C/EBPBeta and Elk-1 synergistically transactivate the

Background The serum response element (SRE) in the c-fos promoter is a convergence point for several signaling pathways that regulate induction of the c-fos gene. Many transcription factors regulate the SRE, including serum response factor (SRF), ternary complex factor (TCF), and CCAAT/enhancer binding protein-beta (C/EBPβ). Independently, the TCFs and C/EBPβ have been shown to interact with SRF and to respond to Ras-dependent signaling pathways that result in transactivation of the SRE. Due to these common observations, we addressed the possibility that C/EBPβ and Elk-1 could both be necessary for Ras-stimulated transactivation of the SRE. Results In this report, we demonstrate that Elk-1 and C/EBPβ functionally synergize in transactivation of both a Gal4 reporter plasmid in concert with Gal4-SRF and in transactivation of the SRE. Interestingly, this synergy is only observed upon activation of Ras-dependent signaling pathways. Furthermore, we show that Elk-1 and C/EBPβ could interact both in an in vitro GST-pulldown assay and in an in vivo co-immunoprecipitation assay. The in vivo interaction between the two proteins is dependent on the presence of activated Ras. We have also shown that the C-terminal domain of C/EBPβ and the N-terminal domain of Elk-1 are necessary for the proteins to interact. Conclusions These data show that C/EBPβ and Elk-1 synergize in SRF dependent transcription of both a Gal-4 reporter and the SRE. This suggests that SRF, TCF, and C/EBPβ are all necessary for maximal induction of the c-fos SRE in response to mitogenic signaling by Ras.

[
  "009:25"
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  "@type": "vcard:Contact",
  "hasEmail": "mailto:info@nih.gov"
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  {
    "@type": "dcat:Distribution",
    "title": "Official Government Data Source",
    "mediaType": "text/html",
    "description": "Visit the original government dataset for complete information, documentation, and data access.",
    "downloadURL": "https://www.ncbi.nlm.nih.gov/pmc/articles/PMC29063/"
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[
  "gene-transactivation",
  "nih",
  "ras-signaling",
  "serum-response-element",
  "transcription-factors"
]

[
  "009:033"
]

{
  "name": "National Institutes of Health",
  "@type": "org:Organization"
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[
  "NIH"
]