Literature DB >> 31263220

DNA double-strand break repair-pathway choice in somatic mammalian cells.

Ralph Scully1, Arvind Panday2, Rajula Elango2, Nicholas A Willis3.   

Abstract

The major pathways of DNA double-strand break (DSB) repair are crucial for maintaining genomic stability. However, if deployed in an inappropriate cellular context, these same repair functions can mediate chromosome rearrangements that underlie various human diseases, ranging from developmental disorders to cancer. The two major mechanisms of DSB repair in mammalian cells are non-homologous end joining (NHEJ) and homologous recombination. In this Review, we consider DSB repair-pathway choice in somatic mammalian cells as a series of 'decision trees', and explore how defective pathway choice can lead to genomic instability. Stalled, collapsed or broken DNA replication forks present a distinctive challenge to the DSB repair system. Emerging evidence suggests that the 'rules' governing repair-pathway choice at stalled replication forks differ from those at replication-independent DSBs.

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Year:  2019        PMID： 31263220      PMCID： PMC7315405          DOI： 10.1038/s41580-019-0152-0

Source DB:  PubMed          Journal:  Nat Rev Mol Cell Biol        ISSN： 1471-0072            Impact factor:   113.915


  277 in total

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4.  APLF (C2orf13) facilitates nonhomologous end-joining and undergoes ATM-dependent hyperphosphorylation following ionizing radiation.

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Journal:  PLoS Genet       Date:  2008-06-27       Impact factor: 6.020
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  279 in total

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Review 4.  The molecular basis and disease relevance of non-homologous DNA end joining.

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Review 5.  A Role for N6-Methyladenine in DNA Damage Repair.

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7.  An unorthodox partnership in DNA repair pathway choice.

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Review 8.  The balancing act of R-loop biology: The good, the bad, and the ugly.

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