Mitotic homologous recombination maintains genomic stability and suppresses tumorigenesis

By M. Moynahan, M. Jasin. Nature reviews. Molecular cell biology, 2010

937 citations recorded by the source corpus.

Mitotic homologous recombination promotes genome stability through the precise repair of DNA double-strand breaks and other lesions that are encountered during normal cellular metabolism and from exogenous insults. As a result, homologous recombination repair is essential during proliferative stages in development and during somatic cell renewal in adults to protect against cell death and mutagenic outcomes from DNA damage. Mutations in mammalian genes encoding homologous recombination proteins, including BRCA1, BRCA2 and PALB2, are associated with developmental abnormalities and tumorigenesis. Recent advances have provided a clearer understanding of the connections between these proteins and of the key steps of homologous recombination and DNA strand exchange.

Subfields: Cell Biology, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/fcd7968edd5453794db5d5b3612f97859ebc37ee

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Citations in the corpus

Genome editing with engineered zinc finger nucleases (2010, background): “All eukaryotic cells efficiently repair DSBs via the homology-directed repair (HDR) or non-homologous end joining (NHEJ) pathway”
How shelterin solves the telomere end-protection problem. (2010, background): “For primary references and more extensive details on these pathways, the reader is referred to excellent recent reviews on these subjects (Hefferin and Tomkinson 2005; Harper and Elledge 2007; Cimprich and Cortez 2008; Jackson and Bartek 2009; Mahaney et al. 2009; Mimitou and Symington 2009; Lieber ”
The DNA damage response and cancer therapy (2012, background): “The major mechanisms that cope with DSBs are homologous recombinatio”
PARP Inhibitors: The First Synthetic Lethal Targeted Therapy (2017, background): “HRR is generally a “conservative” mechanism, in that it restores the original DNA sequence at the site of DNA damage (14).”
Homologous recombination and human health: the roles of BRCA1, BRCA2 and associated proteins (2015, background): “The BRCTrepeats mediate interactions between BRCA1 and several proteins involved in the DNA-damage response, including Abraxas/ FAM175A, BRIP1/BACH1, and CtIP/RBBP8, which are part of the BRCA1-A, -B, -C complexes, respectively (Moynahan and Jasin 2010; Li and Greenberg 2012).”
The DNA Damage Response: Making it safe to play with knives (2010, background): “Patients with BRCA2 mutations have increased incidence of male breast, pancreas, and prostate cancer (Moynahan and Jasin, 2010).”
CRISPR/Cas9-mediated gene editing in human tripronuclear zygotes (2015, background): “HDR of double strand breaks at the HBB gene occurs preferentially through the non-crossover pathway DSBs can be repaired through either error-prone NHEJ or high-fidelity HDR (Ciccia and Elledge, 2010; Moynahan and Jasin, 2010).”
Dynamics of DNA damage response proteins at DNA breaks: a focus on protein modifications. (2011, background): “The pivotal role of protein–protein interactions in the sequential association of repair factors to DDR foci is also illustrated by the recruitment of HR proteins to DSBs (Huen et al. 2010; Moynahan and Jasin 2010).”
Repair of strand breaks by homologous recombination. (2013, background): “Critical mediators are Rad52 in yeast and BRCA2 in mammalian cells, as Rad51 recruitment to DSBs, and hence HR, are substantially impaired when these proteins are disrupted (Sugawara et al. 2003; Lisby et al. 2004; San Filippo et al. 2008; Moynahan and Jasin 2010).”
Epigenetics and aging (2016, background): “Rad51 is a crucial factor required for homologous recombination (HR)–mediated DNA repair pathways (135).”