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

被引:18
作者
NOZAKI, T
MASUTANI, M
AKAGAWA, T
SUGIMURA, T
ESUMI, H
机构
[1] NATL CANC CTR,RES INST,DIV BIOCHEM,CHUO KU,TOKYO 104,JAPAN
[2] UNIV TOKYO,FAC MED,DEPT ORAL & MAXILLOFACIAL SURG,BUNKYO KU,TOKYO 113,JAPAN
[3] NATL CANC CTR,RES INST,KASHIWA,CHIBA 277,JAPAN
来源
JAPANESE JOURNAL OF CANCER RESEARCH | 1994年 / 85卷 / 11期
关键词
POLY(ADP-RIBOSYL)ATION; G1; ARREST; DNA DAMAGE; P53; DNA REPAIR;
D O I
10.1111/j.1349-7006.1994.tb02912.x
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Low-dose gamma-irradiation of mouse embryonic fibroblast C3D2F1 3T3-a cells caused G1 arrest along with G2 arrest and inhibition of replicative DNA synthesis. When the cells were cultured in the presence of inhibitors of poly(ADP-ribose) polymerase [EC 2.4.2.30], such as 3-aminobenzamide, benzamide and luminol, G1 arrest of C3D2F1 3T3-a cells was suppressed and enhancement of G2 arrest was observed. In contrast, 3-aminobenzoic 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 of G1 arrest and is also involved in the pathway of G2 arrest.
引用
收藏
页码:1094 / 1098
页数:5
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