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IGF1 — JUN

Text-mined interactions from Literome

Krause et al., J Biol Chem 2001 : The JNK inhibitor dicumarol suppressed IGF-I mediated activation of JNK and phosphorylation of c-Jun but did not affect p38 and IkappaB phosphorylation or activation of AKT
Walsh et al., Immunology 2002 : We found that IGF-1 transiently induces Akt, jun N-terminal kinases ( JNK ), and c-Jun phosphorylation in activated T cells, with JNK and c-Jun phosphorylation occurring faster than Akt phosphorylation ... Jurkat/IGF-1R cells exhibited enhanced constitutive Akt phosphorylation compared with mock transfected controls, but IGF-1 induced transient phosphorylation of MKK4, JNKs, and c-Jun
Yamagishi et al., Brain Res Mol Brain Res 2003 (Potassium Deficiency) : Comparison of inhibitory effects of brain derived neurotrophic factor and insulin-like growth factor on low potassium induced apoptosis and activation of p38 MAPK and c-Jun in cultured cerebellar granule neurons ... BDNF and IGF-1 suppressed the activation of p38 and c-Jun, but not of c-Jun N-terminal kinase (JNK) , caused by lowering the potassium concentration
Wadsworth et al., Endocrinology 2004 : Saw palmetto extract suppresses insulin-like growth factor-I signaling and induces stress activated protein kinase/c-Jun N-terminal kinase phosphorylation in human prostate epithelial cells
Kim et al., Biochem Biophys Res Commun 2004 (MAP Kinase Signaling System) : Furthermore, IGF-II remarkably increased the DNA binding activities of NF-kappaB and AP-1 , and the IL-8 promoter activity
Chiou et al., Biochem Biophys Res Commun 1992 : Insulin-like growth factor I stimulates transcription of the c-jun proto-oncogene in Balb/C 3T3 cells
Freiss et al., J Steroid Biochem Mol Biol 2005 (Breast Neoplasms) : We have tested the effects of two Eli-Lilly compounds, LY 117, 018 and raloxifene, on E2-regulated and IGF-I induced proliferation or AP-1 activity in human breast cancer cells ... Moreover, raloxifene was the most efficient molecule to prevent IGF-I induced AP-1 activity, with a significant effect observed with a concentration as low as 5 x 10 ( -11 ) M in the presence of IGF-I alone
Kooijman et al., Int J Biochem Cell Biol 2006 : We previously established that stimulation by IGF-I of interleukin (IL)-8 expression in leukocytes required activation of extracellular regulated kinase (ERK) and basal activity of c-Jun N-terminal kinase (JNK)
Grounds et al., Clin Exp Pharmacol Physiol 2008 (Necrosis) : 3. Activation of TNF signalling via the c-Jun N-terminal kinase (JNK) can inhibit IGF-1 signalling by phosphorylation and conformational changes in insulin receptor substrate (IRS)-1 downstream of the IGF-1 receptor
Jia et al., J Cell Mol Med 2011 : These data demonstrate a cross-talk between IGF-1R and AT-1R in AT-II and IGF-1 induced Cx43 expression in SV SMCs involving Erk 1/2 and downstream activation of the AP-1 transcription factor
Yang et al., Biochem J 2011 (Colonic Neoplasms) : IGF-1 induced MAT2A promoter activity and increased nuclear protein binding to USF ( upstream stimulatory factor ) /c-Myb, YY1 ( Yin and Yang 1 ), E2F, AP-1 ( activator protein 1 ) and NF-?B ( nuclear factor ?B ) consensus elements ... IGF-1 increased the expression of c-Jun , FosB, MafG, p65, c-Myb, E2F-1 and YY1 at the pre-translational level
Wang et al., Differentiation 2011 (Diabetes Mellitus...) : Previously, we have shown that the expression of c-Jun in the fibroblastic stroma can promote secretion of IGF-I , which stimulates prostate epithelial cell proliferation through activating specific target genes
Puzik et al., Cytokine 2012 (Infection) : Furthermore the effect of IGF-I on cytokine expression, apoptosis and the DNA binding activity of AP-1 and NF?B was evaluated
Monnier et al., Mol Cell Endocrinol 1994 : To further characterize the molecular mechanism by which IGF-I increases AP1 activity, we analysed the transcription regulation of c-fos and c-jun using reporter genes containing the respective promoters or specific regulatory elements
Okubo et al., J Biol Chem 1998 : In this study, we analyzed the IGF-I effect on the stress activated protein kinase/c-Jun N-terminal kinase (JNK) activity using human embryonic kidney 293 cells, 293 cells transiently expressing hemagglutinin-JNK, and 293 cells stably expressing a hemagglutinin-JNK transgene
Horney et al., Am J Physiol 1998 (Diabetic Nephropathies) : MMCs in HG displayed increased IGF-I stimulated insulin receptor substrate-1/2 phosphorylation and activator protein-1 transcriptional activity compared with NG controls