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.
Publication types
-
Research Support, Non-U.S. Gov't
-
Research Support, U.S. Gov't, P.H.S.
MeSH terms
-
3T3 Cells
-
Animals
-
Apoptosis / genetics
-
Binding Sites
-
Cell Cycle Proteins / genetics*
-
Cell Cycle Proteins / metabolism
-
Cell Line
-
Cell Transformation, Neoplastic / genetics
-
Cloning, Molecular
-
DNA
-
Gene Expression Regulation
-
Humans
-
Mice
-
Molecular Sequence Data
-
Phosphoprotein Phosphatases / genetics*
-
Phosphoprotein Phosphatases / metabolism
-
Protein Binding
-
Proto-Oncogene Mas
-
Proto-Oncogene Proteins c-myc / metabolism*
-
RNA, Messenger / metabolism
-
Transcription, Genetic
-
cdc25 Phosphatases
Substances
-
Cell Cycle Proteins
-
MAS1 protein, human
-
Proto-Oncogene Mas
-
Proto-Oncogene Proteins c-myc
-
RNA, Messenger
-
DNA
-
Phosphoprotein Phosphatases
-
cdc25 Phosphatases