anti-Syntaxin 2 (STX2) Antibodies

Human Syntaxin 2 (STX2) interaction partners

1. STX2 as a crucial modulator of the aggressive colorectal cancer phenotype.

2. he patient showed azoospermia, relatively small testes, and a mildly elevated follicle stimulating hormone level, but no additional clinical features. Testicular histology of the patient showed universal maturation arrest and multinucleated spermatocytes, which have also been observed in mice lacking Stx2. PCR-based cDNA screening revealed wildtype STX2 expression in various tissues including the testis

3. Munc134 mediates human neutrophil elastaseinduced airway mucin5AC hypersecretion by interacting with syntaxin2

4. TGF-beta, bFGF and epimorphin in the extracellular microenvironment cooperatively affect HSF behaviors under the control of a highly sulfated chondroitin sulfate

5. The effects of HIV/HCV co-infection on hepatic fibrosis might be mediated in part by epimorphin (EPM). Strategies to limit the expression of EPM might represent a novel therapeutic approach to prevent the progression of hepatic fibrosis during HIV/HCV co-infection.

6. Identify 3 loci associated with circulating tPA levels, the PLAT region, STXBP5, and STX2. Functional studies implicate a novel role for STXBP5 and STX2 in regulating tPA release.

7. Epimorphin can revert ovarian cancer cells away from their mesenchymal phenotype and toward an epithelial phenotype.

8. epimorphin modulates the signaling pathways mediated by EGFR for epidermal tissue organization

9. Genetic variation in STX2 is associated with von Willebrand factor:Ag levels in patients diagnosed with type 1 von Willebrand Disease.

10. EPM, secreted by activated stellate cells within stroma, promotes invasion and metastasis of hepatocellular cancer cells by activating MMP-9 expression through the FAK-ERK pathway.

11. Genetic variability in STXBP5 and STX2 affects both VWF concentration and activity in young individuals with premature arterial thrombosis.

12. Munc18b binds to syntaxins 1A, 2, and 3 and regulates vesicle transport to the apical plasma membrane

13. These findings suggest that epimorphin contributes to repair of pulmonary fibrosis in nonspecific interstitial pneumonia, perhaps partly by inducing expression of matrix metalloproteinase 2, which is an important proteolytic factor in lung remodeling.

14. expression of SNAP-23 and syntaxin-2 on the extracellular surface of the platelet plasma membrane.

15. Inadequate epimorphin elicits an abnormal differentiation response in keratinocytes, and indicate a causal function of the epimorphin signaling gradient for the establishment of differentiated epidermal structure in the skin.

16. Homology with vesicle fusion mediator syntaxin-1a predicts determinants of epimorphin/syntaxin-2 function in mammary epithelial morphogenesis.(

Mouse (Murine) Syntaxin 2 (STX2) interaction partners

1. he patient showed azoospermia, relatively small testes, and a mildly elevated follicle stimulating hormone level, but no additional clinical features. Testicular histology of the patient showed universal maturation arrest and multinucleated spermatocytes, which have also been observed in mice lacking Stx2. PCR-based cDNA screening revealed wildtype STX2 expression in various tissues including the testis

2. Syn-2 knockout mice exhibited paradoxical superior glucose homeostasis resulting from an enhanced insulin secretion. The increase in insulin exocytosis was attributed mainly to an enhanced recruitment of the larger pool of newcomer secretory granules (SGs) that undergoes no residence time on plasma membrane before fusion and, to a lesser extent, also the predocked SGs.

3. The selectivity in syntaxin binding and apical protein redistribution further suggests that rab17 and syntaxin 2 mediate fusion of transcytotic vesicles at the apical surface.

4. It was concluded that Epim deletion inhibits polyposis in Apcmin/+ mice, associated with increased mucosal TGF-beta signaling and decreased myofibroblast HGF expression and secretion.

5. Overexpression of Epim expression is associated with mammary carcinoma.

6. These results suggest that STX2 plays roles in transport and/or subcellular distribution of sulfoglycolipids.

7. epimorphin modulates the signaling pathways mediated by EGFR for epidermal tissue organization

8. Epimorphin regulates bile duct formation via effects on mitosis orientation

9. Epimorphin has a pivotal role in the repair of renal fibrosis by modulating both extracellular matrix (ECM) degradation and its production.

10. syntaxin 2 enters the membrane of a fused zymogen granule after the opening of the fusion pore

11. Epimorphin is involved in tissue repair following a single injection of carbon tetrachloride, in which distribution and the quantity of epimorphin expression are important, particularly in maintaining hepatocyte function.

12. Upregulated in an in vitro model of pancreatic duct formation; plays an important role during pancreatic ductal proliferation and differentiation.

13. Results suggest that epimorphin is a key stromal regulator of epithelial cell proliferation and growth in the intestine, and demonstrate a novel and critical role for epimorphin in regulating testicular development and growth as well as spermatogenesis.

14. Data show that epimorphin is secreted through a non-classical mechanism, and that secreted epimorphin binds to alphav-integrin-containing receptors on epithelial cells, leading to activation of signaling pathways and induction of epithelial morphogenesis.

15. Epimorphin elicits hepatocyte spheroids by inducing proteases in rodent hepatocytes through NF-kappaB.

16. Inadequate epimorphin elicits an abnormal differentiation response in keratinocytes, and indicate a causal function of the epimorphin signaling gradient for the establishment of differentiated epidermal structure in the skin.

17. the nonsense mutation of the Stx2/Epim gene is responsible for the interruption of spermatogenesis

18. Homology with vesicle fusion mediator syntaxin-1a predicts determinants of epimorphin/syntaxin-2 function in mammary epithelial morphogenesis.(