◀ Back to JUN

JUN — PENK

Text-mined interactions from Literome

Comb et al., NIDA Res Monogr 1992 : In the studies described herein, we demonstrate that AP-1 complexes consisting of different Jun proteins differentially regulate proenkephalin transcription at the CRE-2 element ... c-Jun constitutively activates proenkephalin transcription, whereas JunD activates in a fashion completely dependent on the activation of second-messenger pathways and the cAMP dependent PKA ... Because c-Jun activates proenkephalin transcription constitutively, induction of c-Jun may lead to a further and prolonged activation of proenkephalin gene expression
Tan et al., Mol Cell Biol 1994 : Together, these results indicate that growth factor- and cAMP dependent signaling pathways converge at CRE-2 to synergistically stimulate gene expression and that ATF-3 and c-Jun regulate proenkephalin transcription in response to both growth factor- and cAMP dependent intracellular signaling pathways
Monnier et al., DNA Cell Biol 1998 : However, AP1 by itself is not sufficient to increase PENK transcription, as insulin-like growth factor 1 (IGF1), which stimulates AP1 activity but not cAMP production, is unable to stimulate PENK transcription ... These results indicate a cooperative effect of AP1 and CREB on PENK transcription