The most recent information on INSIG1 is here. Click here for the function of INSIG1. Edit this page in Wiki Genes - INSIG1 or see Wiki Gene. Insulin-induced factitious hypoglycemic coma. Paper-5186484. These genes are PROX1, INSIG-1, NK4, and UBD. Paper-13648755. SGK1 dependence of insulin induced hypokalemia. Paper-13529665. Insulin-induced expression of human heat-shock protein gene hsp70. Paper-6473656. Insulin induced an increase in AGT and AT1R mRNA with similar ED50. Paper-13111298. Insulin-induced hypoglycaemia produced an exaggerated AVP response. Paper-6341915. Insulin induced movement of SNX9 to membrane fractions from the cytosol. Paper-10042709. Insulin-induced hexokinase II expression is reduced in obesity and NIDDM. Paper-1361495. Insulin-induced hypoglycaemia stimulates secretion of parathyroid hormone. Paper-4557214. IGF1R overexpression in VSMCs impaired insulin-induced Akt phosphorylation. Paper-13623049. Alpha-actinin-4 is selectively required for insulin-induced GLUT4 translocation. Paper-12929735. The knock-down of C/ EBP-beta with siRNA abolished the insulin-induced Ccl2 mRNA expression. Paper-12401906. Moreover, insulin-induced membrane ruffling is inhibited by overexpression of Kank. Paper-13591333. Insulin-induced TGS was similar in all three groups as was insulin- stimulated GT. Paper-1650638. Insulin-induced release of plasminogen activator from human blood platelets. Paper-156239. Knockdown of the insulin receptor attenuated insulin-induced translocation of TRPV2. Paper-13559840. Insulin induced a dose dependent increase of the PAI-1 secretion by Hep G2 cell line. Paper-5833675. Fuzzy Logic Analysis of Kinase Pathway Crosstalk in TNF/EGF/ Insulin-Induced Signaling. Paper-13701308. Protein kinase Cdelta participates in insulin-induced activation of PKB via PDK1. Paper-12239767. Insulin induced reciprocal changes in HDL- and low-density lipoprotein (LDL)-receptor activity. Paper-6244966. Ghrelin stimulates insulin-induced glucose uptake in adipocytes. Paper-11334407. Finally, we demonstrate that PPARgamma participates in the insulin-induced IDE expression in neurons. Paper-13765001. Insulin-induced phosphorylation of FKHR ( Foxo1) targets to proteasomal degradation. Paper-10012221. The present study thus explored the contribution of SGK1 to insulin-induced hypokalemia. Paper-13529665. RESULTS: Exposure of corneal epithelial cells to insulin induced phosphorylation of EGFR. Paper-12347944. Involvement of the ERK1/2 MAPK pathway in insulin-induced S6K1 activation in avian cells. Paper-12655646. Chrysin inhibited insulin-induced expression of HIF-1alpha by reducing its stability. Paper-12433585. CONCLUSION: Insulin-induced cardioprotection at reperfusion occurs through activation of STAT3. Paper-12972841. These data demonstrate that the OT response to insulin-induced hypoglycaemia is inhibited by ethanol. Paper-13611325. Insulin-induced hypoglycemia is not aggravated by somatostatin in insulin-dependent diabetes. Paper-3257279. Inhibition of ERK1/2 or overexpression of MPK-1 promoted insulin-induced differentiation. Paper-13522892. Addition of exogenous insulin induced translocation and insertion of TRPV2 to the plasma membrane. Paper-13559840. Knockdown of Rab8A and Rab14, but not of Rab8B or Rab10, inhibited insulin-induced GLUT4 translocation. Paper-13028990. Insulin induced the synthesis of EF-2 within 20 min of treatment, with a half-maximal dose of 10(-11) M. Paper-6445527. Mutant SCAP(Y298C) fails to bind INSIG-1 and is resistant to sterol- mediated inhibition of ER exit. Paper-9541588. Insulin-induced vascular endothelial growth factor expression is mediated by the NADPH oxidase NOX3. Paper-12239991. Attenuated insulin-induced decrease in UEc in DM1 implicates the impaired insulin effect on proteolysis. Paper-12846330. Accordingly, insulin-induced cell hydration was 63% lower in sgk1 ( -/- ) mice than in sgk1 ( +/+ )mice. Paper-13529665. Insulin-induced hypoglycemia caused a modest but significant (p = 0.031) increase in plasma GIP. Paper-3704900. Insulin-induced hypoglycaemia caused a rise in plasma AVP followed by an increase in plasma cortisol. Paper-1666701. Insulin-induced epidermal growth factor activation in vascular smooth muscle cells is ADAM-dependent. Paper-12943721. Insulin-induced hypoglycemia did not increase AVP levels in either DSAP- or SAP-treated rats. Paper-12220110. The difference in the degradation rates is traced to two amino acids: Ser-149 in Insig-1 and Ser-106 in Insig-2. Paper-11411254. Furthermore, BMP2 inhibited Wnt/ beta-catenin signaling that promoted CL6 cardiomyogenesis. Paper-12827279. Insulin-induced phosphorylation of 4E-BP1 was inhibited by Akt-AA in Chinese hamster ovary cells. Paper-1940911. Sterol-regulated degradation of Insig-1 mediated by the membrane- bound ubiquitin ligase gp78. Paper-12357864. Insulin-induced hypoglycaemia produced a 2.2-fold increment in plasma OT levels in the control experiments. Paper-13611325. Permissive action of protein kinase C-zeta in insulin-induced CD36- and GLUT4 translocation in cardiac myocytes. Paper-13739521. Promoter analyses showed that IRS2, HK2 and INSIG1 are direct targets of TFE3. Paper-10825694. Insig required for sterol- mediated inhibition of Scap/ SREBP binding to COPII proteins in vitro. Paper-10769049. Insulin-induced IR phosphorylation and protein levels of IR and IRS-1 were higher in R than in C females. Paper-12309971. We therefore investigated the impact of GH and cortisol on ghrelin secretion during insulin-induced hypoglycaemia. Paper-12163724. NADPH oxidase and hydrogen peroxide mediate insulin-induced calcium increase in skeletal muscle cells. Paper-13579296. Overexpression of INSIG-1 increases the sensitivity of cells to sterol- mediated inhibition of SREBP processing. Paper-9541588. Role of IRS and PHIP on insulin-induced tyrosine phosphorylation and distribution of IRS proteins. Paper-13381675. Our data showed that overexpression of PTP1B effectively attenuated insulin-induced inhibition of Smad2 stimulation. Paper-12260398. The absence of uPAR attenuates insulin-induced vascular smooth muscle cell migration and proliferation. Paper-13089540. Insulin-induced Akt phosphorylation was increased by pravastatin and ERK1/2 phosphorylation attenuated. Paper-12146331. Accelerated degradation of HMG CoA reductase mediated by binding of insig-1 to its sterol-sensing domain. Paper-9787459. The Insig-1/ Scap/ SREBP complex accumulates in the ER, ready for liberation when the cell is again sterol deprived. Paper-11348302. In cells overexpressing the INSIG-1 gene, by contrast, SREBP processing is suppressed and oxysterol regulation is disrupted. Paper-9171744. Experiments with siRNA suggest that this action of INSIG1 is related to SREBP- mediated regulation of PCK2. Paper-12386449. Pretreatment with NF-E2-related factor-2 small-interfering RNA abolished insulin-induced heme oxygenase-1 induction. Paper-12008695. Sterols block transport of the mammalian SCAP/ SREBP-2 complex, but only when mammalian Insig-1 or -2 is co-expressed. Paper-9990954. Insulin-induced translocation of CD36 to the plasma membrane is reversible and shows similarity to that of GLUT4. Paper-12734091. Finally, central leptin treatment markedly increased INSIG-1 mRNA expression and impaired SREBP-1c activation in epididymal WAT. Paper-13560316. These findings suggest that the INSIG-1 protein alters sterol balance by modulating SREBP processing jointly with SCAP. Paper-9171744. BCAA treatment significantly suppressed glucose- and insulin-induced in vitro angiogenesis in the presence of VEGF. Paper-13765870. Some genes, including INSIG1, EGR1, CAV1, LCN2 and CCNG1, were differentially expressed in the two cell lines. Paper-12950262. Pretreatment of Ang II increased ERK1/2 phosphorylation and inhibited insulin-induced Akt phosphorylation. Paper-12468266. PATIENTS AND METHODS: We studied 16 patients (9 pre-pubertal) with ISS and a GH peak >or=40 mU/l to insulin-induced hypoglycaemia. Paper-13171375. Insulin-induced phosphorylation of Akt, AS160, S6K, and S6 was also decreased in skeletal muscle. Paper-13736057. This positive modulation of ENPP1 expression is paralleled by a reduced insulin-induced IR and IRS-1 phosphorylation. Paper-13579414. Insulin induced translocation of vesicles containing NPC1L1 and fluorescent sterol from the ERC to the cell membrane. Paper-12911089. Cholesterol-induced conformational change in SCAP enhanced by Insig proteins and mimicked by cationic amphiphiles. Paper-10029474. The incubation of adipocytes with MMP-3 inhibited insulin-induced glucose uptake in adipocytes. Paper-12765490. Insulin-induced hypoglycemia, L-dopa and arginine stimulate GH secretion through different mechanisms in man. Paper-6652576. In addition, we demonstrated that FXR does not interfere with insulin-induced GLUT4 translocation to plasma membrane. Paper-12985464. Proteolytic activation of sterol regulatory element-binding protein induced by cellular stress through depletion of Insig-1. Paper-10561323. Serum ghrelin levels are suppressed in hypopituitary patients following insulin-induced hypoglycaemia irrespective of GH status. Paper-12163724. Overexpression of dominant negative PKCdelta abrogated insulin-induced association of PKCdelta with both PKB and PDK1. Paper-12239767. TFE3 also induced hexokinase II ( HK2) and insulin-induced gene 1 ( INSIG1). Paper-10825694. By facilitating sterol-dependent ER retention of SCAP, INSIG-1 plays a central role in cholesterol homeostasis. Paper-9541588. Insulin-induced hypoglycemia caused an increase in plasma aldosterone as well as in renin activity and cortisol. Paper-2631645. Increased inflammation was modulated by insulin-induced changes in CSF levels of