c-myc null cells misregulate cad and gadd45 but not other proposed c-Myc targets
Open Access
- 15 December 1998
- journal article
- Published by Cold Spring Harbor Laboratory in Genes & Development
- Vol. 12 (24) , 3797-3802
- https://doi.org/10.1101/gad.12.24.3797
Abstract
We report here that the expression of virtually all proposed c-Myc target genes is unchanged in cells containing a homozygous null deletion of c-myc. Two noteworthy exceptions are the genecad, which has reduced log phase expression and serum induction in c-myc null cells, and the growth arrest gene gadd45, which is derepressed by c-myc knockout. Thus, cad andgadd45 are the only proposed targets of c-Myc that may contribute to the dramatic slow growth phenotype of c-myc null cells. Our results demonstrate that a loss-of-function approach is critical for the evaluation of potential c-Myc target genes.Keywords
This publication has 40 references indexed in Scilit:
- Myc represses the growth arrest gene gadd45Oncogene, 1997
- c-myc activates RCC1 gene expression through E-box elementsOncogene, 1997
- Mnt, a novel Max-interacting protein is coexpressed with Myc in proliferating cells and mediates repression at Myc binding sites.Genes & Development, 1997
- Cdc25 cell-cycle phosphatase as a target of c-mycNature, 1996
- CDC25 Phosphatases as Potential Human OncogenesScience, 1995
- Myc and Max proteins possess distinct transcriptional activitiesNature, 1992
- myc FUNCTION AND REGULATIONAnnual Review of Biochemistry, 1992
- Chimaeras of Myc oncoprotein and steroid receptors cause hormone-dependent transformation of cellsNature, 1989
- c-myc oncogene protein synthesis is independent of the cell cycle in human and avian cellsNature, 1985
- Functional role for c-myc in mitogenic response to platelet-derived growth factorNature, 1984