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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