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INS — RELA

Text-mined interactions from Literome

Bertrand et al., J Biol Chem 1999 : We recently showed that the antiapoptotic function of insulin requires nuclear factor kappaB (NF-kappaB) activation ( Bertrand, F., Atfi, A., Cadoret, A., L'Allemain, G., Robin, H., Lascols, O., Capeau, J., and Cherqui, G. ( 1998 ) J. Biol. Chem. 273, 2931-2938 ) ... Along with its protective effect, overexpressed TRAF2 increased basal and insulin stimulated NF-kappaB activities ... We also show that insulin increased manganese-superoxide dismutase ( Mn-SOD ) mRNA expression through NF-kappaB activation and that Mn-SOD contributed to insulin antiapoptotic signaling since expression of antisense Mn-SOD RNA decreased this process
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 ... These inhibitors abolished insulin induction of NF-kappaB DNA binding activity and kappaB-chloramphenicol acetyltransferase (CAT) promoter activity, maintaining expressed cytosolic IkappaB-alpha protein, and increased AP-1 DNA binding activity and TRE-CAT promoter activity
Sonnenberg et al., Obes Res 2004 (Metabolic Syndrome X...) : Elevated free fatty acid, glucose, and insulin levels enhance this NF-kappa B activation and further downstream modulate specific clinical manifestations of metabolic syndrome
Grempler et al., Biochem J 2004 (Carcinoma, Hepatocellular...) : TNFalpha, but not insulin , led to rapid activation of NFkappaB ( nuclear factor kappaB )
Sinha et al., J Biol Chem 2004 (Insulin Resistance) : Supporting the hypothesis that IKK acts through NFkappaB to cause insulin resistance, the IKK inhibitors acetylsalicylate and parthenolide prevented FA-induced reductions in insulin stimulated glucose uptake and NFkappaB nuclear translocation
Du et al., Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi 2004 : NF-kappaB p65 activity induced by insulin in mesangial cells was inhibited by culture superatants of splenic lymphocytes from oral immune tolerance rats ( P < 0.05 )
De Oliveira et al., J Lab Clin Med 2005 (Diabetes Mellitus, Type 2...) : In the presence of insulin ( 10-100 nmol/L ), the stimulation of NF-kappaB protein expression by AGE-BSA ( 100 microg/mL ) was decreased, whereas the expression of PPAR-gamma, protein was enhanced
Hammar et al., J Biol Chem 2005 : Activation of NF-kappaB by extracellular matrix is involved in spreading and glucose stimulated insulin secretion of pancreatic beta cells
Al-Rasheed et al., J Am Soc Nephrol 2006 (Diabetic Nephropathies) : Phosphatidylinositol 3-kinase but not extracellular signal regulated mitogen activated protein kinase mediated C-peptide and insulin activation of NF-kappaB
Horovitz-Fried et al., Biochem Biophys Res Commun 2007 : We earlier showed that insulin did not affect nuclear NFkappaB levels ... Thus, PKCalpha regulates insulin induced PKCdelta expression levels and this regulation involves activation of SP-1 and NFkappaB
Madonna et al., Int J Immunopathol Pharmacol 2007 : Co-treatment of HUVEC with insulin and SB202190 strongly reverted the stimulatory effect of insulin on NF-KB activation, thus establishing a link between NF-KB activation and p38MAPkinase mediated induction of VCAM-1 by insulin
Kim et al., Biogerontology 2008 : These results indicate that insulin promoted NF-kappaB activation through phosphorylation of FOXO1 by upregulating PI3K/Akt signaling
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
Madonna et al., Biochim Biophys Acta 2008 : Insulin markedly increased TNF-alpha induced NF-kappaB activation and induced phosphorylated IkappaB-alpha accumulation
Martins et al., Cell Physiol Biochem 2008 : In the present study, we investigated the effect of insulin on the LPS induced production of nitric oxide ( NO ) and prostaglandin ( PG ) -E ( 2 ), on the expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase (COX)-2, and on nuclear factor kappa B (NF-kappaB) activation in AMs ... These results show that in AMs stimulated by LPS, insulin prevents nuclear translocation of NF-kappaB , possibly by blocking I-kappaBalpha degradation, and supresses the production of NO and PGE ( 2 ), two molecules that contribute to septic shock
Iwasaki et al., Mol Cell Endocrinol 2009 (Inflammation) : We examined the effect of insulin on the transcriptional activity of NF-kappaB , which mediates the expression of a variety of inflammation/coagulation related genes using hepatocyte cell lines in vitro
Engberding et al., Arterioscler Thromb Vasc Biol 2009 (Diabetes Mellitus, Type 2...) : IGF1R downregulation uncovered an insulin induced reduction in activation of NF-kappaB and inhibition of MCP-1 upregulation in response to TNF-alpha
Sajan et al., J Lipid Res 2009 (Disease Models, Animal...) : In support of a critical mediatory role of aPKC, in both models, inhibition of hepatic aPKC by adenovirally mediated expression of kinase-inactive aPKC markedly diminished diet/insulin dependent activation of hepatic SREBP-1c and NFkappaB , and concomitantly improved hepatosteatosis, hypertriglyceridemia, hyperinsulinemia, and hyperglycemia
