1: Nature 1992 Nov 12;360(6400):177-9

Published erratum appears in Nature 1992 Dec 3;360(6403):491
Abrogation by c-myc of G1 phase arrest induced by RB protein but not by p53.

Goodrich DW, Lee WH

Center for Molecular Medicine, University of Texas Health Science Center, San
Antonio 78245.

Inactivating mutations of the retinoblastoma gene (RB) are found in a wide
variety of tumour cells. Replacement of wild-type RB can suppress the
tumorigenicity of some of these cells, suggesting that the RB protein (Rb) may
negatively regulate cell growth. As activation of c-myc expression promotes cell
proliferation and blocks differentiation, it may positively regulate cell
growth. The c-myc protein is localized in the nucleus and can physically
associate with RB protein in vitro, hence c-myc may functionally antagonize RB
function. Microinjection of Rb in G1 phase reversibly arrests cell-cycle
progression. Here we co-inject RB protein with c-myc, EJ-ras, c-fos or c-jun
protein. Co-injection of c-myc, but not EJ-ras, c-fos or c-jun, inhibits the
ability of Rb to arrest the cell cycle. The c-myc does not inhibit the activity
of another tumour supressor, p53 (ref. 12). Thus, c-myc and RB specifically
antagonize one another in the cell.

MeSH Terms:
G1 Phase/physiology*
Protein p53/physiology*
Proto-Oncogene Proteins c-fos/physiology
Proto-Oncogene Proteins c-jun/physiology
Proto-Oncogene Proteins c-jun/pharmacology
Proto-Oncogene Proteins c-myc/physiology*
Retinoblastoma Protein/physiology*
Support, Non-U.S. Gov't
Support, U.S. Gov't, P.H.S.

Gene Symbols:

Retinoblastoma Protein
Proto-Oncogene Proteins c-myc
Proto-Oncogene Proteins c-jun
Proto-Oncogene Proteins c-fos
Protein p53

PMID: 1436095, UI: 93063346