CyclinG contributes to G2/M arrest of cells in response to DNA damage.

Abstract:

:To investigate regulation mechanisms of G2/M phase transition, we studied the association of cell cycle progression with p53-dependent p21/waf-1 and cyclinG expression. We used doxorubicin (DOX) and sodium butyrate (NaB) to accumulate p53 protein. DOX treatment resulted in an apparent increase of cells in the G2/M fraction, whereas NaB arrested cells at G1. P53 protein induction in response to DOX accompanied up-regulation of p21/waf-1 and cyclinG expression. However, cyclinG was undetectable in NaB-treated cells. These results implied a putative association between increases in the proportion of cells accumulating in the G2/M fraction and enhanced cyclinG expression. Antisense oligo DNAs (AS) complementary to cyclinG mRNA inhibited the cyclinG protein expression induced by DOX treatment. This inhibition resulted in a marked reduction in the number of cells arrested at G2/M and accumulating at G1. A role for cyclinG in G2/M phase transition control is implied.

authors

Shimizu A,Nishida J,Ueoka Y,Kato K,Hachiya T,Kuriaki Y,Wake N

doi

10.1006/bbrc.1997.8004

subject

Has Abstract

pub_date

1998-01-26 00:00:00

pages

529-33

issue

3

eissn

0006-291X

issn

1090-2104

pii

S0006291X97980049

journal_volume

242

pub_type

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