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CRK — INS

Text-mined interactions from Literome

Canesi et al., Gen Comp Endocrinol 2001 : Moreover, both zinc and insulin induced activation of mitogen activated protein kinases ( MAPKs ) ; however, whereas zinc gave a clear effect on the stress activated p-38 MAPK, insulin activated extracellular activated MAPK ( ERK2 ) and inhibited p-38
Sweeney et al., Endocrinology 2001 : Here, leptin pretreatment reduced the extent of insulin stimulated p38 MAP kinase phosphorylation and phosphorylation of cAMP response element binder, a downstream effector of p38 MAP kinase
Somwar et al., Biochem J 2001 (MAP Kinase Signaling System) : Insulin caused a dose- ( EC ( 50 ) =15 nM ) and time- ( t ( 1/2 ) =3 min ) dependent increase in p38 MAPK phosphorylation, which peaked at 10 min ( 2.3+/-0.3-fold )
Liu et al., Mol Cell Biol 2002 : Overexpression of the APS/Y ( 618 ) F mutant in 3T3-L1 adipocytes blocked the insulin stimulated tyrosine phosphorylation of endogenous Cbl and binding to Crk
Kumar et al., J Exp Biol 2002 (Insulin Resistance) : Further investigations into the mitogen activated protein kinase ( MAPK ) pathway revealed that insulin stimulated p38 phosphorylation was impaired, as compared with extracellular-signal regulated kinase ( ERK ) and c-Jun N-terminal kinase (JNK), which were phosphorylated normally in insulin-resistant cells
Standaert et al., Biochemistry 2004 : Interestingly, these mutants inhibited insulin induced increases in ( a ) binding of Cbl to both Crk and the p85 subunit of PI 3-kinase, ( b ) activation of Cbl dependent PI 3-kinase, ( c ) activation and translocation of aPKC to the plasma membrane, ( d ) translocation of Glut4 to the plasma membrane, ( e ) and glucose transport
Hers et al., Biochem J 2005 : The effect of insulin on phosphorylation of both these sites required the activation of PI3K and the MAPKs ( mitogen activated protein kinases ) ERK1/2 ( extracellular-signal regulated kinase 1 and 2 ), but not the activation of mTOR ( mammalian target of rapamycin ) /p70S6 kinase, JNK ( c-Jun N-terminal kinase ) or p38MAPK
Hu et al., Diabetologia 2007 (Adenocarcinoma...) : Treatment of ob/ob mice for 20 days with T33 normalised basal and insulin stimulated glucose uptake and increased phosphorylation of Akt and p38 mitogen activated protein kinase in skeletal muscle
Anilkumar et al., Arterioscler Thromb Vasc Biol 2008 : After angiotensin II or TNFalpha treatment, JNK activation was augmented in Nox2 but not Nox4 transfected cells, whereas insulin augmented phosphorylation of p38MAPK , Akt, and GSK3beta specifically in Nox4 overexpressing cells and JNK specifically in Nox2 overexpressing cells
Bernard et al., Metabolism 2008 (Obesity) : Training did not increase insulin stimulated p38 MAP kinase protein concentration, nor did it have an effect on insulin stimulated p38 MAP kinase phosphorylation at the plasma membrane
Wang et al., J Nutr Biochem 2009 (Insulin Resistance) : Interestingly, CrPic was able to increase the basal and insulin stimulated levels of p38 MAPK activation in the control and insulin-resistant cells
Fomina-Yadlin et al., PloS one 2012 : The induction of Ins2 by GW8510 occurred through p53 in a JNK- and p38 dependent manner
Beitner-Johnson et al., J Biol Chem 1995 (Carcinoma, Embryonal) : In 293 cells, which express both IGF-I and insulin receptors, insulin also induced a dose dependent tyrosine phosphorylation of Crk II, but with somewhat reduced sensitivity, compared to IGF-I
Ishiki et al., Endocrinology 1997 : We examined the potential role of Crk-II in insulin and epidermal growth factor (EGF) signaling in Rat-1 fibroblasts overexpressing insulin receptors ... Basal tyrosine phosphorylation of c-abl and its constitutive association with Crk-II were not further increased by insulin or EGF ... Interestingly, EGF, but not insulin , stimulated tyrosine phosphorylation of c-cbl and its association with Crk-II
Sorokin et al., Oncogene 1998 : Overexpression of c-Crk enhanced insulin- but not PDGF induced activation of MAP kinases when compared to parental cell lines