The role of c-Jun in controlling the EPAC1-dependent induction of the SOCS3 gene in HUVECs

Jolanta Wiejak, Julia Dunlop, Stephen J Yarwood

    Research output: Contribution to journalArticle

    5 Citations (Scopus)

    Abstract

    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.

    Original languageEnglish
    Pages (from-to)1556-1561
    Number of pages6
    JournalFEBS Letters
    Volume588
    Issue number9
    DOIs
    Publication statusPublished - 2 May 2014

    Keywords

    • Animals
    • Base Sequence
    • Binding Sites
    • Cells, Cultured
    • Guanine Nucleotide Exchange Factors
    • Human Umbilical Vein Endothelial Cells
    • Humans
    • Mice
    • Phosphorylation
    • Protein Processing, Post-Translational
    • Proto-Oncogene Proteins c-jun
    • STAT3 Transcription Factor
    • Suppressor of Cytokine Signaling Proteins
    • Transcription Factor AP-1
    • Transcriptional Activation

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