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2016 ; 15
(8
): 1134-43
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FANCI is a negative regulator of Akt activation
#MMPMID27097374
Zhang X
; Lu X
; Akhter S
; Georgescu MM
; Legerski RJ
Cell Cycle
2016[]; 15
(8
): 1134-43
PMID27097374
show ga
Akt is a critical mediator of the oncogenic PI3K pathway, and its activation is
regulated by kinases and phosphatases acting in opposition. We report here the
existence of a novel protein complex that is composed minimally of Akt, PHLPP1,
PHLPP2, FANCI, FANCD2, USP1 and UAF1. Our studies show that depletion of FANCI,
but not FANCD2 or USP1, results in increased phosphorylation and activation of
Akt. This activation is due to a reduction in the interaction between PHLPP1 and
Akt in the absence of FANCI. In response to DNA damage or growth factor
treatment, the interactions between Akt, PHLPP1 and FANCI are reduced consistent
with the known phosphorylation of Akt in response to these stimuli. Furthermore,
depletion of FANCI results in reduced apoptosis after DNA damage in accord with
its role as a negative regular of Akt. Our findings describe an unexpected
function for FANCI in the regulation of Akt and define a previously unrecognized
intersection between the PI3K-Akt and FA pathways.
|Apoptosis
[MESH]
|Cell Line, Tumor
[MESH]
|Enzyme Activation
[MESH]
|Fanconi Anemia Complementation Group D2 Protein/metabolism
[MESH]
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