norepinephrine and apolipoprotein E (both P<.05). Paper-11287004. CONCLUSIONS: Acute insulin-induced hypoglycaemia induces a rise in plasma endothelin concentrations in people with Type 1 diabetes. Paper-13409924. Insulin-induced interaction of caveolin-2 with phospho- ERK was prevented when tyrosine 19 is mutated to alanine. Paper-13527288. Down-regulation of Rac1 or FLJ00068 by RNA interference, on the other hand, abrogated insulin-induced GLUT4 translocation. Paper-13033165. When Glu-214 is changed to alanine, Insig-2 becomes ubiquitinated, but it is still not degraded as rapidly as ubiquitinated Insig-1. Paper-11411254. It is concluded that PKC-zeta, but not any other PKC isoform, is necessary for insulin-induced translocation of GLUT4 and CD36. Paper-13739521. Silencing AS160 or TBC1D1 increased surface GLUT4 in unstimulated cells but did not prevent insulin-induced GLUT4 translocation. Paper-13028990. Insulin-induced hypoglycemia is used for evaluating GH-IGF-I and ACTH-adrenal axes in patients with pituitary disorders. Paper-13416005. Abstract The possible inhibition exerted by ethanol on the oxytocin ( OT) response to insulin-induced hypoglycaemia was tested in man. Paper-13611325. When the new Insig-1 and cholesterol converge on Scap, Scap/ SREBP binds to Insig-1, preventing ubiquitination. Paper-11348302. Ectoenzyme nucleotide pyrophosphate phosphodiesterase 1 ( ENPP1) is an inhibitor of insulin-induced activation of the insulin receptor. Paper-12288936. Insulin-induced hypoglycemia suppresses plasma parathyroid hormone levels in patients with adrenal insufficiency. Paper-10611797. In human endothelial cells amino acids inhibit insulin-induced Akt and ERK1/2 phosphorylation by an mTOR-dependent mechanism. Paper-12124702. Insulin-induced hypoglycemia was the most efficacious stimulus, and caused a similar rise in hPP response in males and females. Paper-4455835. Insig- mediated degradation of HMG CoA reductase stimulated by lanosterol, an intermediate in the synthesis of cholesterol. Paper-11064571. These data indicate that extracellular ATP and statins via the P2X7 receptor modulate insulin-induced Akt signaling in epithelial cells. Paper-12655732. PGRMC1 binding partners include multiple P450 proteins, PAIR-BP1, Insig, and an uncharacterized hormone/drug-binding protein. Paper-13556779. Here, we show that gp78, a membrane bound E3, binds to Insig-1 and is required for sterol-regulated ubiquitination of reductase. Paper-10970449. Expression of an APS mutant unable to bind Enigma increased the insulin-induced Glut 4 translocation to the plasma membrane. Paper-12289832. Pioglitazone and rosiglitazone enhanced insulin-induced inhibition of IGFBP-1 production by 13% and 20%, respectively (P < 0.001). Paper-10998841. Insulin induced an approximately five- and three-fold increase in FAS mRNA content in adipocytes and hepatoma cells, respectively. Paper-1453142. In the GLUTag cells, insulin-induced activation of glu expression occurred through the same TCF site that mediates cat/ TCF activation. Paper-12774793. Insulin-induced hypokalaemia increases plasma renin and angiotensin II levels while decreasing the serum aldosterone concentration. Paper-7418719. Insulin-induced activation of NADPH-dependent H2O2 generation in human adipocyte plasma membranes is mediated by Galphai2. Paper-983965. On the contrary, insulin-induced cell migration was inhibited by blocking the insulin receptor but not the IGF-1 receptor. Paper-11762199. Loss of insulin-induced inhibition of glucagon gene transcription in hamster pancreatic islet alpha cells by long-term insulin exposure. Paper-13023440. Insulin-induced receptor loss in the cultured human lymphocyte: quantitative morphological perturbations in the cell and plasma membrane. Paper-3426847. Furthermore, insulin-induced ML-1 cell proliferation was significantly enhanced by overexpression of cDNA encoding full-length CTCF. Paper-12545290. No inhibition of insulin-induced tyrosine phosphorylation of insulin receptor and insulin-receptor substrate-1 was observed. Paper-11359212. RESULTS: From among 16 agents tested, chronic insulin treatment was found to abolish insulin-induced inhibition of glucagon gene transcription. Paper-13023440. Ventromedial hypothalamic glucokinase is an important mediator of the counterregulatory response to insulin-induced hypoglycemia. Paper-12769264. Insulin-induced F-actin rearrangements took place through both types of receptors, but IGF-1 was a little more specific through its own receptors. Paper-11762199. Three mutations in sterol-sensing domain of SCAP block interaction with insig and render SREBP cleavage insensitive to sterols. Paper-9272220. We now report that LY295427 increases expression of insulin-induced gene-1 ( INSIG-1) and restores SREBP processing in cells treated with oxysterols. Paper-9171744. SiRNA against Nox4 but not Nox1 inhibited insulin-induced differentiation and ROS production but promoted proliferation. Paper-13522892. After exercise training, insulin-induced and IGF-1-induced vasorelaxant responses were evaluated by measuring the isometric tension of aortic rings. Paper-12276760. Insulin-induced hypoglycaemia, which stimulates gastric acid secretion, is associated with an increase in circulating somatostatin levels in man. Paper-4752086. Several new models are proposed from studies on a range of sterol binding proteins including Insig, SCAP, LXR, HMG-CoAR, NPC1 and NPC2. Paper-13761415. PKB activity was required for the insulin-induced activation of phosphodiesterase 3B ( PDE3B) and for the antilipolytic action of insulin. Paper-13681780. Sterols induce binding of SCAP to INSIG-1, as determined by blue native-PAGE, and this is correlated with the inhibition of SCAP exit from the ER. Paper-9541588. The insulin-induced translocation of p47(phox) was PKC delta dependent and attenuated by pravastatin, but independent of the activation of Akt and Rac1. Paper-12146331. In the pancreas, cholecystokinin increased the proliferation of insulin- producing beta cells and reduced insulin-induced hyperphagia. Paper-12576103. Insulin-induced NADPH oxidase activation promotes proliferation and matrix metalloproteinase activation in monocytes/ macrophages. Paper-13772292. Interestingly, local insulin induced an up-regulation of adiponectin expression in the AT of those patients with higher metabolic syndrome disturbances. Paper-13039036. In sterol-depleted cells Insig-1 is degraded at least 15 times more rapidly than Insig-2, owing to ubiquitination of Lys-156 and Lys-158 in Insig-1. Paper-11411254. RESULTS: The present study demonstrates that insulin-induced human haematopoietic myeloblastic ML-1 cell proliferation requires increased CTCF expression. Paper-12545290. Finally, S1P significantly reduced insulin-induced mRNA of ob gene and leptin secretion, whereas S1P increased glycerol release from adipocytes. Paper-12317803. Insulin sensitivity as measured by insulin-induced phosphorylation of Akt and S6 ribosomal protein was also independent of rosiglitazone. Paper-12734528. Inhibition of p38 MAPK with SB-203580 blocked the insulin-induced phosphorylation of Hsp27 and the improved functional recovery. Paper-12687547. In contrast, none of the extracts had any significant effect on MEK whereas only a cake saponin subfraction enhanced insulin-induced PKB/Akt activation. Paper-12206664. Celiac-superior mesenteric ganglionectomy, but not vagotomy, suppresses the sympathoadrenal response to insulin-induced hypoglycemia. Paper-11527526. Pramlintide is used with insulin and has been associated with an increased risk of insulin-induced severe hypoglycemia, particularly in type 1 diabetes. Paper-12027628. In addition, resistin inhibited insulin-induced phosphorylation of Akt in islets as well as other insulin target organs. Paper-12426541. Insulin induced a modest sustained 1.2- and 1.3-fold increase (P < 0.05) in p38 MAPK phosphorylation in the rested and exercised legs, respectively. Paper-9744088. Peroxisome Deficiency Causes a Complex Phenotype because of Hepatic SREBP/ Insig Dysregulation Associated with Endoplasmic Reticulum Stress. Paper-13653403. Isolation of mutant cells lacking Insig-1 through selection with SR-12813, an agent that stimulates degradation of 3-hydroxy-3-methylglutaryl-coenzyme A reductase. Paper-10561310. Insulin-induced protein tyrosine phosphorylation cascade and signalling molecules are localized in a caveolin-enriched cell membrane domain. Paper-1606529. Recently, it was shown that insulin-induced gene (Insig)-1, the key regulator of SREBP activity, is up-regulated by both activation of PPARalpha and PPARgamma. Paper-13633499. We also measured AVP responses to osmotic challenge induced by administration of hypertonic saline (1 M, 15 ml/kg, sc) and to insulin-induced hypoglycemia. Paper-12220110. CONCLUSIONS: Inhibition of EGFR activity decreases cell migration involved in insulin-induced wound repair, an effect that mimics inhibition of MMP activation. Paper-12347944. Knock-down of LAR induced post-receptor insulin resistance with the insulin-induced activation of PKB/Akt and MAP kinases markedly inhibited. Paper-11017556. Insulin induced a transient 2.4-fold increase in ERK1/2 phosphorylation (maximal at approximately 15 min) in skeletal muscle arterioles (P <0.05). Paper-10923049. The insulin receptor and glucose-6-phosphate dehydrogenase were upregulated by mmLDL and OxLDL, whereas insulin-induced gene 1 was significantly down-regulated. Paper-12084922. Crucial step in cholesterol homeostasis: sterols promote binding of SCAP to INSIG-1, a membrane protein that facilitates retention of SREBPs in ER. Paper-9541588. The hypocholesterolemic agent LY295427 up-regulates INSIG-1, identifying the