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

Jolanta Wiejak; Julia Dunlop; Stephen J Yarwood

doi:10.1016/j.febslet.2014.02.038

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 journal › Article › peer-review

8 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 language	English
Pages (from-to)	1556-1561
Number of pages	6
Journal	FEBS Letters
Volume	588
Issue number	9
DOIs	https://doi.org/10.1016/j.febslet.2014.02.038
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

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10.1016/j.febslet.2014.02.038

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title = "The role of c-Jun in controlling the EPAC1-dependent induction of the SOCS3 gene in HUVECs",

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.",

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",

author = "Jolanta Wiejak and Julia Dunlop and Yarwood, {Stephen J}",

year = "2014",

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doi = "10.1016/j.febslet.2014.02.038",

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T1 - The role of c-Jun in controlling the EPAC1-dependent induction of the SOCS3 gene in HUVECs

AU - Wiejak, Jolanta

AU - Dunlop, Julia

AU - Yarwood, Stephen J

PY - 2014/5/2

Y1 - 2014/5/2

N2 - 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.

AB - 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.

KW - Animals

KW - Base Sequence

KW - Binding Sites

KW - Cells, Cultured

KW - Guanine Nucleotide Exchange Factors

KW - Human Umbilical Vein Endothelial Cells

KW - Humans

KW - Mice

KW - Phosphorylation

KW - Protein Processing, Post-Translational

KW - Proto-Oncogene Proteins c-jun

KW - STAT3 Transcription Factor

KW - Suppressor of Cytokine Signaling Proteins

KW - Transcription Factor AP-1

KW - Transcriptional Activation

U2 - 10.1016/j.febslet.2014.02.038

DO - 10.1016/j.febslet.2014.02.038

M3 - Article

C2 - 24631457

VL - 588

SP - 1556

EP - 1561

JO - FEBS Letters

JF - FEBS Letters

SN - 0014-5793

IS - 9

ER -

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

Abstract

Keywords

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