In response to DNA damage and genotoxic stress, the @entity876 @entity5 suppressor triggers either cell cycle arrest or apoptosis. The G(2) arrest after damage is, in part, mediated by the @entity876 target, 14-3-3final sigma (final sigma). @entity14 cells lacking final sigma are exquisitely sensitive to DNA damage. Here we analyzed the mechanism of this sensitivity in final sigma(-/-) as compared with final sigma(+/+) @entity1 @entity14 cells. Exposure to @entity632 resulted in rapid apoptosis only in final sigma(-/-) cells. This was further characterized by @entity522 activation, @entity3544 ( @entity994 ) cleavage, and @entity15308 activation. Moreover, @entity589 was rapidly translocated out of the cytoplasm, and @entity4674 was released in final sigma(-/-) cells. Transient adenovirus-mediated reconstitution of final sigma in the final sigma(-/-) cells led to effective rescue of this phenotype and protected cells against apoptosis. The association of final sigma, @entity589 , and @entity10610 in protein complexes may be the basis for this antiapoptotic mechanism. In conclusion, final sigma not only enforces the @entity876 -dependent G(2) arrest but also delays the apoptotic signal transduction.

The G2/M regulator 14-3-3sigma prevents apoptosis through sequestration of XXXX .

@entity1 :: ('9606', 'Species') :: ['human'] @entity632 :: ('MESH:D004317', 'Chemical') :: ['adriamycin'] @entity10610 :: ('983', 'Gene') :: ['CDK1'] @entity522 :: ('836', 'Gene') :: ['caspase-3'] @entity589 :: ('581', 'Gene') :: ['Bax'] @entity5 :: ('MESH:D009369', 'Disease') :: ['tumor'] @entity4674 :: ('54205', 'Gene') :: ['cytochrome c'] @entity3544 :: ('644914', 'Gene') :: ['p21'] @entity876 :: ('7157', 'Gene') :: ['p53'] @entity15308 :: ('1017', 'Gene') :: ['CDK2'] @entity14 :: ('MESH:D015179', 'Disease') :: ['Colorectal tumor', 'colorectal tumor'] @entity994 :: ('1026', 'Gene') :: ['CIP1']
@entity589 :: (581,Gene) :: ['Bax']