INSIG-1 protein as a mediator of cholesterol homeostasis through SREBP. Paper-9171744. Insulin-induced hypoglycemia is a potent stress stimulating ACTH release, but the factors responsible for this ACTH secretion are not known. Paper-5593947. In support of this conclusion is our finding that suppression of RalGDS expression in cells inhibits both EGF and insulin-induced phosphorylation of Akt. Paper-12766452. Ubiquitination is not necessary for release of Scap/ SREBP from Insig-1, but it establishes a requirement for synthesis of new Insig-1 for feedback inhibition. Paper-11348302. Here we report that hypotonic stress reverses the sterol-mediated inhibition of SREBP proteolytic activation by reducing the level of Insig-1 but not Insig-2. Paper-10561323. Interestingly, leptin as well as insulin induced the expression of phosphotyrosine phosphatase (PTP)-1B, whereas CNTF treatment did not affect its expression. Paper-13638828. The prolyl isomerase Pin1 interacts with a ribosomal protein S6 kinase to enhance insulin-induced AP-1 activity and cellular transformation. Paper-13700363. Insulin-induced hypoglycaemia (ITT) stimulated the release of B- LPH and cortisol in both groups, whereas the B-EP increase was absent in the patients. Paper-5147480. METHODS AND RESULTS: The expression of Nox1 and Nox4 was increased during insulin-induced differentiation, and insulin increased ROS production. Paper-13522892. The relative insulin-induced increase in blood flow corrected for the control substance was higher in lean than obese women ( ANOVA for repeated measures F=3.93, P=0.05). Paper-12747714. Peroxisome proliferator-activated receptor-delta induces insulin-induced gene-1 and suppresses hepatic lipogenesis in obese diabetic mice. Paper-12897625. Peroxisome proliferator-activated receptor-delta induces insulin-induced gene-1 and suppresses hepatic lipogenesis in obese diabetic mice. Paper-13473168. Tribbles is a Drosophila protein that slows cell cycle progression, and its mammalian homolog, TRB3 interferes with insulin-induced activation of AKT. Paper-12364706. The Grem1 action was most effective at the early differentiation stage when CL6 cells were destined to cardiomyogenesis, and was mediated through inhibition of BMP2. Paper-12827279. Fasting C-peptide levels at diagnosis correlated with insulin-induced IFN-gamma (R = 0.52; p = 0.05) and negatively with spontaneous IL-4 secretion (R = -0.62; p < 0.05). Paper-12288993. Conclusion: TLCS induces insulin resistance by a PKC-dependent suppression of insulin-induced IRbeta phosphorylation and the PI 3-kinase/ PKB path. Paper-12700730. Upon sterol deprivation, the Scap/ SREBP complex dissociates from Insig-1, which is then ubiquitinated on lysines 156 and 158 and degraded in proteasomes. Paper-11348302. Both models showed decreased insulin-induced IRS-1 and IRS-2 tyrosine phosphorylation, accompanied by reduced protein levels of IRS-1 and IRS-2. Paper-12203615. CONCLUSION: Amino acids are necessary for insulin-induced activation of mTOR signaling and protein synthesis in both healthy and insulin resistant skeletal muscle. Paper-12833193. Although the insulin-induced increment in ANP concentrations was not different among groups, circulating ANP was strongly associated with glucose tolerance status. Paper-13309637. The mitogen-activated protein kinase ( MAPK) inhibitors PD-098059 and U-0126 attenuated the insulin-induced increase in BK-alpha expression. Paper-12815586. In the investigation of the PKB-independent mechanism, we found that insulin-induced nuclear translocation of beta-catenin (beta-cat), an effector of Wnt signaling. Paper-12656634. We observed that insulin-induced BRET between the IR and PTP1B was markedly reduced by Grb14, suggesting that Grb14 regulated this interaction in living cells. Paper-12304409. Insulin induced changes (P < 0.05) in ET-B mRNA levels in BeWo (+90 and +60% after 24 and 48 h, respectively) and JEG-3 (-70%), but not in JAR and trophoblast cells. Paper-8602417. Here, we use the trypsin assay to show that Insig proteins reduce the concentration of cholesterol needed in vitro to produce the conformational change in SCAP. Paper-10029474. The ectoenzyme ENPP1 (also termed membrane glycoprotein PC-1 or ENPP1/ PC-1) is an inhibitor of insulin-induced activation of the insulin receptor. Paper-13068033. Insulin-induced hypoglycemia, a potent stimulus of adrenomedullary secretion, resulted in 1.7- and 14-fold rises in plasma CgA and epinephrine, respectively. Paper-6541717. Feedback control of cholesterol synthesis is mediated in part by sterol-induced binding of HMG CoA reductase to Insig proteins in the endoplasmic reticulum (ER). Paper-11064571. FOXO1 Transrepresses Peroxisome Proliferator-activated Receptor {gamma} Transactivation, Coordinating an Insulin-induced Feed-forward Response in Adipocytes. Paper-13736003. RESULTS: Insulin-induced SMC proliferation through the IGF-1 receptors; indeed, the blockade of insulin receptors does not inhibit the mitogenic influence of insulin. Paper-11762199. Amino acids are necessary for the insulin-induced activation of mTOR/ S6K1 signaling and protein synthesis in healthy and insulin resistant human skeletal muscle. Paper-12833193. Sterols prevent Insig-1 ubiquitination and degradation by displacing gp78 from Insig-1, an event that results from sterol-induced binding of Scap to Insig-1. Paper-12357864. This insulin-induced redistribution of GLUT4 protein is achieved through a series of highly organized membrane trafficking events, orchestrated by insulin receptor signals. Paper-12132962. Activation of both, PPARalpha and PPARgamma led to increased concentrations of Insig-1 and Insig-2a, with the most prominent effect on Insig-2a after troglitazone incubation. Paper-13633499. In this work we have investigated the intracellular pathways involved in insulin-induced and amino acid- induced p70/ S6-K activations in human endothelial cells. Paper-12124702. FGF-19 also suppressed the insulin-induced expression of sterol regulatory element-binding protein-1c (SREBP-1c), a key transcriptional activator of lipogenic genes. Paper-13703315. Finally, insulin-induced translocation of TRPV2 was observed in cultured mouse beta-cells, and knockdown of TRPV2 reduced insulin secretion induced by glucose. Paper-13559840. AIMS: To determine whether acute insulin-induced hypoglycaemia provokes a detectable alteration in peripheral plasma endothelin (ET) concentrations in humans with Type 1 diabetes. Paper-13409924. Repetitive and profound insulin-induced hypoglycemia in newborn rats can establish a reliable animal model of brain injury resulting from neonatal hypoglycemia. Paper-12971597. In contrast, Pin1(-/-) mouse embryonic fibroblasts (MEFs) exhibited significantly decreased insulin-induced p70S6K phosphorylation compared with Pin1(+/+) MEFs. Paper-13700363. Quantitative RT-PCR analysis of the 4 genes showed reduced expression of 2 genes in cancers: Insulin-induced protein 1 ( INSIG1/ CL-6) and p41 Arp2/3 complex (p41-Arc). Paper-9509753. The insulin-induced glucose uptake was enhanced by berberine in the absence of change in IRS-1 (Ser(307/312)), Akt, p70 S6, and ERK phosphorylation. Paper-12687535. 2. Insulin-induced hypoglycemia and Pitressin administration were associated with nearly equivalent increments of immunoreactive ACTH and beta-LPH concentrations. Paper-3526410. A significant (p = 0.02) reduction in expression of phosphoenolpyruvate carboxykinase ( PCK2) was observed following siRNA inhibition of INSIG1 in human Huh7 hepatoma cells. Paper-12386449. Adaptation of glucokinase gene expression in the rat dorsal vagal complex in a model for recurrent intermediate insulin-induced hypoglycemia: impact of gender. Paper-13555222. CONCLUSIONS: Nox4 acts as a switch from insulin-induced proliferation to differentiation by controlling MKP-1 expression, which limits ERK1/2 signaling. Paper-13522892. To characterize insulin-induced CD36 translocation in intact cells, Chinese hamster ovary (CHO) cells stably expressing CD36 or myc-tagged GLUT4 (GLUT4myc) were created. Paper-12734091. Effects of acute and chronic insulin-induced hypoglycemia on type II glucocorticoid receptor ( GR) gene expression in characterized CNS metabolic loci. Paper-12151879. Insulin induced similar decrements in fractional sodium excretion (N-NIDDM: 43+/-5.9 and 57+/-9.1%,H-N IDDM: 48+/-16.4 and 62+/-12.5%, low and high insulin dose respectively). Paper-651739. Inhibition of EGFR activation by AG1478 or the MMP inhibitor, GM6001, reduced phosphorylation of insulin-induced ERK in the presence of insulin and delayed wound closure. Paper-12347944. TSC is caused by mutation in either TSC1 or TSC2 tumor suppressor genes that negatively regulate insulin-induced S6K activation and cell growth. Paper-12263435. We investigated the ability of insulin to stimulate protein synthesis in growing pubertal children who were given sufficient amino acids to counter insulin-induced hypoaminoacidemia. Paper-11240654. Inhibition of PI(3)K specifically blocked the insulin-induced reduction in ghrelin concentration, whereas inhibition of MAPK had no effect on insulin-mediated actions. Paper-12211172. As observed by siRNA and overexpression, Nox4 controlled the expression of MAP kinase phosphatase-1 ( MKP-1), which reduces insulin-induced ERK1/2 activation. Paper-13522892. Regulation of hepatic cholesterol biosynthesis, lipogenesis, and insulin signaling intersect at the transcriptional level by control of SREBP and Insig genes. Paper-13653403. More recently, Insig-1 and Insig-2 were identified as ER resident proteins that bind the SCAP/ SREBP complex and promote its ER retention when cells are treated with sterols. Paper-10029474. The insulin-induced