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Gene Review

Stxbp3a  -  syntaxin binding protein 3A

Mus musculus

Synonyms: MUNC-18-3, Mammalian homolog of Unc-18c, Munc-18c, Protein unc-18 homolog 3, Protein unc-18 homolog C, ...
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Disease relevance of Stxbp3a


High impact information on Stxbp3a

  • Adipocytes from Munc18c-null mice show increased sensitivity to insulin-stimulated GLUT4 externalization [2].
  • We have now generated mouse embryos deficient in the syntaxin4 binding protein Munc18c and show that the insulin-induced appearance of GLUT4 at the cell surface is enhanced in adipocytes derived from these Munc18c-/- mice compared with that in Munc18c+/+ cells [2].
  • Phosphatidylinositol 3-phosphate, which induced GLUT4 translocation to the cell periphery without externalization in Munc18c+/+ cells, elicited GLUT4 externalization in Munc18c-/- cells [2].
  • To examine the temporal relationship between pre- and post-docking events, we generated a Munc18c temperature-sensitive mutant (Munc18c/TS) by substitution of arginine 240 with a lysine residue [3].
  • Munc18c function is required for insulin-stimulated plasma membrane fusion of GLUT4 and insulin-responsive amino peptidase storage vesicles [4].

Biological context of Stxbp3a


Anatomical context of Stxbp3a


Associations of Stxbp3a with chemical compounds

  • However, after consuming a high-fat diet for only 5 weeks, the Munc18c(-/+) mice manifested severely impaired glucose tolerance compared with high-fat-fed WT mice [9].
  • Stimulus-induced tyrosine phosphorylation of Munc18c was investigated as a potential regulatory mechanism by which the Munc18c-Syntaxin 4 complex can be dissociated in response to divergent stimuli in multiple cell types [6].
  • Use of [(32)P]orthophosphate incorporation, pervanadate treatment, and phosphotyrosine-specific antibodies demonstrated that Munc18c underwent tyrosine phosphorylation [6].
  • Glucose intolerance in Munc18c transgenic mice was reversed by repression of transgene expression using tetracycline or by simultaneous overexpression of Syn4 protein [7].
  • In conclusion, our data suggest that the mechanism by which glucosamine inhibits insulin-stimulated GLUT4 translocation involves modification of Munc18c [12].
  • When overexpressed in MIN6 cells, this Hc-linker region functioned as a competitive inhibitor of endogenous syntaxin 4-Munc18c binding, increased syntaxin 4 binding to VAMP2, and significantly enhanced glucose-stimulated secretion [13].

Physical interactions of Stxbp3a

  • As expected, overexpressed Munc18c was found to co-immunoprecipitate with syntaxin 4 in the basal state [8].
  • Together, these data suggest that Munc18c inhibits the docking/fusion of GLUT4-containing vesicles by blocking the binding of VAMP2 to syntaxin 4 [8].
  • Supporting the notion of Munc18c binding with Syntaxin 4 and Doc2beta in mutually exclusive complexes, in vitro competition with Syntaxin 4 effectively displaced Munc18c from binding to Doc2beta [14].

Regulatory relationships of Stxbp3a

  • Expression of either wild-type Munc18c or the Y521A-Munc18c mutant both resulted in a marked inhibition of insulin-stimulated Glut4 translocation [15].

