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Text-mined interactions from Literome

Standaert et al., Endocrinology 1999 : The activation of c-Jun N-terminal kinase (JNK) by insulin and anisomycin has been reported to result in increases in glycogen synthase ( GS ) activity in rat skeletal muscle ( Moxham et al., J Biol Chem, 1996, 271 : 30765-30773 )
Chapman et al., J Biol Chem 1999 : Moreover, phorbol esters were a much more potent inducer of collagenase-CAT gene transcription than insulin, a difference that may be explained by selective effects of insulin and phorbol esters on AP-1 expression
Wang et al., Mol Cell Biochem 1999 : This mitogenic effect induced by insulin in CSV3-1 cells requires an induction of AP-1 activity associated with c-Jun and JunB
Jormsjö et al., Circ Res 2000 (Coronary Disease...) : Phorbol 12-myristate 13-acetate ( PMA ) and insulin , 2 known activators of AP-1, increased the binding of AP-1 to the MMP-12 promoter, with higher affinity for the A allele
Conejo et al., J Cell Physiol 2001 : Furthermore, insulin induced nuclear factor-kappaB (NF-kappaB) DNA binding activity and down-regulated activating protein-1 (AP-1) DNA binding activity throughout the differentiation process
Morino et al., Endocrinology 2001 : Insulin induced c-Jun N-terminal kinase activation is negatively regulated by protein kinase C delta ... We investigated the role of protein kinase C ( PKC ) in insulin induced c-Jun N-terminal kinase (JNK) activation in rat 1 fibroblasts expressing human insulin receptors
Park et al., J Biol Chem 2002 : Insulin inhibited the anisomycin induced stimulation of both endogenous SEK1 and its substrate c-Jun N-terminal kinase (JNK) , but not that of the upstream kinase MEKK1, in 293T cells
Hurd et al., Biochem J 2002 : Insulin regulates the activity of the AP-1 ( activator protein-1 ) transcriptional complex in several cell types
Lee et al., J Biol Chem 2003 : Activation of the c-Jun N-terminal kinase (JNK) by proinflammatory cytokines inhibits insulin signaling, at least in part, by stimulating phosphorylation of rat/mouse insulin receptor substrate 1 (Irs1) at Ser ( 307 ) ( Ser ( 312 ) in human IRS1 )
Greene et al., J Biol Chem 2003 : Finally, an inhibitor of c-Jun N-terminal kinase, SP600125, at 10 microm did not block IRS-1 degradation and IRS-1 Ser ( 312 ) phosphorylation yet completely blocked insulin stimulated c-Jun phosphorylation ... Further, insulin stimulated c-Jun phosphorylation was not blocked by inhibitors of the phosphatidylinositol 3-kinase and mammalian target of rapamycin, indicating that c-Jun N-terminal kinase is unlikely to be the kinase phosphorylating IRS-1 Ser ( 312 ) in response to insulin
Yumita et al., Int J Cancer 2003 : Suppression of insulin induced AP-1 transactivation by menin accompanies inhibition of c-Fos induction ... Overexpression of menin strongly suppressed insulin induced AP-1 activity in CHO-IR cells, which express high levels of insulin receptor
Fisslthaler et al., Nitric Oxide 2003 : In native endothelial cells, insulin enhanced the DNA binding activity of Sp1 and AP-1 , but not that of NF-kappaB
Inagaki et al., Proc Natl Acad Sci U S A 1992 : c-Jun represses the human insulin promoter activity that depends on multiple cAMP response elements ... Surprisingly, the c-jun protooncogene product ( c-Jun ) repressed the cAMP induced activity of the insulin promoter in a cotransfection assay with the c-Jun expression plasmid
Ueki et al., J Biol Chem 2003 : p85 alpha-/- cells show decreased insulin stimulated Jun N-terminal kinase activity, which is restored by expression of p85 alpha, p85 beta, or a p85 mutant that does not bind to p110, indicating the existence of p85 dependent, but PI 3-kinase independent, signaling pathway
Yi et al., J Med Food 2004 : Insulin induced DNA synthesis and c-Jun protein expression were also reduced by ethanol treatment in Rat-1 fibroblasts overexpressing normal human insulin receptor
Schattenberg et al., J Biol Chem 2005 (Fatty Liver...) : This inhibition of insulin signaling by CYP2E1 overexpression was partially c-Jun N-terminal kinase dependent
Orzechowski et al., Life Sci 2005 : Preincubation with sodium ascorbate potentiates insulin dependent PKB/Akt and c-Jun phosphorylation in L6 rat myoblasts challenged with reactive oxygen/nitrogen species ... Moreover, a 24 h preincubation with ASC also elevated the pS473-Akt and pS63, pS73-c-Jun levels in response to insulin irrespective to ROS/RNS co-treatment
Park et al., Pharmacol Res 2005 (Insulin Resistance) : Fibroin sensitized the insulin stimulated c-Jun accumulation and phosphorylation in insulin-resistant cells
Hui et al., Brain Res 2005 (Brain Ischemia) : In contrast, insulin , a PI3K agonist, not only obviously activated Akt1 during early and later reperfusion, but also inhibited phosphorylation of JNK1/2, c-Jun , and Bcl-2 and attenuated the activation of caspase-3
Romero-Prado et al., J Cell Biochem 2006 : In the absence of FBS and in the presence of insulin or prolactin, cells show cytoskeletal organization and an AP-1 transcription site activity resembling proliferative osteochondrocytes while cells in the presence of dexamethasone and added prolactin or TGF-beta resembled differentiated osteoblasts