LRP1-mediated CR uptake, as demonstrated here, suggests that impaired hepatic LRP1 translocation can contribute to the postprandial lipaemia in insulin resistance. Paper-13747813. The current results identify gp78 as the E3 that initiates sterol-accelerated degradation of reductase, and Insig-1 as a bridge between gp78/VCP and the reductase substrate. Paper-10970449. The insulin-induced protein degradation of LRP1 in J774 cells was mediated by the activation of the PI(3)K/Akt pathway and proteasomal system by an enhanced ubiquitin-receptor conjugation. Paper-13590680. The model predicts and experiments confirm that insulin-induced amplification of mitogenic signaling is abolished by disrupting PIP(3)- mediated positive feedback via GAB1 and IRS. Paper-13711205. Insulin-induced activation of PKC-zeta was confirmed in vitro by its translocation from the cytosol to the membrane fraction, and in vivo by immunohistochemistry studies. Paper-13485335. Insulin induced tyrosine phosphorylation of SHC occurred very rapidly (within 1 min) with a dose curve which paralleled the autophosphorylation of the insulin receptor. Paper-7805898. Insulin induced an approximately 12- to 16-fold increase in luciferase activity in both the 1/1 and 2/2 PAI-1 genotype HUVEC cultures transfected with the p1PAI110/luc construct. Paper-1643163. Elevated free fatty acids attenuate the insulin-induced suppression of PDK4 gene expression in human skeletal muscle: potential role of intramuscular long-chain acyl-coenzyme A. Paper-12522686. Consistent with this, infusion of amino acids into humans leads to S6K1 activation, inhibition of insulin-induced class 1 PI3K activation, and insulin resistance. Paper-12029101. Insulin-induced PI3K/Akt activation is known to inhibit a family of Forkhead transcription factors ( FOXO), which can lead to increased oxidative stress in several model organisms. Paper-12677823. The insulin-induced CD36 translocation was shown to be phosphatidylinositol-3 kinase-dependent, and reversible (as evidenced by insulin wash-out) in a similar time frame as that for GLUT4. Paper-12734091. Scap/ SREBP moves to the Golgi, where SREBP is processed to liberate a nuclear fragment that activates genes for cholesterol synthesis and uptake and the gene for Insig-1. Paper-11348302. Thus, these data suggest that the triacylglycerol reducing effect of fibrates and thiazolidinediones is partially caused by inhibition of SREBP-1 activation via up-regulation of Insig. Paper-13633499. Our findings indicate that exercise training enhances insulin-induced and IGF-1- induced vasorelaxant responses which are mediated through the PI3K- NOS-dependent pathway. Paper-12276760. Insulin induced dose-dependent vasoconstriction of skeletal muscle arterioles (up to -22 +/- 3% of basal diameter; P <0.05) during PI3-kinase inhibition with wortmannin (50 nmol/l). Paper-10923049. Accordingly, insulin-induced proliferation was enhanced by siRNA against MKP-1, whereas inhibition of ERK1/2 or overexpression of MKP-1 attenuated proliferation. Paper-13522892. Inhibitors of insulin receptor tyrosine kinase, PI3K, Akt and mTOR abrogated insulin-induced Nrf2-mediated GCLc expression, redox balance, and IHEC survival. Paper-12319338. Insulin induced Tyr phosphorylation of the insulin receptor ( INS-R) and formation of an INS-R - G(i)alpha(2) complex, suggesting interference with LPS-induced cAMP control. Paper-13498788. Mutation of Ser-411 to Ala ablated insulin-induced Thr-389 phosphorylation and S6K1 activation, whereas mutation mimicking Ser-411 phosphorylation did not show any effect. Paper-13138485. These results support a model whereby AS160, Rab8A, and myosin Vb are required for insulin-induced GLUT4 translocation in muscle cells, potentially as part of a linear signaling cascade. Paper-13028990. When Asp-205 was mutated to alanine, the mutant Insig-1 lost the ability to bind to Scap and, thus, was unable to suppress the cleavage of sterol regulatory element-binding proteins. Paper-11811765. The role of c-Jun N-terminal kinase, p38, and extracellular signal-regulated kinase in insulin-induced Thr69 and Thr71 phosphorylation of activating transcription factor 2. Paper-12154425. Sterol regulation of reductase degradation and SREBP processing is restored when SRD-14 cells are transfected with expression plasmids encoding either Insig-1 or Insig-2. Paper-10561310. Whereas insig-1 binding to SCAP leads to ER retention, insig-1 binding to HMG CoA reductase leads to accelerated degradation that is blocked by proteasome inhibitors. Paper-9787459. Sirpalpha1 can bind SHP-2 in the form of tyrosine phosphorylation by SH2 effect and negatively regulate growth factor, oncogene, or insulin-induced responses as its substrate. Paper-12004788. Therefore, the effect of molecules implicated in conferring insulin resistance in some other tissues was investigated on insulin-induced inhibition of glucagon gene transcription in alpha cells. Paper-13023440. Insulin-induced as well as tolbutamide- induced hypoglycemia clearly provoked hPP secretion (peaks: 1201 +/- 370 pg/ml, P = 0.03, and 520 +/- 112 pg/ml, P = 0.005, respectively). Paper-2980872. Grem1, a known BMP antagonist, enhanced DMSO-induced cardiomyogenesis of P19CL6 embryonal carcinoma cells ( CL6 cells) 10-35 fold in an area of beating differentiated cardiomyocytes. Paper-12827279. Type II glucocorticoid receptor involvement in habituated activation of lateral hypothalamic area orexin-A-immunopositive neurons during recurring insulin-induced hypoglycemia. Paper-12284051. Down-regulation of caveolin-2 by caveolin-2 siRNA arrested the insulin-induced nuclear localization of ERK with no change in the insulin- stimulated ERK activation. Paper-13527288. Here, we identify that a high-fat diet impaired insulin-induced hypothalamic Foxo1 phosphorylation and degradation, increasing the nuclear Foxo1 activity and hyperphagic response in rats. Paper-13772979. IGF1R downregulation uncovered an insulin-induced reduction in activation of NF-kappaB and inhibition of MCP-1 upregulation in response to TNF-alpha. Paper-13623049. Accelerated degradation is inhibited by overexpression of the sterol-sensing domain of SREBP cleavage-activating protein ( SCAP), suggesting that both proteins bind to the same site on insig-1. Paper-9787459. The messenger RNAs for enzymes of fatty acid synthesis and their transcriptional regulator, SREBP-1c, as well as the Insig-1 mRNA, were upregulated two-fold in the OSBP-expressing livers. Paper-13192365. Insulin-induced desensitization of extracellular signal-regulated kinase activation results from an inhibition of Raf activity independent of Ras activation and dissociation of the Grb2-SOS complex. Paper-1900528. Insulin-induced mitogen- activated protein (MAP) kinase phosphatase-1 ( MKP-1) attenuates insulin-stimulated MAP kinase activity: a mechanism for the feedback inhibition of insulin signaling. Paper-1161548. In conclusion, our results demonstrate that NOX3, a ROS generating NADPH oxidase, plays an integral role in insulin-induced p42/44 MAPK signal transmission and VEGF-A production. Paper-12239991. Insig overexpression was associated with a striking reduction in the elevated level of nuclear sterol regulatory element-binding protein (SREBP)-1c, the activated form of the transcription factor. Paper-10206725. Genes consistently induced ( ATF3, CCNG2, CDKN1A, EGR1, INSIG1, and MAF) or repressed ( CCND1 and VGF) in both cell lines, were also found after gemcitabine treatment. Paper-12464314. Indeed, we found that this distinct insulin-induced PM accumulation of Akt kinases is translated into a differential regulation by the Akt isoforms of AS160, a RabGAP that regulates GLUT4 trafficking. Paper-13755212. U0126, an inhibitor of the ERK MAPK pathway, completely abolished insulin-induced S6K1 phosphorylation and activity in chicken myoblasts, whereas its effect was only partial in LMH cells. Paper-12655646. We conclude that sequential activation and nuclear appearance of ERK1/2 and JNK, rather than p38, underlies the two-step insulin-induced ATF2 phosphorylation in JNK-expressing cells. Paper-12154425. Lastly, overexpression of a fragment of myosin Vb, a recently identified Rab8A-interacting protein, inhibited insulin-induced GLUT4 translocation and altered the subcellular distribution of GTP-loaded Rab8A. Paper-13028990. This in vitro inhibition is dependent on the presence of Insig-1, an ER resident protein that is necessary for sterol- mediated inhibition of Scap/ SREBP transport in intact cells. Paper-10769049. The distribution of caveolar and noncaveolar phosphorylated IR was unaffected but insulin-induced IR activation was significantly enhanced following consumption of the high-cholesterol diet (120%, P < 0.001). Paper-13494298. The rate of HSP60 transcription and mRNA accumulation were measured in rat H4IIE hepatoma cells and insulin-induced expression of HSP60 was predominantly via the MEK/ ERK pathway. Paper-13503655. Repetitive and profound insulin-induced hypoglycemia results in brain damage in newborn rats: an approach to establish an animal model of brain injury induced by neonatal hypoglycemia. Paper-12971597. Here, we report that the ubiquitin ligase gp78, which binds with much higher affinity to Insig-1 than Insig-2, is required for ubiquitination and degradation of Insig-1 in sterol-depleted cells. Paper-12357864. OBJECTIVE: Circulating ghrelin is suppressed during insulin-induced hypoglycaemia in healthy subjects, but it is unknown whether this is determined by feedback inhibition from counter-regulatory hormones. Paper-12163724. The alphaIGF-1R antibody, A12, was capable of arresting IGF-1 or insulin-induced FD/ IGF-1R cell proliferation in the G1 phase