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. Author manuscript; available in PMC: 2013 Jun 1.
Published in final edited form as: Clin Cancer Res. 2012 Oct 15;18(23):6400–6406. doi: 10.1158/1078-0432.CCR-11-3150

Fig 1.

Fig 1

The BRCA and RAD52 pathways of DNA double-strand break (DSB) repair. Various DNA lesions lead to DSBs that can be repaired by homologous recombination (HR) or single-strand annealing (SSA). A) In the HR pathway, after activation of the DNA damage response pathway, DNA ends are resected to expose 3’ single-stranded DNA (ssDNA) which become substrates for binding by RPA. BRCA2 or, in its absence, Rad52 can recruit Rad51 for loading onto ssDNA, displacing RPA, allowing for homology searching and strand invasion by the Rad51 nucleofilament. Subsequently, noncrossover or crossover ligation products are generated in the double-strand break repair (DSBR) pathway or only noncrossover products when synthesis-dependent strand-annealing (SDSA) is utilized. B) SSA requires repetitive sequences around the DSB. After resection, Rad52 mediates annealing of the exposed complementary sequences. After removal of the 3’-flaps, ligation leads to repair, with loss of the intervening sequence. *There is currently no clear evidence that 1-end DSBs or daughter-strand gaps are repaired by single-strand annealing.

The left half of panel A is adapted by permission from Macmillan Publishers Ltd: Nature Reviews Molecular Cell Biology (66), copyright 2006.