Skip NavigationSkip to Content
Return Return to Search Results

SNIP1 is a candidate modifier of the transcriptional activity of c-Myc on E box-dependent target genes

  1. Author:
    Fujii, M.
    Lyakh, L. A.
    Bracken, C. P.
    Fukuoka, J.
    Hayakawa, M.
    Tsukiyama, T.
    Soil, S. J.
    Harris, M.
    Rocha, S.
    Roche, K. C.
    Tominaga, S. I.
    Jen, J.
    Perkins, N. D.
    Lechleider, R. J.
    Roberts, A. B.

  2. Author Address

    NCI, Lab Cell Regulat & Carcinogenesis, Bethesda, MD 20892 USA. Univ Dundee, Div Gene Regulat & Express, Coll Life Sci, Dundee DD1 5EH, Scotland. NCI, Lab Populat Genet, Bethesda, MD 20892 USA. Jichi Med Univ, Dept Biochem, Minami Kawachi, Tochigi 3290498, Japan. NCI, Canc & Dev Biol Lab, Frederick, MD 21702 USA. NCI, Mol Oncol Res Unit, Bethesda, MD 20892 USA.;Lechleider, RJ, NCI, Lab Cell Regulat & Carcinogenesis, Bethesda, MD 20892 USA.;fujiim@jichi.ac.jp lechleiderr@mail.nih.gov
    1. Year: 2006
    2. Date: Dec
  2. Journal: Molecular Cell
    1. 24
    2. 5
    3. Pages: 771-783
  4. Type of Article: Article
  5. ISSN: 1097-2765
  1. Abstract:

    Using a yeast two-hybrid screen, we found that SNIP1 (Smad nuclear-interacting protein 1) associates with c-Myc, a key regulator of cell proliferation and transformation. We demonstrate that SNIP1 functions as an important regulator of c-Myc activity, binding the N terminus of c-Myc through its own C terminus, and that SNIP1 enhances the transcriptional activity of c-Myc both by stabilizing it against proteosomal degradation and by bridging the c-Myc/p300 complex. These effects of SNIP1 on c-Myc likely contribute to synergistic effects of SNIP1, c-Myc, and H-Ras in inducing formation of foci in an in vitro transformation assay and also in supporting anchorage-independent growth. The significant association of SNIP1 and c-Myc staining in a non-small cell lung cancer tissue array is further evidence that their activities might be linked and suggests that SNIP1 might be an important modulator of c-Myc activity in carcinogenesis.

    See More

  1. Keywords:

External Sources

  1. View Full Text
  2. DOI: 10.1016/j.molcel.2006.11.006
  3. View record in Web of Science®
  4. WOS: 000242812000013

Library Notes

  1. No notes added.
NCI at Frederick

You are leaving a government website.

This external link provides additional information that is consistent with the intended purpose of this site. The government cannot attest to the accuracy of a non-federal site.

Linking to a non-federal site does not constitute an endorsement by this institution or any of its employees of the sponsors or the information and products presented on the site. You will be subject to the destination site's privacy policy when you follow the link.

ContinueCancel