Ignet

Gene Information

Gene symbol: SNTG1

Gene name: syntrophin, gamma 1

HGNC ID: 13740

Synonyms: SYN4, G1SYN

Related Genes

#	Gene Symbol	Number of hits
1	INS	1 hits
2	SLC2A4	1 hits
3	STX4	1 hits
4	STXBP3	1 hits

Related Sentences

#	PMID	Sentence
1	12882905	Insulin resistance in tetracycline-repressible Munc18c transgenic mice.
2	12882905	To investigate the physiological effects of modulating the abundance of Munc18c or syntaxin 4 (Syn4) proteins on the regulation of glucose homeostasis in vivo, we generated tetracycline-repressible transgenic mice that overexpress either Munc18c or Syn4 proteins in skeletal muscle, pancreas and adipose tissue seven-, five-, and threefold over endogenous protein, respectively.
3	12882905	Munc18c transgenic mice displayed whole-body insulin resistance during hyperinsulinemic-euglycemic clamp resulting from >41% reductions in skeletal muscle and white adipose tissue glucose uptake, but without alteration of hepatic insulin action.
4	12882905	Glucose intolerance in Munc18c transgenic mice was reversed by repression of transgene expression using tetracycline or by simultaneous overexpression of Syn4 protein.
5	12882905	In addition, Munc18c transgenic mice had depressed serum insulin levels, reflecting a threefold reduction in insulin secretion from islets isolated therefrom, thus uncovering roles for Munc18c and/or Syn4 in insulin granule exocytosis.
6	12882905	Taken together, these results indicate that balance, more than absolute abundance, of Munc18c and Syn4 proteins directly affects whole-body glucose homeostasis through alterations in insulin secretion and insulin action.
7	12882905	Insulin resistance in tetracycline-repressible Munc18c transgenic mice.
8	12882905	To investigate the physiological effects of modulating the abundance of Munc18c or syntaxin 4 (Syn4) proteins on the regulation of glucose homeostasis in vivo, we generated tetracycline-repressible transgenic mice that overexpress either Munc18c or Syn4 proteins in skeletal muscle, pancreas and adipose tissue seven-, five-, and threefold over endogenous protein, respectively.
9	12882905	Munc18c transgenic mice displayed whole-body insulin resistance during hyperinsulinemic-euglycemic clamp resulting from >41% reductions in skeletal muscle and white adipose tissue glucose uptake, but without alteration of hepatic insulin action.
10	12882905	Glucose intolerance in Munc18c transgenic mice was reversed by repression of transgene expression using tetracycline or by simultaneous overexpression of Syn4 protein.
11	12882905	In addition, Munc18c transgenic mice had depressed serum insulin levels, reflecting a threefold reduction in insulin secretion from islets isolated therefrom, thus uncovering roles for Munc18c and/or Syn4 in insulin granule exocytosis.
12	12882905	Taken together, these results indicate that balance, more than absolute abundance, of Munc18c and Syn4 proteins directly affects whole-body glucose homeostasis through alterations in insulin secretion and insulin action.
13	12882905	Insulin resistance in tetracycline-repressible Munc18c transgenic mice.
14	12882905	To investigate the physiological effects of modulating the abundance of Munc18c or syntaxin 4 (Syn4) proteins on the regulation of glucose homeostasis in vivo, we generated tetracycline-repressible transgenic mice that overexpress either Munc18c or Syn4 proteins in skeletal muscle, pancreas and adipose tissue seven-, five-, and threefold over endogenous protein, respectively.
15	12882905	Munc18c transgenic mice displayed whole-body insulin resistance during hyperinsulinemic-euglycemic clamp resulting from >41% reductions in skeletal muscle and white adipose tissue glucose uptake, but without alteration of hepatic insulin action.
16	12882905	Glucose intolerance in Munc18c transgenic mice was reversed by repression of transgene expression using tetracycline or by simultaneous overexpression of Syn4 protein.
17	12882905	In addition, Munc18c transgenic mice had depressed serum insulin levels, reflecting a threefold reduction in insulin secretion from islets isolated therefrom, thus uncovering roles for Munc18c and/or Syn4 in insulin granule exocytosis.
18	12882905	Taken together, these results indicate that balance, more than absolute abundance, of Munc18c and Syn4 proteins directly affects whole-body glucose homeostasis through alterations in insulin secretion and insulin action.
19	12882905	Insulin resistance in tetracycline-repressible Munc18c transgenic mice.
