| microRNA-15b contributes to depression-like behavior in mice by affecting synaptic protein levels and function in the nucleus accumbens. | microRNA-15b contributes to depression-like behavior in mice by affecting synaptic protein levels and function in the nucleus accumbens.
Guo L, Zhu Z, Wang G, Cui S, Shen M, Song Z, Wang JH., Free PMC Article | 12/26/2020 |
| Pancreatic acini from Munc18c-depleted mice (Munc18c(+/-)) and human pancreas (lenti-Munc18c-shRNA-treated) exhibit normal apical exocytosis of zymogen granules (ZGs) in response to physiologic stimulation with the intestinal hormone cholecystokinin (CCK-8). | Depletion of the membrane-fusion regulator Munc18c attenuates caerulein hyperstimulation-induced pancreatitis.
Dolai S, Liang T, Orabi AI, Xie L, Holmyard D, Javed TA, Fernandez NA, Xie H, Cattral MS, Thurmond DC, Thorn P, Gaisano HY., Free PMC Article | 02/9/2019 |
| observed an almost complete absence of exocytosis in Munc18-2-deficient MCs but intact exocytosis in MCs lacking Munc18-1 or Munc18-3 | Munc18-2, but not Munc18-1 or Munc18-3, controls compound and single-vesicle-regulated exocytosis in mast cells.
Gutierrez BA, Chavez MA, Rodarte AI, Ramos MA, Dominguez A, Petrova Y, Davalos AJ, Costa RM, Elizondo R, Tuvim MJ, Dickey BF, Burns AR, Heidelberger R, Adachi R., Free PMC Article | 01/26/2019 |
| Investigated the use of Escherichia coli as an expression host for Munc18c. Three N-terminal His-tagged constructs were engineered, two with a tobacco etch virus (TEV) or thrombin protease cleavage site to enable removal of the fusion tag. | Milligram quantities of homogeneous recombinant full-length mouse Munc18c from Escherichia coli cultures.
Rehman A, Jarrott RJ, Whitten AE, King GJ, Hu SH, Christie MP, Collins BM, Martin JL., Free PMC Article | 08/30/2014 |
| PTP1B is the first known tyrosine phosphatase for Munc18c and a regulator of its phosphorylation and function in adipocytes. | Regulation of the SNARE-interacting protein Munc18c tyrosine phosphorylation in adipocytes by protein-tyrosine phosphatase 1B.
Bakke J, Bettaieb A, Nagata N, Matsuo K, Haj FG., Free PMC Article | 02/22/2014 |
| Ectopic expression of syntaxin3 affects behaviors of B16 melanoma by controlling actin dynamics. | Ectopic expression of syntaxin3 affects behaviors of B16 melanoma by controlling actin dynamics.
Shono M, Yoshioka R, Chatani Y, Hirai Y. | 10/26/2013 |
| Munc18c provides stimulus-specific regulation of GLUT4 trafficking, but not FA transporter trafficking | Munc18c provides stimulus-selective regulation of GLUT4 but not fatty acid transporter trafficking in skeletal muscle.
Jain SS, Snook LA, Glatz JF, Luiken JJ, Holloway GP, Thurmond DC, Bonen A., Free PMC Article | 10/13/2012 |
| The Using 3T3-L1 adipocytes subjected to small interfering ribonucleic acid reduction of Munc18c as a model of impaired insulin-stimulated GLUT4 vesicle exocytosis. | Munc18c phosphorylation by the insulin receptor links cell signaling directly to SNARE exocytosis.
Jewell JL, Oh E, Ramalingam L, Kalwat MA, Tagliabracci VS, Tackett L, Elmendorf JS, Thurmond DC., Free PMC Article | 06/18/2011 |
| Munc18c(L) gene is closely related to syntaxin-binding protein, Munc18c.It comprises 2 exons separated by a 600bp intron with non-consensus donor & acceptor sites.Exons 1 & 2 of Munc18c(L) overlap with exons 1 through half of 9 of Munc18c gene. | Cloning and characterization of Munc18c(L), a novel murine Munc18c gene paralog.
Schlaepfer IR, Pulawa LK, Eckel RH. | 01/21/2010 |
| We conclude, therefore, that Munc18c is not rate-limiting for cardiac substrate uptake, neither under basal conditions nor when maximally stimulated metabolically. | Munc18c is not rate-limiting for glucose and long-chain fatty acid uptake in the heart.
