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FOS — INS

Text-mined interactions from Literome

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
Hurd et al., Biochem J 2002 : Insulin regulates the activity of the AP-1 ( activator protein-1 ) transcriptional complex in several cell types
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
Ao et al., Pancreas 2005 (Hypoglycemia) : Maintaining euglycemia prevents insulin induced Fos expression in brain autonomic regulatory circuits ... Maintaining blood glucose levels within physiological range by hyperinsulinemic/euglycemic clamp prevented insulin infusion induced Fos expression in the PVN, DMV, and NTS
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
Solomon et al., Neuropeptides 2006 : NTS c-Fos expression was significantly augmented by insulin , while it was significantly decreased by the AGA
Kale et al., Neurosci Res 2006 (Hypoglycemia) : Insulin induced hypoglycemia (IIH) upregulates prepro-orexin mRNA and Fos immunostaining of LHA ORX-A neurons
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
Boghossian et al., Am J Physiol Regul Integr Comp Physiol 2009 (Anorexia...) : CeA insulin increased c-Fos in multiple brain regions, including the arcuate nucleus/paraventricular nucleus region of the hypothalamus
Kim et al., J Biol Chem 1994 : Insulin stimulates phosphorylation of c-Jun, c-Fos , and Fos related proteins in cultured adipocytes ... Insulin also stimulated phosphorylation of c-Fos and several Fos related proteins ( pp72, pp45, and pp39 ) as indicated by precipitation with anti-c-Fos antibody following exposure to denaturating conditions
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 ... 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
Stumpo et al., J Biol Chem 1994 : As in our previous studies, c-Fos mRNA accumulation in response to insulin was essentially normal in the down-regulated HIRc-B and H4IIEC3 cells, whereas the response to re-added PMA was completely abolished
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
Porter et al., Neurosci Lett 1997 : Effect of intracerebroventricular and intravenous insulin on Fos-immunoreactivity in the rat brain ... The insulin had no effect on Fos expression in any brain nuclei
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
Torres-Aleman et al., Neuroscience 1998 : In addition, insulin-like growth factor-I increased intracellular Ca2+ levels in Purkinje cells and c-Fos in dividing glioblasts
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