Molecular and Cellular Biology
Geisel School of Medicine
In normal cells, induction of quiescence is accompanied by the increased expression of growth arrest-specific genes (gas). One of them, gas1, is regulated at the transcriptional level and codes for a membrane-associated protein (Gas1) which is down regulated during the G0-to-S phase transition in serum-stimulated cells. Gas1 is not expressed in growing or transformed cells, and when overexpressed in normal fibroblasts, it blocks the G0-to-S phase transition. Moreover, Gas1 blocks cell proliferation in several transformed cells with the exception of simian virus 40- or adenovirus-transformed cell lines. In this paper, we demonstrate that overexpression of Gas1 blocks cell proliferation in a p53-dependent manner and that the N-terminal domain-dependent transactivating function of p53 is dispensable for Gas1-induced growth arrest. These data therefore indicate that the other intrinsic transactivation-independent functions of p53, possibly related to regulation of apoptosis, should be involved in mediating Gas1-induced growth arrest.
Del Sal G, Ruaro EM, Utrera R, Cole CN, Levine AJ, Schneider C. Gas1-induced growth suppression requires a transactivation-independent p53 function. Mol Cell Biol. 1995;15(12):7152-7160. doi:10.1128/mcb.15.12.7152
Dartmouth Digital Commons Citation
Del Sal, Giannino; Ruaro, Elisabetta M.; Utrera, Rene; and Cole, Charles N., "Gas1-induced Growth Suppression Requires a Transactivation-independent p53 Function." (1995). Dartmouth Scholarship. 1159.