Liang et al., J Huazhong Univ Sci Technolog Med Sci 2009 : However, in G4, G5, and G6 groups, apoptosis rate of islet cells, NF-kappaB expression, Bax activity, and Cyt C release were all significantly increased, and insulin secretion was impaired as compared with G1, G2, and G3 groups ( P < 0.05 )
Yan et al., Zhonghua Wai Ke Za Zhi 2009 (Disease Models, Animal...) : To investigate the effects of nuclear factor kappa B (NF-kappaB) on insulin signaling in skeletal muscle cells of rat with sepsis
Salminen et al., Cell Signal 2010 : We will discuss the evidence that insulin/IGF-1 signaling can enhance the NF-kappaB signaling and subsequently potentiate the aging process and aggravate age related degenerative diseases
Shapiro et al., Inflammation 2010 (Acute Lung Injury...) : For instance, insulin inhibits NF-kappaB -- dependent synthesis of pro-inflammatory factors and attenuates production of ROS
Zhang et al., Zhonghua Shao Shang Za Zhi 2010 (Burns) : To study the inhibitory effects of insulin on nuclear factor-kappa B (NF-kappaB) nuclear translocation of vascular endothelial cells induced by burn serum and its correlative mechanism
Di Santo et al., Journal of thrombosis and haemostasis : JTH 2011 (Thrombosis) : The results demonstrated that, in MN interacting with activated PLT : ( i ) TF activity, antigen and mRNA were low until 8-10 h and dramatically increased thereafter, up to 24 h ; ( ii ) according to the kinetics of TF expression in MN, GSK3ß undergoes phosphorylation on serine 9, a process associated with down-regulation of enzyme activity ; ( iii ) pharmacological blockade of GSK3 further increased TF expression and was accompanied by increased accumulation of NF-kB , in the nucleus ; ( iv ) blockade of phosphoinositide-3 kinase ( PI(3)K ) by wortmannin inhibited PLT induced TF expression ; and ( v ) according to the established role of the GSK3 downstream insulin receptor, insulin increased PLT induced TF expression in a PI(3)K dependent manner
Bertrand et al., J Biol Chem 1995 : We examined the effect of insulin on nuclear factor kappa B (NF-kappa B) activity in Chinese ovary ( CHO ) cells overexpressing wild-type ( CHO-R cells ) or -defective insulin receptors mutated at Tyr1162 and Tyr1163 autophosphorylation sites ( CHO-Y2 cells ) ... In CHO-R cells, insulin caused a specific, time-, and concentration dependent activation of NF-kappa B ... Insulin activation of NF-kappa B : 1 ) was related to insulin receptor number and tyrosine kinase activity since it was markedly reduced in parental CHO cells which proved to respond to insulin growth factor-1 and phorbol 12-myristate 13-acetate ( PMA ) activation, and was dramatically decreased in CHO-Y2 cells ; 2 ) persisted in the presence of cycloheximide and was blocked by pyrrolidine dithiocarbamate, aspirin and sodium salicylate, three compounds interfering with I kappa B degradation and/or NF-kappa B.I kappa B complex dissociation ; 3 ) was independent of both PMA-sensitive and atypical ( zeta ) protein kinases C ; and 4 ) was dependent on Raf-1 kinase activity since insulin stimulated NF-kappa B DNA binding activity was inhibited by 8-bromo-cAMP, a Raf-1 kinase inhibitor ... Moreover, insulin activation of NF-kappa B-driven luciferase reporter gene expression was blocked in CHO-R cells expressing a Raf-1 dominant negative mutant
Zhou et al., J Biol Chem 1997 (Liver Neoplasms, Experimental) : Finally, expression of either the antisense p65 subunit of NF-kappaB or dominant negative Raf-1 kinase blocked insulin 's induction of the mdr1b promoter activity
Benoliel et al., J Cell Sci 1997 : These compounds inhibited the insulin induced nuclear translocation of NF-kappa B as detected by confocal laser scanning microscopy
Bertrand et al., J Biol Chem 1998 : We now investigated whether the activation of NF-kappaB by insulin could serve an antiapoptotic function ... We also show that insulin antiapoptotic signaling but not insulin activation of NF-kappaB involved phosphatidylinositol 3-kinase ( PI 3-kinase ), as supported by the inhibition of the former but not of the latter process by the PI 3-kinase inhibitor LY294002 ... Insulin antiapoptotic signaling: (i) was dependent on IR number and IR tyrosine kinase activity since it was reduced in parental CHO cells and was abolished in CHO-Y2 cells overexpressing IRs mutated at Tyr1162/1163 ; ( ii ) was, like insulin activation of NF-kappaB , dependent on Raf-1 but not on mitogen activated protein kinase activity since both processes were decreased by the dominant negative Raf-1 mutant Raf-C4 whereas they persisted in mitogen activated protein kinase depleted cells ; and ( iii ) required NF-kappaB activation since it was decreased by proteasome inhibitors and the dominant negative IkappaB-alpha ( A32/36 ) mutant and was mimicked by overexpression of the NF-kappaB c-Rel subunit