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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 (zeige SNAP23 ELISA Kits)) and vesicle-associated membrane protein 2 (VAMP2 (zeige VAMP2 ELISA Kits)). Fibrosarcoma/adenocarcinoma cell lines were used in these studies. (MUNC18C = syntaxin binding protein MUNC18C; STX4 = syntaxin 4)
The analysis revealed three candidate genes GSK3B (zeige GSK3b ELISA Kits), PTPN1 (zeige PTPN1 ELISA Kits), STX4 that are differentially expressed in study subjects. GSK3B (zeige GSK3b ELISA Kits) 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 (zeige PTPN1 ELISA Kits) 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 (zeige INS ELISA Kits) granules underlying biphasic glucose-stimulated insulin (zeige INS ELISA Kits) secretion in human pancreatic beta cells
Increased level of SNAP23 (zeige SNAP23 ELISA Kits)-Syntaxin4-VAMP7 (zeige VAMP7 ELISA Kits) interaction correlates with decreased Syntaxin4 phosphorylation and trafficking of MT1-MMP (zeige MMP14 ELISA Kits) to invadopodia during cellular invasion.
upregulation of Syntaxin 4 is sufficient to significantly improve insulin (zeige INS ELISA Kits) 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 (zeige STX2 ELISA Kits) and syntaxin4 on keratinocyte cornification.
Syntaxin 4 activation and insulin (zeige INS ELISA Kits) release in the absence of the glucose stimulus, consistent with nitrosative stress and dysfunctional exocytosis
Syn4 transgenic mice with high level expression of Syn4 had a significant extension of lifespan (33% increase in median) and showed increased peripheral insulin (zeige INS ELISA Kits) sensitivity, even at ages where controls exhibited age-related insulin (zeige INS ELISA Kits) 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 (zeige SLC2A4 ELISA Kits) to the plasma membrane is mediated by formation of functional SNARE (zeige VTI1B ELISA Kits) complexes containing syntaxin4, SNAP23 (zeige SNAP23 ELISA Kits), and VAMP2 (zeige VAMP2 ELISA Kits).
data support a mechanistic model for gelsolin's role in insulin (zeige INS ELISA Kits) exocytosis: gelsolin (zeige GSN ELISA Kits) clamps unsolicited soluble N-ethylmaleimide-sensitive factor (zeige NSF ELISA Kits) attachment receptor-regulated exocytosis through association with Syn4 which is relieved upon stimulus-induced calcium influx to activate gelsolin (zeige GSN ELISA Kits) to facilitate insulin (zeige INS ELISA Kits) exocytosis
functions as the necessary t-SNARE (zeige VTI1B ELISA Kits) protein responsible for correct fusion of the GLUT8 (zeige SLC2A8 ELISA Kits)-containing vesicle with the plasma membrane in the mouse blastocyst
Interacts with tomosyn (zeige STXBP5 ELISA Kits) and plays a role in insulin (zeige INS ELISA Kits)-stimulated GLUT4 (zeige SLC2A4 ELISA Kits) 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 (zeige PDGFA ELISA Kits) induction of Glut4 (zeige SLC2A4 ELISA Kits) translocation is the suppression of the Munc18c negative regulation of Syntaxin 4 function.
Potentially involved in docking of synaptic vesicles at presynaptic active zones (By similarity).
, syntaxin 4
, renal carcinoma antigen NY-REN-31
, syntaxin 4A (placental)