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INS — NPY4R

Text-mined interactions from Literome

Liu et al., J Biol Chem 2000 : Phosphorylation of G ( M ) has been postulated to govern activity of PP1 in response to adrenaline and insulin ... In this study, we used biochemical assays and G ( M ) expression in living cells to examine the effects of insulin on the phosphorylation of G ( M ), and the binding of PP-1 to G ( M )
Wada et al., Mol Cell Biol 2001 : In addition, insulin induced phosphorylation of GSK-3beta and activation of PP1 followed by activation of glycogen synthase and glycogen synthesis were decreased by expression of WT-SHIP2 and increased by the expression of Delta IP-SHIP2
Suzuki et al., Mol Cell Biol 2001 (Insulin Resistance) : However, PP1G/RGL is not required for insulin activation of GS in skeletal muscle, and rather another GS-specific phosphatase appears to be involved
Shi et al., Invest Ophthalmol Vis Sci 2002 : I ( Cl, vol ) was not activated under isosmotic conditions by the simultaneous inhibition of PKC with calphostin and activation of PP-1 by insulin
Semiz et al., Mol Cell Biochem 2002 : Interestingly, this treatment stimulated muscle GSFA by 2-fold ( p < 0.05 ) and increased insulin stimulated PP1 activity by 77 % ( p < 0.05 ) in the fatty rats as compared to untreated rats
Delibegovic et al., Diabetes 2003 (Glucose Intolerance...) : PP1-R5/PTG , another glycogen targeted form of PP1, was not significantly stimulated by insulin in the skeletal muscle of WT mice but showed compensatory stimulation by insulin in G ( M ) ( -/- ) mice
Munro et al., FEBS J 2005 (Diabetes Mellitus, Experimental) : Stimulation of glycogen targeted protein phosphatase 1 (PP1) activity by insulin contributes to the dephosphorylation and activation of hepatic glycogen synthase ( GS ) leading to an increase in glycogen synthesis
McCarty et al., Med Hypotheses 2006 (Hyperparathyroidism...) : Thus, the PKC activation associated with fat overexposure might be expected to boost basal [ Ca2+ ] i in skeletal muscle, potentially impeding insulin mediated activation of PP-1
Metallo et al., Arch Biochem Biophys 1991 (Diabetes Mellitus, Experimental) : FA and CK-II activate PP-1 in vitro and might be involved in the activation of PP-1 by insulin
Ghosh et al., Endocrinology 2007 (Insulin Resistance) : TNFalpha increased serine/threonine phosphatase activity of protein phosphatase 1 (PP1) in response to C6, but not insulin , suggesting a ceramide-specific effect
Kida et al., J Clin Invest 1992 (Insulin Resistance) : These results suggest that insulin activation of PP-1 could contribute to the stimulation of glycogen synthase by this hormone in human muscle ... Lower fasting PP-1 activity in cytosol and glycogen fractions plus lower insulin stimulated PP-1 activity could explain, in part, reduced insulin stimulated glycogen synthase in skeletal muscle of insulin-resistant subjects
Kuehnen et al., Endocrinology 2011 (Insulinoma) : Protein phosphatase 1 (PP-1) dependent inhibition of insulin secretion by leptin in INS-1 pancreatic ß-cells and human pancreatic islets ... In addition, glucose induced insulin secretion was inhibited by nuclear inhibitor of PP-1 and calyculin A, which was in part mediated by a reduction of PP-1 dependent calcium influx into INS-1 ß-cells
Hatou et al., Cornea 2011 : The effect of insulin is mediated by the protein kinase C, PP1 , and/or PP2A pathways
Geetha et al., J Endocrinol 2012 (Diabetes Mellitus, Type 2...) : These findings provide evidence for the involvement of a particular PP1 complex, PPP1R12A/PP1cd, in insulin signaling and may lead to a better understanding of dysregulated IRS1 phosphorylation in insulin resistance and T2D
Srinivasan et al., J Biol Chem 1994 : In this study, we examined the role of insulin , protein kinase C ( PKC ) and mitogen activated protein kinase ( MAPK ) cascade in activation of protein phosphatase-1 (PP-1) by using three complementary approaches ... ML-9, a myosin light chain kinase inhibitor, blocked the effects of insulin and TPA on both MAPK and PP-1 activation ... In these cells subsequent effects of insulin on MAPK and PP-1 activation were blocked, without an effect on basal enzyme levels
Begum et al., J Biol Chem 1995 : In this study, we examined the distribution of protein serine/threonine phosphatase-1 (PP-1) and analyzed the effect of insulin on PP-1 and its mechanism of activation in freshly isolated rat adipocytes ... Insulin rapidly stimulated PF PP-1 in a time- and dose dependent manner ( maximum stimulation at 5 min with 4 nM insulin ) ... The insulin effect on MAP kinase and PP-1 activation was blocked by a GTP antagonist, guanyl-5'-yl thiophosphate ... We conclude that insulin rapidly activates a membrane associated PP-1 in adipocytes, which may be similar to rabbit skeletal muscle PP-1G, and the activation is mediated by p21Ras/MAP kinase pathway
