SUPPRESSION OF G1 ARREST AND ENHANCEMENT OF G2 ARREST BY INHIBITORS OF POLY(ADP-RIBOSE) POLYMERASE - POSSIBLE INVOLVEMENT OF POLY(ADP-RIBOSYL)ATION IN CELL-CYCLE ARREST FOLLOWING GAMMA-IRRADIATION

Authors
NOZAKI T MASUTANI M AKAGAWA T SUGIMURA T ESUMI H
Citation
T. Nozaki et al., SUPPRESSION OF G1 ARREST AND ENHANCEMENT OF G2 ARREST BY INHIBITORS OF POLY(ADP-RIBOSE) POLYMERASE - POSSIBLE INVOLVEMENT OF POLY(ADP-RIBOSYL)ATION IN CELL-CYCLE ARREST FOLLOWING GAMMA-IRRADIATION, Japanese journal of cancer research, 85(11), 1994, pp. 1094-1098
Citations number
17
Categorie Soggetti
Oncology
Journal title
Japanese journal of cancer research → ACNP
ISSN journal
09105050
Volume
85
Issue
11
Year of publication
1994
Pages
1094 - 1098
Database
ISI
SICI code
0910-5050(1994)85:11<1094:SOGAAE>2.0.ZU;2-O
Abstract
Low-dose gamma-irradiation of mouse embryonic fibroblast C3D2F1 3T3-a cells caused G1 arrest along with G2 arrest and inhibition of replicat ive DNA synthesis. When the cells were cultured in the presence of inh ibitors of poly(ADP-ribose) polymerase [EC 2.4.2.30], such as 3-aminob enzamide, benzamide and luminol, G1 arrest of C3D2F1 3T3-a cells was s uppressed and enhancement of G2 arrest was observed. In contrast, 3-am inobenzoic acid, a non-inhibitory analog of 3-aminobenzamide, did not suppress G1 arrest following gamma-irradiation. These results suggest that the poly(ADP-ribosyl)ation reaction is critical for the pathway o f G1 arrest and is also involved in the pathway of G2 arrest.