UNASSIGNED: DNA damage response (DDR) consists of both proapoptotic and prosurvival signaling branches. Superiority of each signaling branch determines the outcome of DNA damage: death or allowing the repair. The present authors have previously shown that an increased intracellular level of cAMP disrupts @entity876 -mediated apoptosis in @entity1 pre-B @entity1 cells and inhibition of NF-kB prevents prosurvival effect of cAMP during DNA damage. @entity584 /PKB (protein kinase B) is a general mediator of survival signaling. @entity584 signaling inhibits @entity876 -mediated transcription and apoptosis. The results of present study showed that cAMP disrupted DNA damage/ @entity876 -mediated apoptosis through @entity584 and subsequent NF-kB activation. These results suggested that @entity584 may be found as part of a complex with scaffolding proteins, beta-arrestins and @entity20224 . cAMP disarticulated the complex through binding to @entity20224 compartment. It seems that release of @entity584 protein potentiated DDR activated pro-survival @entity584 in @entity1 cells. Taken together, the present data indicated that regulation of @entity584 signaling may determine the fate of cells exposed to genotoxic stress.

PI3K/AKT and Mdm2 activation are associated with inhibitory effect of cAMP increasing agents on DNA damage-induced cell death in @entity1 pre-B XXXX cells.

@entity876 :: ('7157', 'Gene') :: ['p53'] @entity1 :: ('9606', 'Species') :: ['human', 'NALM-6'] @entity584 :: ('207', 'Gene') :: ['AKT'] @entity20224 :: ('5144', 'Gene') :: ['PDE4D']
@entity1 :: (9606,Species) :: ['NALM-6']
