TFII-I enhances activation of the c-fos promoter through interactions with upstream elements

Dae Won Kim, Venugopalan Cheriyath, Ananda L. Roy, Brent H. Cochran

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21 Citations (Scopus)


The transcription factor TFII-I was initially isolated as a factor that can hind to initiator elements in core promoters. Recent evidence suggests that TFII-I may also have a role in signal transduction. We have found that overexpression of TFlI-I can enhance the response of the wild-type c-fos promotor to a variety of stimuli. This effect depends on the c-fos c-sis- platelet-derived growth factor-inducible factor binding element (SIE) and serum response element (SRE). There is no effect of cotransfected TFII-I on the TATA box containing the c-fos basal promoter. Three TFII-I binding sites can be found in c-fos promoter. Two of these overlap the c-fos SIE and SRE, and another is located just upstream of the TATA box. Mutations that distinguish between serum response factor (SRF), STAT, and TFII-I binding to the c-fos SIE and SRE suggest that the binding of TFII-I to these elements is important for c-fos induction in conjunction with the SRF and STAT transcription factors. Moreover, TFII-I can form in vivo protein-protein complexes with the c-fos upstream activators SRF, STAT1, and STAT3. These results suggest that TFII-I may mediate the functional interdependence of the c-fos SIE and SRE elements. In addition, the ras pathway is required for TFII-I to exert its effects on the c-fos promoter, and growth factor stimulation enhances tyrosine phosphorylation of TFII-I. These results indicate that TFII-I is involved in signal transduction as well as transcriptional activation of the c-fos promoter.

Original languageEnglish
Pages (from-to)3310-3320
Number of pages11
JournalMolecular and cellular biology
Issue number6
Publication statusPublished - 1998 Jun

All Science Journal Classification (ASJC) codes

  • Molecular Biology
  • Cell Biology


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