Abstract:
:The Fanconi anemia (FA) pathway, of which the FANCD2 protein is a key component, plays crucial roles in the maintenance of hematopoietic stem cells and suppression of carcinogenesis. However, the function of FANCD2 remains unclear. Here, we report that FANCD2 is a novel and specific substrate of caspase 3. Cleavage of FANCD2 by caspase 3 did not require either the FA core complex or mono-ubiquitylation of FANCD2, and was stimulated by p53. In addition, we identified the cleavage sites and generated cell lines that stably express a caspase-resistant FANCD2 mutant. Our data suggest that FANCD2 is regulated by caspase-mediated degradation during apoptosis induced by DNA damage.
journal_name
FEBS Lettjournal_title
FEBS lettersauthors
Sakai W,Sugasawa Kdoi
10.1016/j.febslet.2014.08.027subject
Has Abstractpub_date
2014-10-16 00:00:00pages
3778-85issue
20eissn
0014-5793issn
1873-3468pii
S0014-5793(14)00629-2journal_volume
588pub_type
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