of the cell cycle and resulted in apoptotic induction. Paper-12128576. These data imply that cholesterol interacts with SCAP directly by inducing it to bind to Insigs, whereas 25-HC works indirectly through a putative 25-HC sensor protein that elicits SCAP- Insig binding. Paper-10561374. In contrast, blockage of the ERK-specific MAP kinase MEK with PD98059, that prevents phosphorylation of ERK1/ ERK2, abrogated insulin-induced CXCL8 release in primary monocytes. Paper-13039141. Testicular regulation of neuronal glucose and monocarboxylate transporter gene expression profiles in CNS metabolic sensing sites during acute and recurrent insulin-induced hypoglycemia. Paper-13175716. Treatment of H4IIE liver cells with anisomycin inhibited insulin-induced tyrosine phosphorylation of IRS-2; inhibition was reversed by pretreatment with the JNK and GSK-3 inhibitors. Paper-12729734. Insulin-induced phosphorylation of the signaling proteins Akt/ PKB and ERK-2 was analyzed using a bead-based fluorescence detection system and was correlated to BMI and fat cell size. Paper-13658586. Akt2 Regulation of Cdc2-Like Kinases ( Clk/ Sty), Serine/Arginine-Rich (SR) Protein Phosphorylation, and Insulin-Induced Alternative Splicing of PKC{beta}II Messenger Ribonucleic Acid. Paper-13728437. Glycogen Synthase Kinase 3{beta} Is a Novel Regulator of High Glucose- and High Insulin-induced Extracellular Matrix Protein Synthesis in Renal Proximal Tubular Epithelial Cells. Paper-13067140. Furthermore, activation of HER1 is required for the insulin-induced increase in expression of the HER1 ligands heparin- binding epidermal growth factor-like growth factor, amphiregulin and epiregulin. Paper-12325338. Aldosterone inhibits insulin-induced glucose uptake by degradation of insulin receptor substrate (IRS) 1 and IRS2 via a reactive oxygen species-mediated pathway in 3T3-L1 adipocytes. Paper-13679924. Thus, the drugs which restore the impaired insulin-induced PI 3-kinase/ AKT activation, for example, by suppressing JNK or p70S6K, PTEN or SHIP2, could be novel agents to treat diabetes mellitus. Paper-13429451. In these situations, an increase in the insulin-induced IRS/ PI 3-kinase/Akt pathway occurs in the ovary, suggesting that the activation of this pathway may have a role in the development of PCOS. Paper-12171015. The effects of leptin on the expression of several enzymes of the sphingolipid metabolism, sterol regulatory element binding protein (SREBP)-1c, and insulin-induced gene 1 ( INSIG-1) in this tissue were studied. Paper-13560316. The decrease in IRS-1 amount resulted in a reduction in its tyrosine phosphorylation and the alteration of insulin-induced protein kinase B activation and AS160 phosphorylation. Paper-12379297. Corroborating these results, constitutively active Akt upregulated the signaling molecules involved in insulin-induced relaxation such as iNOS, cGK1alpha, and MBP activity, even in the absence of insulin stimulation. Paper-12313230. Chondrogenic differentiation by combined treatment with bone morphogenetic protein-2 and insulin induced cartducin expression along with type II and IX collagen expression in chondrogenic progenitor N1511 cells. Paper-10842494. Overexpression of IRS1 and IRS2 impaired insulin-induced internalization of the IR in a dose-dependent manner suggesting that IRS proteins prevent endosome-associated receptor dephosphorylation/inactivation. Paper-13104027. Exogenous TNF-alpha infusion increased c-Jun N-terminal kinase phosphorylation and insulin receptor substrate-1 serine 307 phosphorylation, and inhibited insulin-induced signaling in liver. Paper-12790724. The aim of this study was to determine whether the response of pituitary hormones, cortisol, plasma renin activity, aldosterone and catecholamines to insulin-induced hypoglycaemia is changed in hypertension. Paper-12128789. CONCLUSIONS: Our results indicate that CTCF is indeed a protein with multifunctional activity that plays a significant role in modulating signalling pathways to mediate insulin-induced ML-1 cell proliferation. Paper-12545290. Moreover, the nonadditivity of arsenite-induced glucose uptake and insulin-induced glucose uptake indicates that arsenite recruits GLUT4 from insulin-responsive intracellular stores. Paper-12273652. Insulin-induced phosphorylation of Akt (at 15 and 30 minutes) is not accompanied by the phosphorylation of the downstream kinase p70/ S6-K, indicating the existence of a negative feedback at this level. Paper-12124702. Estrogen receptors consist of two isoforms, estrogen receptors-alpha (ER-alpha) and -beta ( ER-beta), but their roles in insulin-induced glucose uptake in mature adipose tissue have yet to be clarified. Paper-12367959. RANKL-induced Akt phosphorylation was strongly inhibited by berberine; however, neither monocyte/macrophage-colony stimulating factor (M-CSF)-induced nor insulin-induced Akt activation was inhibited by the drug. Paper-12688244. Since skeletal muscle is an important insulin target tissue and accounts for much of insulin-induced glucose disposal, it is important to determine its role in injury/infection-induced hyperglycemia. Paper-13094275. CONCLUSIONS/INTERPRETATION: These results show that an extended exposure of alpha cells to insulin induces IR downregulation and loss of insulin-induced inhibition of glucagon gene transcription. Paper-13023440. Insulin-induced antilipolysis was investigated in fat cells obtained after an overnight fast and 60 min after glucose ingestion in seven non-obese patients with non-insulin-dependent diabetes mellitus ( NIDDM). Paper-6105985. In cultured neonatal rat cardiomyocytes, activation of AMPK with 5-aminoimidazole-4-carboxamide-1-beta-D-ribofuranoside ( AICAR) prevented IGF-I/ insulin-induced cardiomyocyte hypertrophy. Paper-13058848. The current study demonstrates that animal cells, in response to either hypotonic shock or ER stress, can bypass the cholesterol inhibition of SREBP processing, an effect that is attributable to the rapid turnover of Insig-1. Paper-10561323. Insulin-induced increase in TGF-beta1 concentration was not abrogated by actinomycin D, however, stimulation by insulin, in the presence of cycloheximide led to a dose-dependent decrease in TGF-beta1 production. Paper-9089368. Here we examined the effect of knockdown of AS160, TBC1D1, and Rabs 8A, 8B, 10, and 14 ( in vitro substrates of AS160 and TBC1D1 Rab-GAP activities) on insulin-induced GLUT4 translocation in L6 muscle cells. Paper-13028990. Simultaneously, overexpression of SOD1 in db/db mice enhanced the inactivation of forkhead box class O1, another regulator of PGC-1alpha expression, without the changes of insulin-induced Akt phosphorylation in liver. Paper-12888636. A physiological link between increased expression of Enigma and an alteration in insulin-induced glucose uptake was suggested by the increase in Enigma mRNA expression in adipose tissue of diabetic obese patients. Paper-12289832. Recently, a common genetic polymorphism (rs7566605) associated with a higher BMI was found in proximity to the insulin induced protein 2 ( INSIG2 ) gene, with replication in four unrelated populations living in Western countries. Paper-12707552. Our findings suggest that insulin activates PKC-zeta, and Akt/ PKB downstream of PI3K, and that these pathways contribute to the insulin-induced increase of L-dopa uptake into PTCs. Paper-13485335. Insulin induced hypoglycemia (< 3 mmol/l) and clonidine induced depression of noradrenergic tone were used to assess the acute effects of cortisol, human growth hormone ( hGH), and norepinephrine ( NE). Paper-8008521. Suppression of SirT1 activity also selectively inhibited insulin-induced tyrosine phosphorylation of insulin receptor substrate 2 ( IRS-2), whereas it had minimal effect on that of IRS-1. Paper-12614966. These results suggest that after islet transplantation and in response to insulin-induced hypoglycemia, endogenous insulin secretion is appropriately suppressed and glucagon secretion may be partially restored. Paper-11527512. We demonstrate that the insulin-induced expression of HB-EGF, AR, and EPI mRNA is completely prevented by the specific PI3K inhibitor Wortmannin, suggesting an involvement of the PI3K. Paper-13108606. In conclusion, for the first time, we demonstrated that insulin-induced forearm glucose oxidation and forearm cGMP release were increased whereas forearm endothelin-1 release was decreased during trimetazidine treatment. Paper-10824817. Lack of an AVP response to insulin-induced hypoglycemia in intact rats therefore indicates that responses to hypovolemia and hypoglycemia are mediated by different catecholamine neurons under distinct sensory controls. Paper-12220110. When cellular cholesterol levels are high, Insig proteins bind to SREBP cleavage-activating protein, retaining it in the ER and preventing it from escorting SREBPs to the site of proteolytic activation in the Golgi complex. Paper-10561323. Moreover, overexpression of JNK and GSK-3 in H4IIE cells reduced insulin-induced tyrosine phosphorylation of IRS-2 and its association with the p85 regulatory subunit of phosphatidylinositol 3-kinase. Paper-12729734. IKKbeta siRNA protected against TNF-alpha-induced impairments in glucose metabolism, since insulin-induced increases in glucose uptake (1.5-fold; P < 0.05) and glycogen synthesis (3.5-fold; P < 0.05) were restored. Paper-12888623. Iressa inhibited not only the activation of HER1 caused by insulin but also the insulin-induced increase in the three ligands ( heparin-binding epidermal growth factor-like growth factor, epiregulin and amphiregulin). Paper-12325338. Thus, three different point mutations, each within the sterol-sensing domain of SCAP, prevent sterol-induced binding