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Text-mined interactions from Literome

Fujishiro et al., J Biol Chem 2001 : p38 mitogen activated protein kinase ( MAPK ), which is situated downstream of MAPK kinase ( MKK ) 6 and MKK3, is activated by mitogenic or stress inducing stimuli, as well as by insulin
Somwar et al., J Biol Chem 2001 : In contrast, insulin dependent p38 MAPK phosphorylation was efficiently reduced in cells pretreated with wortmannin, with an IC ( 50 ) of 7 nm
Carlson et al., Diabetes 2003 (Diabetes Mellitus, Type 2...) : To test the potential for members of the mitogen activated protein ( MAP ) kinase family to contribute to type 2 diabetes, we examined basal and insulin stimulated Erk 1/2, JNK, and p38 phosphorylation in adipocytes isolated from healthy and type 2 diabetic individuals
Li et al., Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi 2003 : High glucose, AGE, high insulin and H ( 2 ) O ( 2 ) could activate P38MAPK by oneself, and increased notably expression of phosphorylated-P38MAPK and P-selectin on cell line ECV304 ; Expression of P-selectin was inhibited significantly by SB203580
Kumar et al., Mol Cell Biochem 2004 : The treatment of cells with p38 MAPK inhibitor, SB203580, blocked the insulin stimulated glucose uptake in sensitive as well as resistant cells and it also prevented the activation of p38 by insulin
Cao et al., Zhong Nan Da Xue Xue Bao Yi Xue Ban 2007 (Atherosclerosis...) : However, it seems clear that p38 does not play a significant role in insulin secretion
Boden et al., Diabetes 2008 (Hyperinsulinism) : FFA augmented the insulin mediated increases in MMP-2 ( from approximately 6- to approximately 11-fold ), MMP-9 ( from approximately 3- to approximately 23-fold ), MT1-MMP ( from approximately 8- to approximately 20-fold ), MMP-2 gelatinolytic activity ( from 2- to 3-fold ), and JNK and p38 mitogen activated protein kinase ( MAPK ) activities but decreased insulin mediated activation of PI3K and ERK1/2
Zare et al., J Leukoc Biol 2008 : In contrast, Plg production did not require NF-kappaB, was only partly down-regulated by p38 MAPK inhibitor, and was efficiently inhibited by insulin , indicating a different mechanism for its induction
Seto-Young et al., Horm Metab Res 2011 (MAP Kinase Signaling System) : Differential roles of MAPK-Erk1/2 and MAPK-p38 in insulin or insulin-like growth factor-I (IGF-I) signaling pathways for progesterone production in human ovarian cells
Harbrecht et al., Am J Physiol Gastrointest Liver Physiol 2012 (MAP Kinase Signaling System) : However, insulin did not increase p38 activation and inhibition of p38 signaling with a dominant negative p38 plasmid had no effect on cytokine- or insulin mediated effects on iNOS
Fomina-Yadlin et al., PloS one 2012 : Further, inhibition of Jun N-terminal kinase (JNK) and p38 kinase activities suppressed insulin induction by GW8510
Mar et al., Int J Cardiol 2013 : Phlorizin ( Na ( + ) -glucose co-transport inhibitor ), insulin , tiron ( radical scavenger ), PD98059 ( ERK inhibitor ) and SB203580 ( p38 inhibitor ) were used
Prasannarong et al., Biochim Biophys Acta 2012 (Insulin Resistance) : Compared with SHAM, ovariectomy induced skeletal muscle insulin resistance, which was associated with decreases ( 32-70 % ) in tyrosine phosphorylation of the insulin receptor and insulin receptor substrate-1 (IRS-1), IRS-1 associated p85 subunit of phosphatidylinositol 3-kinase ( PI3-kinase ), and Akt Ser ( 473 ) phosphorylation whereas insulin stimulated phosphorylation of IRS-1 Ser ( 307 ), SAPK/JNK Thr ( 183 ) /Tyr ( 185 ), and p38 mitogen activated protein kinase ( MAPK ) Thr ( 180 ) /Tyr ( 182 ) was increased ( 24-62 % )
Hirabara et al., J Nutr Biochem 2013 : This effect was associated with increased insulin stimulated p38 MAP kinase phosphorylation and lower n-6/n-3 fatty acid ratio, but not with activation of proteins from insulin signaling ( IR, IRS-1 and Akt )
Kummer et al., J Biol Chem 1997 : Unlike the extracellular signal regulated kinases ( p42 and p44 MAP kinases ), which are stimulated by insulin in many cell types, p38 activity is inhibited by insulin in postmitotic fetal neurons for which insulin is a potent survival factor ( Heidenreich, K. A., and Kummer, J. L. ( 1996 ) J. Biol. Chem. 271, 9891-9894 )
Guan et al., Am J Physiol 1998 : Our data also indicate that both insulin and IGF-I enhance IL-1 beta induced p38 mitogen activated protein kinase ( MAPK ) phosphorylation and SAPK activation