Open AccessSuppression of Gl 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 γ‐Irradiation
Author(s) -
Nozaki Tadashige,
Masutani Mitsuko,
Akagawa Tetsuya,
Sugimura Takashi,
Esumi Hiroyasu
Publication year - 1994
Publication title -
japanese journal of cancer research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.035
H-Index - 141
eISSN - 1349-7006
pISSN - 0910-5050
DOI - 10.1111/j.1349-7006.1994.tb02912.x
Subject(s) - poly adp ribose polymerase , benzamide , cell cycle checkpoint , polymerase , fibroblast , microbiology and biotechnology , chemistry , cell cycle , biology , in vitro , biochemistry , cell , dna , stereochemistry
Low‐dose γ‐irradiation of mouse embryonic fibroblast C3D2F1 3T3‐a cells caused Gl 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, Gl 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 Gl arrest following γ‐irradiation. These results suggest that the poly(ADP‐ribosyDation reaction is critical for the pathway of Gl arrest and is also involved in the pathway of G2 arrest.