◀ Back to CREB5
CREB5 — PRL
Text-mined interactions from Literome
Ishida et al., Am J Physiol Endocrinol Metab 2007
:
Expression of a dominant negative form of
CREB ( MCREB ), which was effective in suppressing CRE mediated transcription induced by the adenylate cyclase activator forskolin,
inhibited basal and forskolin induced
PRL promoter activity and PRL mRNA expression ... These results suggest that
CREB is
involved in the regulation of cell proliferation and the
PRL promoter in normal lactotrophs and that dopamine inhibition of these lactotroph functions is at least in part due to inhibition of the cAMP-PKA-CREB pathway
Levina et al., Cancer Res 2009
(Genital Neoplasms, Female) :
Binding of
PRL to its receptor was
followed by rapid phosphorylation of extracellular signal regulated kinase ( ERK ) 1/2, mitogen activated protein kinase/ERK kinase 1, signal transducer and activator of transcription 3,
CREB , ATF-2, and p53 and activation of 37 transcription factors in ovarian and endometrial carcinoma cells
Hong et al., Biochem Mol Biol Int 1997
:
We suggest that
PRL negatively
regulates the PCNA-gene transcription by interfering with the cAMP/PKA mediated induction of
CREB binding to the CRE-sequences and thereby suppresses DNA synthesis in regenerating rat liver
Yan et al., Mol Cell Endocrinol 1994
:
A constitutively active form of
CREB can
activate expression of the rat
prolactin promoter in non-pituitary cells ... Since the PRL promoter contains an asymmetrical form of a cyclic AMP response element ( termed the CLE ), we investigated whether
CREB could also
induce PRL promoter activity in non-pituitary cells ... CREB-VP16 did not stimulate expression in C6 cells of any of three control promoter-CAT constructs, implying that the strong
response of the
PRL promoter to activated
CREB is both promoter-specific, and is not due to non-specific transcriptional effects of the potent VP16 moiety of CREB-VP16 ... These results imply that
CREB can strongly and specifically
activate expression of the
PRL promoter in non-pituitary cells, via a mechanism different from that employed by Pit-1