20	12882905	To investigate the physiological effects of modulating the abundance of Munc18c or syntaxin 4 (Syn4) proteins on the regulation of glucose homeostasis in vivo, we generated tetracycline-repressible transgenic mice that overexpress either Munc18c or Syn4 proteins in skeletal muscle, pancreas and adipose tissue seven-, five-, and threefold over endogenous protein, respectively.
21	12882905	Munc18c transgenic mice displayed whole-body insulin resistance during hyperinsulinemic-euglycemic clamp resulting from >41% reductions in skeletal muscle and white adipose tissue glucose uptake, but without alteration of hepatic insulin action.
22	12882905	Glucose intolerance in Munc18c transgenic mice was reversed by repression of transgene expression using tetracycline or by simultaneous overexpression of Syn4 protein.
23	12882905	In addition, Munc18c transgenic mice had depressed serum insulin levels, reflecting a threefold reduction in insulin secretion from islets isolated therefrom, thus uncovering roles for Munc18c and/or Syn4 in insulin granule exocytosis.
24	12882905	Taken together, these results indicate that balance, more than absolute abundance, of Munc18c and Syn4 proteins directly affects whole-body glucose homeostasis through alterations in insulin secretion and insulin action.
25	15331531	Syntaxin 4 transgenic mice exhibit enhanced insulin-mediated glucose uptake in skeletal muscle.
26	15331531	Insulin-stimulated translocation of GLUT4 vesicles from an intracellular compartment to the plasma membrane in 3T3L1 adipocytes is mediated through a syntaxin 4 (Syn4)- and Munc18c-dependent mechanism.
27	15331531	Increases in Syn4 caused increases in Munc18c protein, indicating that Syn4 regulates Munc18c expression in vivo.
28	15331531	Insulin-stimulated glucose uptake in skeletal muscle was increased by twofold in Syn4 transgenic mice compared with wild-type mice as assessed by hyperinsulinemic-euglycemic clamp analysis, consistent with a twofold increase in insulin-stimulated GLUT4 translocation in skeletal muscle.
29	15331531	Moreover, insulin content and glucose-stimulated insulin secretion by islets isolated from Syn4 transgenic mice did not differ from that of wild-type mice.
30	15331531	In sum, these data suggest that increasing the number of Syn4-Munc18c "fusion sites" at the plasma membrane of skeletal muscle increases the amount of GLUT4 available to increase the overall rate of insulin-mediated glucose uptake in vivo.
31	15331531	Syntaxin 4 transgenic mice exhibit enhanced insulin-mediated glucose uptake in skeletal muscle.
32	15331531	Insulin-stimulated translocation of GLUT4 vesicles from an intracellular compartment to the plasma membrane in 3T3L1 adipocytes is mediated through a syntaxin 4 (Syn4)- and Munc18c-dependent mechanism.
33	15331531	Increases in Syn4 caused increases in Munc18c protein, indicating that Syn4 regulates Munc18c expression in vivo.
34	15331531	Insulin-stimulated glucose uptake in skeletal muscle was increased by twofold in Syn4 transgenic mice compared with wild-type mice as assessed by hyperinsulinemic-euglycemic clamp analysis, consistent with a twofold increase in insulin-stimulated GLUT4 translocation in skeletal muscle.
35	15331531	Moreover, insulin content and glucose-stimulated insulin secretion by islets isolated from Syn4 transgenic mice did not differ from that of wild-type mice.
36	15331531	In sum, these data suggest that increasing the number of Syn4-Munc18c "fusion sites" at the plasma membrane of skeletal muscle increases the amount of GLUT4 available to increase the overall rate of insulin-mediated glucose uptake in vivo.
37	15331531	Syntaxin 4 transgenic mice exhibit enhanced insulin-mediated glucose uptake in skeletal muscle.
38	15331531	Insulin-stimulated translocation of GLUT4 vesicles from an intracellular compartment to the plasma membrane in 3T3L1 adipocytes is mediated through a syntaxin 4 (Syn4)- and Munc18c-dependent mechanism.
39	15331531	Increases in Syn4 caused increases in Munc18c protein, indicating that Syn4 regulates Munc18c expression in vivo.
40	15331531	Insulin-stimulated glucose uptake in skeletal muscle was increased by twofold in Syn4 transgenic mice compared with wild-type mice as assessed by hyperinsulinemic-euglycemic clamp analysis, consistent with a twofold increase in insulin-stimulated GLUT4 translocation in skeletal muscle.
41	15331531	Moreover, insulin content and glucose-stimulated insulin secretion by islets isolated from Syn4 transgenic mice did not differ from that of wild-type mice.
42	15331531	In sum, these data suggest that increasing the number of Syn4-Munc18c "fusion sites" at the plasma membrane of skeletal muscle increases the amount of GLUT4 available to increase the overall rate of insulin-mediated glucose uptake in vivo.