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INS — RHO

Text-mined interactions from Literome

Begum et al., Mol Endocrinol 2000 (Diabetes Mellitus, Type 2...) : The decrease observed in MBS phosphorylation was due to insulin induced inhibition of Rho kinase activity ... Insulin also prevented a thrombin mediated increase in Rho kinase activation and abolished the thrombin induced increase in MBS phosphorylation and MBP inactivation
Sandu et al., Diabetes 2000 (Diabetes Mellitus, Type 2) : VSMCs isolated from Goto-Kakizaki ( GK ) diabetic rats ( a model for type 2 diabetes ) exhibited marked impairment in MBP activation by insulin that was accompanied by failure of insulin to decrease the phosphorylation of a regulatory myosin bound subunit (MBS) of MBP and inhibit Rho kinase activity resulting in increased myosin light-chain (MLC)20 phosphorylation and VSMC contraction
Sandu et al., J Appl Physiol 2001 (Hypertension) : Collectively, these results indicate that insulin inhibits Rho signaling by decreasing RhoA translocation via the NO/cGMP signaling pathway to cause MBP activation via site-specific dephosphorylation of its regulatory subunit MBS
Kowluru et al., Diabetes 2005 (Insulinoma) : Rho guanosine diphosphate-dissociation inhibitor plays a negative modulatory role in glucose stimulated insulin secretion
Nakamura et al., Biochem Biophys Res Commun 2006 (Diabetes Mellitus) : Northern blot analysis showed that insulin mRNA levels were markedly increased by Rho-kinase inhibitors, Y-27632 and fasudil, in beta-cell derived HIT-T15 cells ... These results imply that Rho/Rho-kinase activation is involved in the suppression of insulin expression found in diabetes and that suppression of the Rho/Rho-kinase pathway could be a useful tool to augment insulin gene transcription
Petersen et al., Mol Cell Biol 2008 : Suppression of Rho-kinase impaired proadipogenic insulin/insulin-like growth factor 1 signaling, which was restored by activation of Epac
Standaert et al., Endocrinology 1996 : Insulin stimulates phospholipase D-dependent phosphatidylcholine hydrolysis, Rho translocation, de novo phospholipid synthesis, and diacylglycerol/protein kinase C signaling in L6 myotubes
Karnam et al., J Biol Chem 1997 : Our findings suggest that : ( a ) insulin translocates Rho by a PI 3-kinase dependent mechanism, but another factor is responsible for GTP loading of Rho ; ( b ) both Rho and ARF may contribute to PC-PLD activation during insulin action ; and ( c ) Rho may be required for insulin stimulation of glucose transport
Standaert et al., J Biol Chem 1998 : Comparative effects of GTPgammaS and insulin on the activation of Rho , phosphatidylinositol 3-kinase, and protein kinase N in rat adipocytes ... Our findings suggest that ( a ) GTPgammaS and insulin activate Rho , PI 3-kinase, and PKN, albeit by different mechanisms ; ( b ) each of these signaling substances appears to be required for, and may contribute to, increases in glucose transport ; and ( c ) PKC-zeta may contribute to increases in glucose transport during insulin, but not GTPgammaS, action