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 language | English |
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Pages (from-to) | 1556-1561 |
Number of pages | 6 |
Journal | FEBS Letters |
Volume | 588 |
Issue number | 9 |
DOIs | |
Publication status | Published - 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