Beard et al., Diabetes 2006 : In contrast, insulin stimulated extracellular signal regulated kinase1/2 and Jun NH2-terminal kinase (JNK) activation were decreased in the presence of bradykinin, accompanied by decreased IRS-1 Ser307 phosphorylation
Xu et al., Endocrinology 2008 (Acute Disease...) : 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
Pathak et al., Cardiovascular diabetology 2008 (Diabetic Angiopathies...) : Insulin induced increases in c-Jun NH2-terminal kinase-1 (JNK1) activity were partially inhibited by m7E3 and eptifibatide whereas antagonism of alphavbeta3 integrins had no effect on insulin induced increases in extracellular signal regulated kinase ( ERK ) activity
Lee et al., Carcinogenesis 2009 (Carcinoma, Hepatocellular...) : The prolyl isomerase Pin1 interacts with a ribosomal protein S6 kinase to enhance insulin induced AP-1 activity and cellular transformation
Karpac et al., Aging Cell 2009 (MAP Kinase Signaling System) : Repression of Insulin/IGF Signaling (IIS) by stress-responsive Jun-N-terminal Kinase (JNK) signaling is emerging as a conserved mechanism that allows reallocating resources from anabolic to repair processes under stress conditions
Hitomi et al., Am J Hypertens 2011 (Hypertrophy...) : Insulin increased p38MAP kinase and c-Jun N-terminal kinase (JNK) phosphorylation ; in the presence of Ang II, p38MAP kinase, and JNK were further activated by insulin
Fomina-Yadlin et al., PloS one 2012 : Further, inhibition of Jun N-terminal kinase (JNK) and p38 kinase activities suppressed insulin induction by GW8510
Kim et al., J Biol Chem 1994 : Insulin stimulates phosphorylation of c-Jun , c-Fos, and Fos related proteins in cultured adipocytes ... In differentiated 3T3-F442A adipocytes, insulin stimulated rapid and transient phosphorylation of c-Jun
Yamauchi et al., Mol Cell Biol 1994 : Consistent with the Shc-Grb2 pathway as the major route for insulin stimulated c-Fos and AP-1 transcriptional activation, the IRS1 mediated inhibition was reversed by transfection with an expression plasmid for Grb2
Henderson et al., Mol Cell Biol 1994 : It was previously shown that the c-jun proto-oncogene can repress insulin gene transcription
Miller et al., Biochemistry 1996 : Both insulin stimulated JNK activity and insulin induced AP-1 transcriptional activity were found to be Ras dependent
Huang et al., Mol Cell Biol 1996 (Cell Transformation, Neoplastic) : ( i ) EGF not only induced a high level of PI 3-kinase activity by itself but also enhanced insulin induced PI 3-kinase activity in JB6 P+ cells, the EGF induced PI-3 kinase activity could be blocked by constitutive overexpression of a dominant negative P85 subunit of PI 3-kinase ( deltaP85 ), and insulin could markedly promote EGF induced AP-1 activity in a dose dependent manner in JB6 P+ cells as well as promote EGF induced JB6 P+ cell transformation ... ( ii ) Inhibition of PI-3 kinase with wortmannin or LY294002 markedly decreased the AP-1 activity induced by insulin, EGF, or EGF and insulin in a dose dependent manner, while wortmannin did not block UVB induced AP-1 activity ... ( iii ) AP-1 activation by insulin, EGF, or EGF and insulin could be completely inhibited by overexpression of deltaP85 in all the dose and time courses studied ... These results demonstrate for the first time that PI 3-kinase appears to be required for EGF- or insulin induced AP-1 transactivation and cell transformation but not cell proliferation in JB6 cells
Wang et al., Mol Cell Biochem 1997 : We now report that both insulin and vanadate induce a significant increase in AP-1 DNA binding activity in CSV3-1 cells but not in 3T3T cells ... Gel supershift assays and Western blot analysis using specific antibodies demonstrate that the increased AP-1 binding activity induced by insulin and vanadate in CSV3-1 cells is primarily contributed by an increase in the expression of c-Jun and JunB protein levels
Kim et al., Biochem J 1997 : By using gel-shift assays, it has been shown that insulin also stimulates nuclear protein binding to an AP-1 site with kinetics similar to MEK translocation and MAP kinase and CKII activation
Zeng et al., Oncol Res 1997 : The early transcription of c-fos, c-jun, and c-myc proto-oncogenes and the increased expression of transcription factors AP-1 and AP-2, induced by DZA and insulin , appear to be crucial events in the differentiation of the 3T3-L1 fibroblasts to adipocytes
Agadir et al., Cancer Res 1997 (Breast Neoplasms) : In this study, we present evidence that RME can down-regulate AP-1 activity induced by the tumor promoter 12-O-tetradecanoylphorbol-13-acetate, insulin , growth factors, and the nuclear proto-oncogenes c-Jun and c-Fos
Teruel et al., J Cell Physiol 1998 : In addition, insulin induced AP-1 DNA binding activity, this effect being totally prevented in the presence of MEK-1 inhibitor
Griffiths et al., Biochem J 1998 : The activator protein-1 (AP-1) transcriptional complex is made up of members of the Fos ( c-Fos, FosB, Fra1, Fra2 ) and Jun ( c-Jun, JunB, JunD ) families and is stimulated by insulin in several cell types
Choi et al., DNA Cell Biol 1998 : An electrophoretic mobility shift assay ( EMSA ) using insulin treated HepG2 nuclear extracts showed that insulin actually enhanced the binding of nuclear proteins to the HBV E element as well as to the consensus AP-1 binding site