of SCAP to insig proteins and abolish feedback regulation of SREBP processing by sterols. Paper-9272220. These results suggest a possible regulatory effect of SirT1 on insulin-induced tyrosine phosphorylation of IRS-2, a vital step in insulin signaling pathway, through deacetylation of IRS-2 protein. Paper-12614966. We show that low concentration of atorvastatin, a drug inhibiting HMG-CoA reductase and cholesterol metabolism, or the natural agonist extracellular ATP rapidly decreased the level of insulin-induced phosphorylated Akt in the nucleus. Paper-12655732. Insulin-induced MKP-1 expression was mediated by extracellular signal- regulated protein kinases ( ERK) 1/2, c-Jun NH2-terminal kinases ( JNK) MAPK, and phosphatidylinositol 3-kinase (PI3K)/Akt pathways. Paper-12591936. Because actin rearrangement is important for insulin-induced glucose transporter 4 ( Glut 4) translocation, we studied the potential involvement of Enigma in insulin-induced glucose transport in 3T3-L1 adipocytes. Paper-12289832. However, in WT mice, preincubation with AICAR completely inhibited insulin-induced phosphorylation of mTOR targets, suggesting that mTOR signaling is blocked by prior AMPK activation. Paper-12762787. The present study explores the relationship between insulin-induced vasodilatory and fibrinolytic properties of the endothelium in women with polycystic ovary syndrome, frequently affected by insulin resistance and early atherosclerosis. Paper-11020908. In conclusion, we demonstrated here that insulin-induced VSMC relaxation is dependent on Akt activation via iNOS, cGK1alpha, and MBP activation, as well as the decreased phosphorylations of MYPT1 and MLC20 and decreased ROKalpha activity. Paper-12313230. Moreover, IRS-1 protein expression and insulin-induced protein kinase B activation, AS160 phosphorylation, and Glut 4 translocation were partially recovered after treatment with the ERK inhibitor. Paper-12379297. Adiponectin decreased (P<0.05) insulin-induced progesterone and androstenedione production as well as attenuated IGF-I- induced LHR, CYP11A1, and CYP17A1 gene expression in theca cells. Paper-12768150. In mammalian cells, the ER membrane protein Insig has emerged as a key component of homeostatic regulation by controlling both the activity of SREBP and the sterol-dependent degradation of the biosynthetic enzyme HMG-CoA reductase. Paper-12641565. Moreover, Western blot analysis showed a significant increase in nNOS (16.5+/-0.4-fold; P<0.05; n=4) phosphorylation after insulin injection, whereas the PI3K inhibitor LY294002 abolished the insulin-induced effects. Paper-13645329. In addition, using both BRET and co-immunoprecipitation experiments, we demonstrated that insulin induced the dimerization of Grb14, most likely as a result of simultaneous binding of two Grb14 molecules on the activated IR. Paper-12304409. OxLDL increased the S-glutathiolation of p21ras, and adenoviral transfection with either a mutant p21ras (C118S) lacking the predominant site of S-glutathiolation or a dominant-negative mutant restored insulin-induced Akt phosphorylation. Paper-12280171. Insulin-induced phosphorylation of the insulin receptor, IRS proteins, Akt and extracellular signal-regulated kinase-1/2 was more rapid and tended to decrease at earlier time-points in visceral than in subcutaneous adipocytes. Paper-12657113. We discuss: (1) how distinct steps in GLUT4 traffic may be regulated by discrete Rab proteins, and (2) the importance of Rac1 activation in insulin-induced actin remodelling in muscle cells, a key element for the net gain in surface GLUT4. Paper-12676329. These findings suggest a pivotal role for NADPH oxidase in insulin-induced proliferation and proteolytic activation in monocytes and macrophages, respectively, and identify a pathway that may play a pathological role in hyperinsulinemic states. Paper-13772292. Insulin-induced cell proliferation was not seen until concentration of the hormone reached the microgram (10 micrograms/ml) level, producing an increase in EGF receptor binding affinity (Ka 8.2 +/- .05 x 10(9)M-1 to 1.25 +/- .05 10(10) M-1). Paper-6479228. In the present study, insulin-induced hypoglycemia in nondiabetic male subjects is associated with increased proinflammatory cytokines ( TNF-alpha, IL-1beta, IL-6, and IL-8), markers of lipid peroxidation, ROS, and leukocytosis. Paper-13678323. By contrast, CD36 expression in non- stimulated cells and the insulin-induced increase in PM CD36 were not paralleled by a rise in LCFA uptake, suggesting that in these cells, such increase requires additional proteins, or a protein activation step. Paper-12734091. Ectonucleotide pyrophosphatase/phosphodiesterase 1 ( ENPP1), originally described as a plasma cell allo-antigen and named plasma cell membrane glycoprotein ( PC-1), is an inhibitor of insulin-induced activation of the insulin receptor. Paper-12780892. Using time-lapse fluorescent microscopy of green fluorescent protein-actin, we demonstrated that the overexpression of Enigma altered insulin-induced actin rearrangements, whereas the expression of Enigma without its LIM domains was without effect. Paper-12289832. Several genes involved in lipid and cholesterol metabolism, including Scd1, Acly, Gpam, Elov16, Acsl5, Mvd, Insig1, and Apoa4, were found to be upregulated (> or = 30% increase) in Nas1-/- mice. Paper-12063046. Insulin-induced IL-6 gene expression is mediated by cGMP/ cyclic GMP-dependent protein kinase/ cAMP response element binding protein, whereas MAPK is involved in the insulin- stimulated IL-6 synthesis/release. Paper-13047201. CONCLUSION(S): Mevastatin inhibits proliferation of theca-interstitial cells by a mechanism that involves depletion of mevalonic acid and selective inhibition of basal and insulin-induced activity of Erk1/2 pathway, but not Akt/ PKB pathway. Paper-11991832. Of 40 identified insulin-induced effectors, 7 have not previously been described in insulin signaling, including SDR, PKCdelta binding protein, LRP-6, and PISP/ PDZK11, a potential calcium ATPase binding protein. Paper-12751517. Moreover, the phosphoinositide affinity-disrupting mutations of IRS-1 significantly impaired but did not completely abrogate the insulin-induced translocation of IRS-1 to the plasma membrane, which was further suppressed by IRS1-N overexpression. Paper-13381675. RESULTS: Pioglitazone increased insulin- stimulated glucose disappearance (p < 0.01) and increased insulin-induced suppression of glucose production (p < 0.01), gluconeogenesis (p < 0.05) and glycogenolysis (p < 0.05) during IL/H. Paper-13023443. Estradiol (E) enhances expression of the neuronal monocarboxylate transporter MCT2 in the DVC during insulin-induced hypoglycemia (IIH), evidence that this hormone may promote local lactate utilization during systemic glucose shortages. Paper-12707294. Conversely, IGF1R downregulation by siRNA allowed assembly of insulin holoreceptors, enhanced insulin-induced phosphorylation of its receptor, Akt, Erk1/2, and further augmented insulin-induced glucose uptake. Paper-13623049. Insulin-induced intracellular signaling is conducted via multiple pathways, including the MAP kinase ( MEK/ ERK) and the phosphatidylinositol 3-kinase ( PI3K) pathways, which in turn activate multiple downstream signaling molecules. Paper-13503655. GK VSMCs had impaired basal and insulin-induced Akt phosphorylation as well as increases in basal MYPT1 phosphorylation, inducible nitric oxide synthase ( iNOS) expression, and nitrite/ nitrate production compared with Wistar-Kyoto controls. Paper-13522200. Insulin-induced eNOS activity in vivo was reduced by hyperglycemia and hexosamine activation, which was coupled to increased activation and expression of matrix metalloproteinase-2 and -9; these phenomena were reversed by inhibition of the hexosamine pathway. Paper-9517702. The distinct signaling pathways underlying insulin-induced and contraction- induced FAT/ CD36 translocation will be discussed and a comparison will be made with the well-defined glucose transport system involving the glucose transporter GLUT4. Paper-11280054. Because JNK is also capable of phosphorylating ATF2, we assessed the involvement of JNK, ERK1/2 and p38 in the insulin-induced two-step ATF2 phosphorylation in JNK-expressing A14 fibroblasts and 3T3L1-adipocytes. Paper-12154425. Results suggest that dietary SPI, by decreasing circulating insulin levels and colon FASN expression, attenuates insulin-induced DNA damage and FASN-mediated anti-apoptosis during carcinogenesis, resulting in an overall reduced tumorigenic state. Paper-12756546. Increased intracellular PAM concentrations facilitated S1P- and insulin-induced mTOR activation as well as p70S6K and 4EBP1 phosphorylation while genetic deletion of PAM decreased S1P- and insulin-induced mTOR activation. Paper-13554803. Insulin-induced transcription of beta-actin mRNA was evident within 5 min and was maximal by 10-15 min at 1000% above control levels. beta-Actin transcription was induced at insulin concentrations as low as 5 x 10(-12) M insulin and was maximal at 5 x 10(-9) M. Paper-52657. This increase in insulin sensitivity was associated with an increase in insulin-induced insulin receptor ( IR) tyrosine phosphorylation and, in parallel, a decrease in IR serine phosphorylation and association with PTP1B. Paper-12661395. OBJECTIVE: To ascertain whether recovery from insulin-induced hypoglycaemia with an oral glucose solution produces a different response of growth hormone ( GH) and cortisol at different times of the study compared with spontaneous recovery from hypoglycaemia. Paper-13110279. GLUT4 colocalized with ACTN4 along the insulin-induced cortical actin mesh and ACTN4 knockdown prevented GLUT4-actin colocalization