Begum et al., Am J Physiol 1994 : In particulate fractions, insulin stimulated PP-1 activity ( 40 % increase over basal with phosphorylase a ) in a time- and dose dependent manner ( half-maximal effect of 0.89 nM in 1 min ) ... Addition of PAO ( 5 microM ) before or after insulin treatment abolished insulin 's effect on PP-1 activation
Begum et al., J Biol Chem 1993 : In this study, we examined the effect of insulin on protein phosphatase 1 (PP-1) activity and phosphorylation in cells expressing wild-type human insulin receptor ( HIRc ) and HIR delta CT cells using phosphorylase alpha as substrate in the presence of 3 nM okadaic acid ... Insulin stimulated PP-1 activity in HIRc cells ( 25-30 % increase over basal activity ) in a time- and dose dependent manner ... We conclude that the COOH-terminal domain of the insulin receptor is an important element in mediating the effect of insulin on PP-1 and suggest that activation of PP-1 may be linked to signaling insulin 's metabolic actions
Begum et al., Endocrinology 1996 : In this study, the acute effects of tumor necrosis factor (TNF)-alpha on insulin stimulated glucose uptake, glycogen synthesis, and protein phosphatase-1 (PP-1) activation were examined in cultured rat skeletal muscle cell line, L6 ... As reported by us earlier ( Srinivasan, M., and N. Begum, J Biol Chem 269 : 16662-16667, 1994 ), insulin rapidly stimulated PP-1 and concomitantly inhibited PP-2A activities in L6 cells ... Pretreatment with TNF- alpha for 10-60 min blocked subsequent insulin induced activation of PP-1
Begum et al., Eur J Biochem 1996 : As reported by us earlier, insulin rapidly stimulated PP-1 and concomitantly inhibited PP-2A activities in control cells ... TNF-alpha treatment blocked insulin induced activation of PP-1
Barriocanal et al., Diabet Med 1995 (Diabetes Mellitus, Type 2) : These data indicate that in vivo insulin dependent activation of muscle PP1 is transient in normal subjects but is delayed in NIDDM
Ragolia et al., Endocrinology 1997 : Compared to the neo control, overexpression of PP-1G resulted in a 3-fold increase in insulin stimulated PP-1 catalytic activity bound to PP-1G immunoprecipitates
Brady et al., J Biol Chem 1997 : The stimulation of glycogen targeted protein phosphatase 1 (PP1) , glycogen synthase, and glycogen synthesis by insulin was examined during the differentiation of 3T3-L1 fibroblasts into adipocytes
Begum et al., Metabolism 1998 (Diabetes Mellitus, Type 2...) : In adipocytes isolated from control rats, insulin ( 5 nmol/L ) stimulated particulate serine/threonine protein phosphatase-1 (PP-1) activity ( 56 % increase over the basal value after 5 minutes ) ... In contrast, adipocytes from diabetic GK rats exhibited a 32 % decrease in basal ( P < .05 ) and a 65 % decrease in insulin stimulated PP-1 activity compared with values in control Wistar rats ... We conclude that ( 1 ) a rapid activation of PP-1 along with concomitant inhibition of cytosolic PP-2A may be important in the mechanism of insulin action in a normal cell, and ( 2 ) the resistance to insulin in terms of glucose uptake and glycogen synthesis observed in diabetic GK rats is partly due to defective regulation of PP-1, PP-2A, and MAPK caused by multiple defects in the upstream insulin signaling components ( IRS-1/phosphatidylinositol-3-kinase [ PI3-kinase ] and Grb2/Sos ) that participate in insulin mediated activation of PP-1 and inactivation of PP-2A
Brady et al., J Biol Chem 1998 : Both agents caused a comparable inhibition of GSK-3 activity in the adipocytes, whereas only insulin activated PP1 ... Finally, wortmannin completely blocked the stimulation of PP1 by insulin in 3T3-L1 adipocytes, indicating that PI3-K inhibition can impinge on PP1 activation ... Cumulatively these results suggest that the weak activation of glycogen synthase in 3T3-L1 fibroblasts is mediated by GSK-3 inactivation, whereas in the more metabolically active adipocytes, the insulin-specific activation of glycogen synthase is mediated by PP1 activation
Ragolia et al., Mol Cell Biochem 1998 : It appears that any agent or condition which interferes with the insulin induced phosphorylation and activation of PP-1 , will decrease the magnitude of insulin 's effect on downstream metabolic processes