Habets DD, Thurmond DC, Coumans WA, Bonen A, Glatz JF, Luiken JJ., Free PMC Article | 01/21/2010 |
| Essential positive role for Munc18c in second-phase glucose-stimulated insulin secretion. | Munc18c depletion selectively impairs the sustained phase of insulin release.
Oh E, Thurmond DC., Free PMC Article | 01/21/2010 |
| tyrosine phosphorylation of Munc18c induces a switch in binding specificity from syntaxin 4 to Doc2beta | The tyrosine phosphorylation of Munc18c induces a switch in binding specificity from syntaxin 4 to Doc2beta.
Jewell JL, Oh E, Bennett SM, Meroueh SO, Thurmond DC., Free PMC Article | 01/21/2010 |
| One mechanism accounting for the PDGF induction of Glut4 translocation is the suppression of the Munc18c negative regulation of Syntaxin 4 function. | 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 JE, Mori M. | 01/21/2010 |
| our data suggest that the mechanism by which glucosamine inhibits insulin-stimulated GLUT4 translocation involves modification of Munc18c. | Glucosamine-induced insulin resistance is coupled to O-linked glycosylation of Munc18c.
Chen G, Liu P, Thurmond DC, Elmendorf JS. | 01/21/2010 |
| balance, more than absolute abundance, of Munc18c and Syn4 proteins directly affects whole-body glucose homeostasis through alterations in insulin secretion and insulin action. | Insulin resistance in tetracycline-repressible Munc18c transgenic mice.
Spurlin BA, Thomas RM, Nevins AK, Kim HJ, Kim YJ, Noh HL, Shulman GI, Kim JK, Thurmond DC. | 01/21/2010 |
| Cellular munc18c levels can modulate glucose transport rate and GLUT4 translocation in 3T3L1 cells. | Cellular munc18c levels can modulate glucose transport rate and GLUT4 translocation in 3T3L1 cells.
Macaulay SL, Grusovin J, Stoichevska V, Ryan JM, Castelli LA, Ward CW. | 01/21/2010 |
| novel and conserved mechanism for the dissociation of Munc18c-Syntaxin 4 complexes in a stimulus-dependent manner to facilitate the increase in Syntaxin 4-VAMP2 association and to promote vesicle/granule fusion | The stimulus-induced tyrosine phosphorylation of Munc18c facilitates vesicle exocytosis.
Oh E, Thurmond DC., Free PMC Article | 01/21/2010 |
| Data show that Munc18c binds to monomeric syntaxin4 and the N-terminal 29 amino acids of syntaxin4 are necessary for this interaction. | Molecular dissection of the Munc18c/syntaxin4 interaction: implications for regulation of membrane trafficking.
Latham CF, Lopez JA, Hu SH, Gee CL, Westbury E, Blair DH, Armishaw CJ, Alewood PF, Bryant NJ, James DE, Martin JL. | 01/21/2010 |
| support a sequential two-state model for SM/soluble NSF attachment protein receptors binding involving an initial interaction via the Syntaxins N-peptide | Structure of the Munc18c/Syntaxin4 N-peptide complex defines universal features of the N-peptide binding mode of Sec1/Munc18 proteins.
Hu SH, Latham CF, Gee CL, James DE, Martin JL., Free PMC Article | 01/21/2010 |
| The interaction between syntaxin4 and Munc18c in adipocytes results in enhancement of insulin-stimulated GLUT4 externalization. | 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., Free PMC Article | 01/21/2010 |
| To define the molecular machinery required for platelet exocytosis, platelets from Munc18c heterozygous knockout mice were analyzed. These platelets show a decrease in Munc18c but no apparent reduction in other secretory machinery components | Platelets from Munc18c heterozygous mice exhibit normal stimulus-induced release.
Schraw TD, Crawford GL, Ren Q, Choi W, Thurmond DC, Pessin J, Whiteheart SW. | 01/21/2010 |
| Glucose intolerance and insulin secretion in knockout mice heterozygous for Munc18c are reported. | Munc18c heterozygous knockout mice display increased susceptibility for severe glucose intolerance.
Oh E, Spurlin BA, Pessin JE, Thurmond DC. | 01/21/2010 |