RAD51 is a key protein of DNA repair and homologous recombination in humans

Alexander V. Mazin, Olga M. Mazina

Research output: Chapter in Book/Report/Conference proceedingChapter

2 Scopus citations


Ionizing radiation and various chemotherapeutic agents kill cancer cells by inducing DNA double-strand breaks (DSBs) or interstrand DNA cross links. Cells however can resist the killing effect by repairing these lesions using the homologous recombination (HR) pathway [1-3]. HR achieves highfidelity of repairing DNA breaks through the unique mechanism that employs homologous DNA as a template [4]. The initial step of HR involves exonucleolytic processing of the DNA ends into a resected DNA duplex with protruding 3'-ssDNA tails (Fig. 1) [5]. Then, RAD51 protein loads onto the ssDNA to form a contiguous helical nucleoprotein filament that promotes a search for the homologous dsDNA [6, 7]. Once the homologous sequence is found, RAD51 promotes the exchange of DNA strands that resulted in formation of joint molecules [8, 9]. Joint molecules provide both a template and a primer for the DNA synthesis that is required for retrieving the information lost at the site of the break and for the consequent restoration of a contiguous DNA structure.

Original languageEnglish (US)
Title of host publicationAdvances in DNA Repair in Cancer Therapy
PublisherSpringer New York
Number of pages22
ISBN (Electronic)9781461447412
ISBN (Print)9781461447405
StatePublished - Jan 1 2013
Externally publishedYes

ASJC Scopus subject areas

  • General Medicine


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