Cdc25 cell-cycle phosphatase as a target of c-myc

Galaktionov, K., Chen, X., Beach, D. (August 1996) Cdc25 cell-cycle phosphatase as a target of c-myc. Nature, 382 (6591). pp. 511-7. ISSN 0028-0836 (Print)

Abstract

The product of the proto-oncogene c-myc, in partnership with Max, forms a transcription factor that can promote either oncogenic transformation or apoptosis. The Myc/Max heterodimer binds to elements in the cdc25A gene and activates transcription. Like myc, cdc25A, itself a proto-oncogene, can induce apoptosis in cells depleted of growth factor, and Myc-induced apoptosis also requires cdc25A. These findings indicate that cdc25A is a physiologically relevant transcriptional target of c-myc.

Item Type: Paper
Uncontrolled Keywords: 3T3 Cells Animals Apoptosis/genetics Binding Sites Cell Cycle Proteins/ genetics/metabolism Cell Line Cell Transformation, Neoplastic/genetics Cloning, Molecular Dna Gene Expression Regulation Humans Mice Molecular Sequence Data Phosphoprotein Phosphatase/ genetics/metabolism Protein Binding Proto-Oncogene Proteins c-myc/ metabolism RNA, Messenger/metabolism Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, P.H.S. Transcription, Genetic cdc25 Phosphatase
Subjects: bioinformatics > genomics and proteomics > genetics & nucleic acid processing > DNA, RNA structure, function, modification > transcription
bioinformatics > genomics and proteomics > genetics & nucleic acid processing > DNA, RNA structure, function, modification > genes, structure and function > genes: types > Myc
organs, tissues, organelles, cell types and functions > cell types and functions > cell functions > apoptosis
bioinformatics > genomics and proteomics > genetics & nucleic acid processing > DNA, RNA structure, function, modification > genes, structure and function > genes: types > oncogene
CSHL Authors:
Communities: CSHL labs > Beach lab
Depositing User: Matt Covey
Date: 8 August 1996
Date Deposited: 22 May 2014 18:36
Last Modified: 22 May 2014 18:36
Related URLs:
URI: https://repository.cshl.edu/id/eprint/30156

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