Other interactions of Stxbp3a


Analytical, diagnostic and therapeutic context of Stxbp3a


  1. Recombinant expression of Munc18c in a baculovirus system and interaction with syntaxin4. Hu, S.H., Gee, C.L., Latham, C.F., Rowlinson, S.W., Rova, U., Jones, A., Halliday, J.A., Bryant, N.J., James, D.E., Martin, J.L. Protein Expr. Purif. (2003) [Pubmed]
  2. Adipocytes from Munc18c-null mice show increased sensitivity to insulin-stimulated GLUT4 externalization. Kanda, H., Tamori, Y., Shinoda, H., Yoshikawa, M., Sakaue, M., Udagawa, J., Otani, H., Tashiro, F., Miyazaki, J., Kasuga, M. J. Clin. Invest. (2005) [Pubmed]
  3. Discrimination of GLUT4 vesicle trafficking from fusion using a temperature-sensitive Munc18c mutant. Thurmond, D.C., Pessin, J.E. EMBO J. (2000) [Pubmed]
  4. Munc18c function is required for insulin-stimulated plasma membrane fusion of GLUT4 and insulin-responsive amino peptidase storage vesicles. Thurmond, D.C., Kanzaki, M., Khan, A.H., Pessin, J.E. Mol. Cell. Biol. (2000) [Pubmed]
  5. Platelets from Munc18c heterozygous mice exhibit normal stimulus-induced release. Schraw, T.D., Crawford, G.L., Ren, Q., Choi, W., Thurmond, D.C., Pessin, J., Whiteheart, S.W. Thromb. Haemost. (2004) [Pubmed]
  6. The stimulus-induced tyrosine phosphorylation of Munc18c facilitates vesicle exocytosis. Oh, E., Thurmond, D.C. J. Biol. Chem. (2006) [Pubmed]
  7. Insulin resistance in tetracycline-repressible Munc18c transgenic mice. Spurlin, B.A., Thomas, R.M., Nevins, A.K., Kim, H.J., Kim, Y.J., Noh, H.L., Shulman, G.I., Kim, J.K., Thurmond, D.C. Diabetes (2003) [Pubmed]
  8. Regulation of insulin-stimulated GLUT4 translocation by Munc18c in 3T3L1 adipocytes. Thurmond, D.C., Ceresa, B.P., Okada, S., Elmendorf, J.S., Coker, K., Pessin, J.E. J. Biol. Chem. (1998) [Pubmed]
  9. Munc18c heterozygous knockout mice display increased susceptibility for severe glucose intolerance. Oh, E., Spurlin, B.A., Pessin, J.E., Thurmond, D.C. Diabetes (2005) [Pubmed]
  10. Characterization of Munc-18c and syntaxin-4 in 3T3-L1 adipocytes. Putative role in insulin-dependent movement of GLUT-4. Tellam, J.T., Macaulay, S.L., McIntosh, S., Hewish, D.R., Ward, C.W., James, D.E. J. Biol. Chem. (1997) [Pubmed]
  11. Evidence of a role for Munc18-2 and microtubules in mast cell granule exocytosis. Martin-Verdeaux, S., Pombo, I., Iannascoli, B., Roa, M., Varin-Blank, N., Rivera, J., Blank, U. J. Cell. Sci. (2003) [Pubmed]
  12. Glucosamine-induced insulin resistance is coupled to O-linked glycosylation of Munc18c. Chen, G., Liu, P., Thurmond, D.C., Elmendorf, J.S. FEBS Lett. (2003) [Pubmed]
  13. The tyrosine phosphorylation of Munc18c induces a switch in binding specificity from syntaxin 4 to Doc2beta. Jewell, J.L., Oh, E., Bennett, S.M., Meroueh, S.O., Thurmond, D.C. J. Biol. Chem. (2008) [Pubmed]
  14. Doc2beta is a novel Munc18c-interacting partner and positive effector of syntaxin 4-mediated exocytosis. Ke, B., Oh, E., Thurmond, D.C. J. Biol. Chem. (2007) [Pubmed]
  15. Tyrosine phosphorylation of Munc18c regulates platelet-derived growth factor-stimulated glucose transporter 4 translocation in 3T3L1 adipocytes. Umahara, M., Okada, S., Yamada, E., Saito, T., Ohshima, K., Hashimoto, K., Yamada, M., Shimizu, H., Pessin, J.E., Mori, M. Endocrinology (2008) [Pubmed]
  16. Molecular identification of two novel Munc-18 isoforms expressed in non-neuronal tissues. Tellam, J.T., McIntosh, S., James, D.E. J. Biol. Chem. (1995) [Pubmed]
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