In:
Genes & Development, Cold Spring Harbor Laboratory, Vol. 14, No. 13 ( 2000-07-01), p. 1584-1588
Abstract:
It is believed that multiple effectors independently control the checkpoints permitting transitions between cell cycle phases. However, this has not been rigorously demonstrated in mammalian cells. The p53-induced genes p21 and 14-3-3ς are each required for the G 2 arrest and allow a specific test of this fundamental tenet. We generated human cells deficient in both p21 and 14-3-3ς and determined whether the double knockout was more sensitive to DNA damage than either single knockout. p21 −/− 14-3-3ς −/− cells were significantly more sensitive to DNA damage or to the exogenous expression of p53 than cells lacking only p21 or only 14-3-3ς. Thus, p21 and 14-3-3ς play distinct but complementary roles in the G 2 /M checkpoint, and help explain why genes at the nodal points of growth arrest pathways, like p53, are the targets of mutation in cancer cells.
Type of Medium:
Online Resource
ISSN:
0890-9369
,
1549-5477
DOI:
10.1101/gad.14.13.1584
Language:
English
Publisher:
Cold Spring Harbor Laboratory
Publication Date:
2000
detail.hit.zdb_id:
1467414-2
SSG:
12
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