◀ Back to FOS

FOS — SRC

Text-mined interactions from Literome

Funakoshi-Tago et al., Eur J Biochem 2003 : TRAF6 and C-SRC induce synergistic AP-1 activation via PI3-kinase-AKT-JNK pathway ... We found that IL-1 mediated c-Src activation was required for AP-1 activation, but not for NF-kappa B activation and also revealed that c-Src induced AP-1 activation was enhanced synergistically by the coexpression of TNF receptor associated factor 6 (TRAF6) ... During the TRAF6 and c-Src induced AP-1 activation, phosphatidylinositol 3 (PI3)-kinase, its downstream signaling molecule, Akt and c-Jun N-terminal kinase (JNK) were significantly activated and inhibition of these kinase activities down-regulated AP-1 activation through the suppression of c-fos expression
Chandrasekar et al., J Biol Chem 2005 : Src kinase inhibitors PP1 and PP2, phosphatidylinositol 3-kinase (PI3K) inhibitors wortmannin and LY294002, Akt inhibitor, the c-Jun N-terminal kinase (JNK) inhibitor SP600125, antisense JNK and dominant negative MyD88, interleukin-1 receptor associated kinase ( IRAK)-1, IRAK4, and phosphatidylinositol 3-kinase expression all attenuated IL-18 mediated AP-1 binding and reporter activity, CXCL16 promoter-reporter activity, and CXCL16 expression
Lo et al., Cell Signal 2006 : The participation of PLCbeta, c-Src/Janus kinase 2 (JAK2) and extracellular signal regulated kinase ( ERK ) signaling pathways in Galpha(16)QL induced c-Fos transcriptional activation was demonstrated by the use of their specific inhibitors
Jeong et al., Exp Mol Med 2007 : Interestingly, co-expression of E12A mutant, lack of TRAF6 binding, with cellular Src ( Src ) results in decreased transcriptional activity of Stat3 and AP-1 , a novel target of STP-A11 compared to that of wild type
Hsieh et al., Biochim Biophys Acta 2008 : Moreover, thrombin stimulated activation of NF-kappaB, AP-1 , and COX-2 promoter activity was blocked by the inhibitors of c-Src , PKC, EGFR, MEK1/2, AP-1 and NF-kappaB, suggesting that thrombin induces COX-2 promoter activity mediated through PKC ( delta ) /c-Src dependent EGFR transactivation, MEK-ERK1/2, AP-1, and NF-kappaB
Scodelaro Bilbao et al., Arch Biochem Biophys 2010 : In this work, we studied the involvement of PKC and Src in the phosphorylation of ERK1/2, p38 and JNK1 MAPKs and in the modulation of ATF-1, c-Fos , c-Jun and Jun D transcription factors by ATP in MCF-7 breast cancer cells
Han et al., FEBS Lett 2011 : Structural-functional studies suggest that the proline-rich motif in the N-terminus of AFAP is critical for c-Src activation, and subsequent SRE/AP-1 transactivation and the actin binding domain in the AFAP C-terminus is negatively involved in the regulation of AFAP/c-Src mediated SRE/AP-1 transactivation
Yang et al., Biochem Pharmacol 2013 : c-Src dependent MAPKs/AP-1 activation is involved in TNF-a induced matrix metalloproteinase-9 expression in rat heart derived H9c2 cells
Muppala et al., PloS one 2013 : In a series of colon and breast cancer cell lines, we found that CD24 activates Src , and induces the activation of c-Jun and expression of c-Jun and c-Fos
Frame et al., Mol Biol Cell 1994 (Cell Transformation, Neoplastic) : However, in CEF that had been made quiescent by serum deprivation, v-Src induced stimulation of AP-1 DNA binding activity was substantially reduced
Fincham et al., Cell Biol Int 1994 (Cell Transformation, Neoplastic) : Transient early AP-1 activation requires proper location of v-Src at the cell periphery and it is essential for mitogenesis
Jalali et al., Arterioscler Thromb Vasc Biol 1998 : Thus, p60src plays a critical role in the shear stress activation of MAPK pathways and induction of Activating Protein-1 (AP- 1)/TRE and Elk-1/SRE mediated transcription in ECs