking
Data show that syntaxin-4 directly associates with DOC2 in an intracellular Ca(2+)-dependent manner.
Potentially involved in docking of synaptic vesicles at presynaptic active zones (By similarity).
, syntaxin 4
, renal carcinoma antigen NY-REN-31
, syntaxin 4A (placental)