without impeding actin remodeling or Akt phosphorylation, maintaining GLUT4 in a tight perinuclear location. Paper-12929735. These results imply that Pin1 amplifies insulin signaling in hepatocarcinoma cells through its interaction with p70S6K, suggesting that Pin1 plays an important role in insulin-induced tumorigenesis and is a potential therapeutic target in hepatocarcinoma. Paper-13700363. Liver-specific PTP1B(-/-) mice have increased hepatic insulin signaling, decreased expression of gluconeogenic genes PEPCK and G-6-Pase, enhanced insulin-induced suppression of hepatic glucose production, and improved glucose tolerance. Paper-13634452. Cellular inflammation and insulin resistance were assessed by measuring phospho- IkappaBalpha and insulin-induced phosphorylation of Akt, respectively, in extracts of thoracic aorta, liver, skeletal muscle, and visceral fat. Paper-13051783. Insulin-induced glucose uptake was markedly reduced in obese patients (19.5+/-1.9 micromol/min kg FFM) and improved with weight loss, but in the third study, it was still lower than that observed in controls (35.9+/-4.0 vs 52.9+/-2.2 micromol/min kg FFM). Paper-9881134. We therefore hypothesized that the major genes involved in the SREBP activation of fatty acids and cholesterol production ( SREBF1, SREBF2, SCAP, INSIG1 and INSIG2) would be strong candidate genes for interindividual variation in drug-induced weight gain. Paper-13638292. To test whether the action of oxysterols on SREBP processing is mediated through endogenous INSIG-1 protein, we used RNAi to lower the expression of the INSIG-1 gene, and found that reduced INSIG-1 protein levels caused the loss of SREBP regulation by oxysterols. Paper-9171744. Individually, inhibitors of either phosphatidylinositide 3-kinase ( PI3K) or MEK1/2 partially blocked the insulin-induced reduction in caspase-3 activity; in combination, the inhibitors completely prevented insulin from attenuating caspase-3 activity. Paper-13481366. Angiotensin II acting through the AT1 receptor can inhibit insulin-induced nitric oxide (NO) production by activating ERK 1/2 and JNK and enhances the activity of NADPH oxidase that leads to an increased reactive oxygen species generation. Paper-13035284. Insulin-induced rise in IL-6 correlated negatively to BMI (P = .001), waist to hip ratio (P = .05), and baseline (fasting) insulin (P = .03) and IL-6 (P = .02) levels and positively to insulin-stimulated glucose uptake in isolated adipocytes (P = .07). Paper-13776018. Insulin was also found to activate the mitogen-activated protein kinase cascades p38 and extracellular signal-related kinase; however, inhibition of these pathways with SB202190 and PD98059 did not alter insulin-induced heme oxygenase-1 expression. Paper-12008695. Applying this technology to membrane protein complexes, we discovered a previously unknown direct interaction of the progesterone-binding membrane protein PGRMC1 with Insig-1, a key regulator of cholesterol homeostasis. Paper-10988371. Additionally, both protein kinase C and phosphatidylinositol 3-kinase are presumably involved in insulin-induced ROS generation because bisindolylmaleimide, a nonspecific protein kinase C inhibitor, and LY290042, an inhibitor of phosphatidylinositol 3-kinase, inhibited this increase. Paper-13579296. Small-interfering RNA-specific gene silencing targeted specifically against Nox2 reduced the cognate protein expression, decreased insulin-induced O(2)(-) production, inhibited the turn on of NFkappaB, p38MAPK, and ERK 1/2, and reduced cell proliferation in macrophages. Paper-13772292. Effects of caudal hindbrain lactate infusion on insulin-induced hypoglycemia and neuronal substrate transporter glucokinase and sulfonylurea receptor-1 gene expression in the ovariectomized female rat dorsal vagal complex: Impact of estradiol. Paper-12707294. MATERIALS AND METHODS: The effect of CTCF on insulin-induced ML-1 cell proliferation was investigated by studying insulin- stimulated extracellular signal-regulated kinase ( Erk) and Akt signalling pathways, and the alterations of CTCF activity in these cells. Paper-12545290. Insulin-induced gene expression is inhibited by the presence of the phosphoinositide (PI) 3-kinase inhibitor LY294002 and the dominant negative mutant of the p85 subunit of PI 3-kinase, whereas hypoxia-induced gene expression is not. Paper-10044110. Insulin-induced phosphorylation of Akt, one of the molecules downstream of PI3-kinase, was inhibited by expression of wild-type SHIP2, whereas it was increased by expression of 5'-phosphatase-defective (DeltaIP) SHIP2 in whole cell lysates. Paper-10207545. In addition to providing a mechanism for sterol-regulated degradation of Insig-1, these results help to explain why Scap is subject to endoplasmic reticulum retention upon Insig-1 binding, whereas 3-hydroxy-3-methylglutaryl coenzyme A reductase is ubiquitinated and degraded. Paper-12357864. Hypertensive rats manifested metabolic IR (36% reduction in the glucose infusion rate by insulin clamp), impaired NO-mediated insulin-induced EDR (E(max): 12 +/- 5 vs. 32 +/- 4% in NS, P < 0.05), and impaired insulin activation of PI3K/endothelial NO synthase. Paper-13643849. In cultured cells Insig-1 and Insig-2 have been shown to block lipid synthesis in a cholesterol-dependent fashion by inhibiting proteolytic processing of sterol regulatory element-binding proteins (SREBPs), membrane-bound transcription factors that activate lipid synthesis. Paper-10206719. METHODS AND RESULTS: ApoCIII inhibited insulin-induced tyrosine phosphorylation of insulin receptor substrate 1 ( IRS-1), decreasing phosphatidylinositol 3-kinase (PI3K)/Akt activation in human umbilical vein endothelial cells. Paper-12904939. These findings suggest that both insulin-induced tyrosine phosphorylation and the cell surface targeting of IRS proteins may be regulated in a similar manner through a target molecule common to the members of the IRS family, and distinct from phosphoinositides or PHIP. Paper-13381675. Moreover, overexpression of wild-type cytPTPepsilon reduced insulin-induced tyrosine phosphorylation of IR, IRS-1, and phosphorylation of protein kinase B and glycogen synthase kinase-3 and insulin-induced stimulation of glucose uptake. Paper-12700844. Following treatment with insulin, a five-fold increase in heme oxygenase-1 mRNA and a four-fold increase in protein expression were observed in renal adenocarcinoma cells; insulin-induced heme oxygenase-1 expression was also demonstrated in mouse primary tubular epithelial cells. Paper-12008695. In the present article, we have investigated the dopamine (DA) content, homovanillic acid (HVA)/DA turnover ratio, DA D(1) and DA D(2) receptors in the hippocampus of insulin-induced hypoglycaemic (IIH) and streptozotocin induced diabetic rats where brain functions are impaired. Paper-13738979. Hyperosmotic dehydration in different cell types produces inactivation of signalling components around mTOR, thereby attenuating insulin-induced glucose uptake, glycogen synthesis, and lipogenesis in adipocytes, and MAP-kinase phosphatase MKP-1 expression in hepatoma cells. Paper-12115496. Global gene expression profiling demonstrated regulation of genes associated with lipid metabolism, most notably an upregulation of genes coding for insulin-induced gene 1 ( Insig-1), low-density lipoprotein receptor ( LDL-R) and of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA). Paper-13720734. We conclude that: (i) INSIG-1 gene expression is suppressed by oxysterols; (ii) LY295427 treatment counters the suppressive effects of oxysterols on SREBP processing, resulting in the expression of the INSIG-1 gene; and (iii) INSIG-1 gene expression affects SREBP processing. Paper-9171744. Compared with placebo, trimetazidine induced 1) an increase in insulin-induced forearm glucose uptake and glucose oxidation accompanied by a reduction in forearm lipid oxidation and citrate release and 2) a decrease of endothelin-1 release paralleled by a significant increase in forearm cGMP release. Paper-10824817. Insulininduced phosphorylation of Akt ( protein kinase B) and GSK-3beta ( Glycogen synthase kinase), subsequent dephosphorylation of glycogen synthase and glycogen synthesis were increased by inhibiting the expression of SKIP, whereas the insulin-induced glycogen synthesis was decreased by overexpression of WT-SKIP. Paper-13639525. Computational modeling unveils how critical network nodes, the adaptor proteins GAB1 and insulin receptor substrate ( IRS), Src kinase, and phosphatase SHP2, convert insulin-induced increase in the phosphatidylinositol-3,4,5-triphosphate (PIP(3)) concentration into enhanced Ras/ ERK activity. Paper-13711205. We demonstrated for the first time the presence of Akt-independent iNOS expression in the GK diabetic model and that the defective insulin-induced vasodilation observed in the diabetic vasculature can be restored by the overexpression of active Akt, which advocates a novel therapeutic strategy for treating diabetes. Paper-13522200. We found that knockdown of cytPTPepsilon by RNA silencing increased insulin-induced tyrosine phosphorylation of IR and IR substrate (IRS)-1 as well as phosphorylation of protein kinase B and glycogen synthase kinase-3 and insulin-induced stimulation of glucose uptake. Paper-12700844. The beneficial effects of insulin were abrogated by insulin receptor (IR)/insulin-like growth factor receptor ( IGFR) or phosphoinositide-3 kinase ( PI3-K) blockade, suggesting that insulin-induced EC proliferation and viability are mediated through pIR/pIGFR and PI3-K effectors. Paper-13595933. Furthermore, Pin1 enhanced the insulin-induced extracellular signal- regulated protein kinase (ERK)1/2 phosphorylation through