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JUN — PRKAR1B

Text-mined interactions from Literome

de Groot et al., Oncogene 1992 : Here we show that Jun/AP-1 is activated by the cAMP dependent protein kinase A (PKA) ... Here we show that Jun/AP-1 is activated by the cAMP dependent protein kinase A (PKA)
Li et al., Exp Cell Res 2004 : The protein kinase A (PKA) inhibitor, H-89, completely blocked PGE2 mediated induction of CRE-Luc and c-Fos promoter-Luc promoters, and partially inhibited induction of AP-1-Luc , while the protein kinase C ( PKC ) inhibitor Go-6976 partially inhibited all three promoters, demonstrating substantial cross-talk between these signaling pathways
Boonyaratanakornkit et al., FASEB J 2005 : Since NF-kappaB, AP-1 , and CREB are all regulated by PKA and are transcription factors predicted by microarray analysis to be involved in the altered gene expression in vectorless gravity, the data suggest that PKA is a key player in the loss of T-cell activation in altered gravity
Chedid et al., J Immunol 1991 (Thymoma) : However, the induction of AP-1 activity by IL-1 and phorbol esters is dependent upon the presence of PKA , as evidenced by the loss of AP-1 inducibility in cells transfected with a cDNA encoding protein kinase inhibitor, a specific inhibitor of PKA
Yen et al., J Biol Chem 2011 (MAP Kinase Signaling System) : We show that PGE2 induced MMP-9 expression is mediated primarily through the EP2/EP4  cAMP  protein kinase A (PKA)/PI3K  ERK signaling pathway, leading to c-Fos expression, and through JNK mediated activation of c-Jun in a PKA/PI3K/ERK independent manner
Marti et al., Oncogene 1994 : Comparing nuclear extracts from normal mammary glands with nuclear extracts from glands which had been cleared of all epithelial cells 3 weeks after birth, revealed that PKA activation, AP-1 induction and Oct-1 inactivation all are dependent on the presence of the epithelial compartment ... The increased Fos/Jun expression and the inactivation of Oct-1 may be consequences of the increased PKA activity