◀ Back to FOS

FOS — PRKCA

Text-mined interactions from Literome

Chen et al., J Biol Chem 1999 : Using a specific inhibitor of the Ca ( 2+ ) -dependent PKC isoforms, Gö6976, and CaCo-2 cells stably transfected with antisense PKC-alpha cDNA, demonstrated that PKC-alpha mediated the AP-1 activation induced by this secosteroid
Chen et al., J Environ Pathol Toxicol Oncol 2000 (MAP Kinase Signaling System) : These data demonstrate that PKCdelta, PKCepsilon, and PKCalpha mediate arsenite induced AP-1 activation in JB6 cells through different MAP kinase ( Erks, JNKs, and p38 kinases ) pathways
Soh et al., J Biol Chem 2003 : A dominant negative mutant of c-Jun inhibited activation of the cyclin D1 promoter in a concentration dependent manner, providing further evidence that AP-1 activity is required for activation of the cyclin D1 promoter by PKC-alpha and PKC-epsilon
Ding et al., Am J Physiol Lung Cell Mol Physiol 2006 (MAP Kinase Signaling System) : Furthermore, overexpression of dominant negative mutant (DNM) of PKCalpha or PKCepsilon markedly blocked AP-1 activation as well as phosphorylation of ERKs and p38 kinase induced by freshly fractured silica
Liao et al., Neurochem Int 2007 : The inductive action of manganese was accompanied by generation of oxidative stress, activation of mitogen activated protein kinases ( MAPKs ), AKT, and protein kinase C-alpha (PKC-alpha) , and increased NF-kappaB and AP-1 DNA binding activities
Miraoui et al., Hum Mol Genet 2010 (Acrocephalosyndactylia) : Investigation of the underlying molecular mechanisms revealed that activated FGFR2 enhances EGFR and PDGFRalpha mRNA expression via activation of PKCalpha dependent AP-1 transcriptional activity
Gruber et al., Exp Cell Res 1995 (Melanoma) : These results suggest a hypothesis whereby RA-induced nuclear PKC alpha might lead to increased AP-1 activity and show that RA-induced growth inhibition and differentiation are not always accompanied by an inhibition of AP-1 activity as has been proposed by other investigators
Baier-Bitterlich et al., Mol Cell Biol 1996 : Importantly, the critical AP-1 enhancer element was differentially modulated by these two distinct PKC isoenzymes, since only PKC-theta but not PKC-alpha overexpression resulted in an approximately 2.8-fold increase in AP-1-collagenase promoter CAT expression in comparison with the vector control