its interaction with p70S6K, whereas the inhibition of p70S6K activity by rapamycin suppressed insulin-induced ERK1/2 phosphorylation in SK-HEP-1 cells. Paper-13700363. RESULTS: Following combined thiazolidinedione-metformin therapy, increases in glucose disposal and increases in sub-maximal and maximal insulin-induced activities of all four muscle signalling factors, IR, IRS-1-dependent PI3K ( IRS-1/ PI3K), aPKC and PKBbeta, were observed. Paper-13491520. Insulin provocative test revealed a severe GH deficiency in these patients, defined by a peak response to insulin-induced hypoglycemia less than 3 ng/dl and IGF1 concentrations less than - 2SDS.We didn't find multiple pituitary hormone deficiency and we noticed only a severe GH deficiency in all three patients. Paper-13634229. Since the silencing of gC1qR by small RNA interference abolished adipogenesis and blocked insulin-induced activation of insulin receptor, insulin receptor substrate-1 ( IRS-1), Akt, and Erk1/2, we can conclude that gC1qR is an essential molecule involved in adipogenesis and insulin signaling. Paper-13749491. In the present studies, we investigated whether insulin-induced HIF-1alpha expression is a prerequisite for insulin to induce other trophic effects in MiaPaCa2 human pancreatic cancer cells and whether inhibition of HIF-1alpha expression would decrease tumor glycolysis and improve host energy homeostasis. Paper-12438681. Insig-1 and Insig-2, closely related endoplasmic reticulum membrane proteins, mediate transcriptional and post-transcriptional mechanisms that assure cholesterol homeostasis through their sterol-induced binding to Scap ( SREBP cleavage-activating protein) and 3-hydroxy-3-methylglutaryl coenzyme A reductase. Paper-12357864. Isoproterenol stimulation failed to induce expression of MKP-1; moreover, insulin resistance induced by long-term beta-adrenergic stimulation inhibited insulin-evoked expression of MKP-1 by impairing insulin-induced phosphorylation of both ERK1/2 and JNK without affecting Akt kinase activity. Paper-12591936. Our results suggest that, in HFD, the differential regulation of insulin-induced glucose uptake between skeletal muscle and adipose tissue may, in part, be a consequence of the CAP/Cbl/ C3G pathway, since the expression of CAP and Cbl, and also the activation of this pathway were increased in adipose tissue but not in muscle. Paper-12199186. In parallel, it was observed that LY294002 and rapamycin almost completely blocked the effects of insulin and IGF-1 on MCT2 protein expression, whereas PD98059 and SB202190 (a p38K inhibitor) had no effect on insulin-induced MCT2 expression and only a slight effect on IGF-1- induced MCT2 expression. Paper-12684724. Furthermore, Ang II abolished insulin-induced tyrosine phosphorylation of insulin receptor substrate 1 ( IRS1), activation of protein kinase B (Akt), and glucose transporter-4 ( GLUT4) translocation to the plasma membrane, which was reversed by pretreating myotubes with losartan or apocynin. Paper-12311247. The early onset of vascular inflammation was accompanied by biochemical evidence of both endothelial dysfunction (reduced nitric oxide production; induction of intracellular adhesion molecule-1 and vascular cell adhesion molecule-1) and insulin resistance (impaired insulin-induced phosphorylation of Akt and eNOS). Paper-13051783. Insulin-induced membrane ruffling was inhibited by microinjection of rho GDI, an inhibitory GDP/GTP exchange regulator for both rho p21 and rac p21 small GTP-binding proteins, but not inhibited by microinjection of botulinum exoenzyme C3, known to selectively ADP-ribosylate rho p21 and to impair its function. Paper-116216. These results demonstrate that insulin simultaneously activates both Akt and JNK, and the latter further increases the phosphorylation of Akt which attenuates MI/R injury and improves heart function; this cross-talk between Akt and JNK in the insulin signaling is involved in insulin-induced cardioprotective effect. Paper-12576508. Nutrient overload induces constitutive S6K1 ( S6 kinase 1) activation, which leads to insulin resistance by suppressing insulin-induced class I PI3K ( phosphoinositide 3-kinase) signalling [Um, Frigerio, Watanabe, Picard, Joaquin, Sticker, Fumagalli, Allegrini, Kozma, Auwerx and Thomas (2004) Nature 431, 200-205]. Paper-12462151. Estradiol, estradiol-BSA and insulin stimuli increased the PKC epsilon, phosphorylated ERK 1/2 and Pit-1 expression, although combined treatments with estradiol/ insulin or estradiol-BSA/ insulin induced a significant reduction in these levels, in close correlation with the decrease of lactotroph cell proliferation. Paper-12767713. In cultured skin fibroblasts from human volunteers exposed to high insulin concentration, either in the presence or in the absence of pravastatin, insulin induced translocation of the p47(phox) subunit of NAD(P)H oxidase from the cytosol to the membrane and generation of radical oxygen species through a PKC delta-dependent mechanism. Paper-12146331. Although pSer307- IRS1 showed decreased insulin-induced tyrosine phosphorylation and interaction with phosphatidylinositol 3-kinase ( PI3K) in response to insulin, pSer632- IRS1 molecules were normally tyrosine- phosphorylated and exhibited typical associated PI3K activity. Paper-12211157. Although sortilin over-expression in C2C12 myotubes improved insulin-induced 2-deoxyglucose uptake, as previously reported, this effect apparently resulted from a decrease in the cellular content of GLUT1 and an increase in GLUT4 via differentiation-dependent alterations at both the gene transcriptional and the post-translational level. Paper-12774724. A marked decrease of basal and insulin- stimulated AKT phosphorylation, which correlated with the increase of patients' insulin resistance, and a significant increase of IRS total protein expression, together with a lower ( IRS-2) or absent ( IRS-1) increase of insulin-induced tyrosine phosphorylation, were found. Paper-12155769. Taken together, these data strongly suggest that the interaction between APS and Enigma is involved in insulin-induced Glut 4 translocation by regulating cortical actin remodeling and raise the possibility that modification of APS/ Enigma ratio could participate in the alteration of insulin-induced glucose uptake in adipose tissue. Paper-12289832. Lowest glucose tolerances were found in HsF and particularly in LC-HsF-HP-fed animals irrespective of line, but this paralleled reduced plasma adiponectin levels, elevated plasma resistin levels, higher retroperitoneal fat masses, and reduced insulin sensitivity (indexed by insulin-induced hypoglycemia) only in Wistar rats. Paper-12300805. Overproduction of constitutively active protein kinase B ( PKB) still inhibited glucagon gene transcription after chronic insulin treatment; together with a markedly reduced insulin-induced phosphorylation and, thus, activation of PKB, this indicates that targets upstream of PKB within the insulin signalling pathway are affected. Paper-13023440. Addition of rCD40L to adipocytes induced mitogen activated protein kinase ( MAPK) activation, stimulated inflammatory adipocytokine production, and decreased insulin-induced glucose transport in parallel with a downregulation of IRS1 and GLUT4 (also known as SCL2A4). rCD40L decreased the expression of lipogenic genes and increased lipolysis. Paper-13745368. In the present study, we demonstrated that TNFalpha- IKKbeta- mediated inactivation of TSC1 resulted in increasing phosphorylation of IRS1 serine 307 and serine 636/639, impaired insulin-induced glucose uptake, tyrosine phosphorylation of IRS1, and the association between IRS1 and PI3K p85. Paper-13052894. In C2C12 myocytes, insulin-induced upregulation of musclin mRNA was significantly decreased by treatment of phosphatidylinositol 3-kinase ( PI3K) inhibitor, LY294002, and was abolished in C2C12 myocytes stably expressing a constitutively active Foxo1 (Foxo1-3A), suggesting the involvement of Foxo1 in the regulation of musclin mRNA. Paper-12588216. Resveratrol effectively inhibits insulin-induced Akt and MAPK ( mitogen-activated protein kinase) activation mainly through disruption of the interactions between insulin receptor substrates and its downstream binding proteins including p85 regulatory subunit of phosphoinositide 3-kinase and Grb2 ( growth factor receptor-bound protein 2). Paper-12061992. But lower levels of PI-3-K and mTOR inhibitors were required to block insulin-induced phosphorylation of RPS6 than EGF-induced phosphorylation, and insulin-induced phosphorylation of elF4E and 4E-BP1 was not completely mTOR dependent suggesting some diversity of signaling for EGF and insulin. Paper-12254191. These synonyms are used for gene INSIG1 (insulin induced gene 1): MGC1405, Insulin-induced gene 1 protein, INSIG-1, CL-6, CL6. These accession numbers are used for gene INSIG1: Q53XW8 (UNIPROT__AC), AAP35891 (NCBI_GENBANK__AC), AAM44086 (NCBI_GENBANK__AC), A4D2M9 (UNIPROT__AC). INSIG1 is a homologue of RCJMB04_1d1 (insulin induced gene 1) from Gallus gallus. INSIG1 is a homologue of LOC100150144 (similar to insulin induced gene 1) from Danio rerio. INSIG1 is a homologue of INSIG1 (insulin induced gene 1) from Bos taurus. INSIG1 is a homologue of INSIG1 (insulin induced gene 1) from Pan troglodytes. INSIG1 is a homologue of INSIG1 (insulin induced gene 1) from Canis lupus familiaris. INSIG1 is a homologue of Insig1 (insulin induced gene 1) from Mus musculus. INSIG1 is a homologue of Insig1 (insulin induced gene 1) from Rattus norvegicus. INSIG1 is a homologue of insig1 (insulin induced gene 1) from Danio rerio. Important links ! iHOP - Information Hyperlinked over Proteins . Concept & Implementation by Robert Hoffmann.