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Unformatted text preview: x FANCD2-Ub connects the
caused by replication blocks other than ICLs with uncharacterBRCA and RAD51 proteins to replisome components to stabilize
ized implications for tumorigenesis (Howlett et al., 2005; Lanstalled forks and prevent fork collapse (Figure 6). This protection
gevin et al., 2011; Naim and Rosselli, 2009; Rosado et al.
mechanism provides a functional explanation for the observa2011). Here the discovery of a role for FANCD2-Ub in preventing
tions that upon replication stalling both BRCA1 and BRCA2
degradation of nascent DNA strands containing PCNA (Chen
rapidly relocalize to replication foci in vivo independent of ICL
processing complements and extends existing with PCNA and
et al., 1998). Moreover, FANCD2 colocalizes results. Notably
FANCD2-Ub functions epistatically (Hussain et al., 2004 and
RAD51 to foci in response to HU with RAD51 at stalled )forks
within this distinct pathway, as does BRCA2, which provides
FANCD2 is found localized to sister chromatids upon replication
a more complete...
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This document was uploaded on 02/14/2014.
- Fall '14