Premium
The role of c‐Jun in controlling the EPAC1‐dependent induction of the SOCS3 gene in HUVECs
Author(s) -
Wiejak Jolanta,
Dunlop Julia,
Yarwood Stephen J.
Publication year - 2014
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2014.02.038
Subject(s) - socs3 , gene , chemistry , biology , microbiology and biotechnology , biochemistry , suppressor
The cyclic AMP sensor, EPAC1, activates AP1‐mediated transcription in HUVECs. Correspondingly, induction of the SOCS3 minimal promoter by EPAC1 requires a single AP1 site that constitutively binds phosphorylated (Ser63) c‐Jun in DNA‐pull‐down assays. c‐Jun (Ser63) becomes further phosphorylated following cyclic AMP stimulation and specific activation of protein kinase A (PKA), but not through selective activation of EPAC1. Moreover, despite a requirement for c‐Jun for SOCS3 induction in fibroblasts, phospho‐null c‐Jun (Ser63/73Ala) had little effect on SOCS3 induction by cyclic AMP in HUVECs. AP1 activation and SOCS3 induction by EPAC1 in HUVECs therefore occur independently of c‐Jun phosphorylation on Ser63.