Oncology 401 Lecture 14 2013

Oncology 401

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Unformatted text preview: ications for tumorigenesis (Howlett et al., 2005; Langevin et al., 2011; Naim and Rosselli, 2009; Rosado et al. 2011). Here the discovery of a role for FANCD2-Ub in preventing degradation of nascent DNA strands in vivo independent of ICL processing complements and extends existing results. Notably FANCD2-Ub functions epistatically with RAD51 at stalled forks within this distinct pathway, as does BRCA2, which provides a more complete understanding of how these proteins maintain replication fork fidelity in the context of ICL and other DNA stresses. FANCD2 monoubiquitination involves an interaction with the replisome component proliferating cell nuclear antigen (PCNA DISCUSSION (Howlett et al., 2009). Because BRCA2/RAD51 functionally interacts with FANCD2 (Long et al., 2011; Wang et al., 2004) and Because of the exquisite sensitivity of FA genes to ICL lesions BRCA2/RAD51 alone is insufficient for fork protection in the most studies thus far have focused on their role in ICL repair absence of FANCD2-Ub, a testable mechanistic model is that Yet, the FA machinery prevents genome instability and lethality as part of a protein supercomple...
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This document was uploaded on 02/14/2014.

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