Ontology highlight
ABSTRACT:
SUBMITTER: Lachaud C
PROVIDER: S-EPMC4075355 | biostudies-literature | 2014 Jul
REPOSITORIES: biostudies-literature
Lachaud Christophe C Castor Dennis D Hain Karolina K Muñoz Ivan I Wilson Jamie J MacArtney Thomas J TJ Schindler Detlev D Rouse John J
Journal of cell science 20140502 Pt 13
Defects in SLX4, a scaffold for DNA repair nucleases, result in Fanconi anemia (FA), due to the defective repair of inter-strand DNA crosslinks (ICLs). Some FA patients have an SLX4 deletion removing two tandem UBZ4-type ubiquitin-binding domains that are implicated in protein recruitment to sites of DNA damage. Here, we show that human SLX4 is recruited to sites of ICL induction but that the UBZ-deleted form of SLX4 in cells from FA patients is not. SLX4 recruitment does not require either the ...[more]