Antagonism of Myc functions by Arf.

Cancer cell ·Vol. 6 ·No. 4 ·2004-10-00 ·Pages 309-11

Cleveland JL, Sherr CJ

Abstract

The Arf-Mdm2-p53 tumor suppressor pathway is activated by sustained hyperproliferative signals emanating from oncoproteins such as Myc. A recent study reveals a novel level of feedback control, whereby induced p19(Arf) binds to Myc and blocks cell proliferation by selectively impairing its transactivation functions.

MeSH Terms

Animals Cell Division Humans Nuclear Proteins/metabolism Proto-Oncogene Proteins/metabolism Proto-Oncogene Proteins c-mdm2 Proto-Oncogene Proteins c-myc/antagonists & inhibitors,metabolism Signal Transduction Tumor Suppressor Protein p14ARF/metabolism Tumor Suppressor Protein p53/metabolism

Chemicals

Nuclear Proteins Proto-Oncogene Proteins Proto-Oncogene Proteins c-myc Tumor Suppressor Protein p14ARF Tumor Suppressor Protein p53 MDM2 protein, human Proto-Oncogene Proteins c-mdm2

Authors & Affiliations

2 authors, click to expand affiliations / ORCID

Cleveland John L

Department of Biochemistry, St. Jude Children's Research Hospital, Memphis, TN 38105, USA.

Sherr Charles J

Article Info

Journal

Cancer cell

Abbr.

Cancer Cell

ISSN

1535-6108

DOI

10.1016/j.ccr.2004.09.020

Published

2004-10-00

Pages

309-11

Language

English

Region

United States

NLM ID

101130617

Subset

External Links

PubMed source DOI: 10.1016/j.ccr.2004.09.020 View journal details

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Antagonism of Myc functions by Arf.

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