Abstract
The maintenance of genome integrity is critical for cell survival. Homologous recombination (HR) is considered the major error-free repair pathway in combatting endogenously generated double-stranded lesions in DNA. Nevertheless, a number of alternative repair pathways have been described as protectors of genome stability, especially in HR-deficient cells. One of the factors that appears to have a role in many of these pathways is human RAD52, a DNA repair protein that was previously considered to be dispensable due to a lack of an observable phenotype in knock-out mice. In later studies, RAD52 deficiency has been shown to be synthetically lethal with defects in BRCA genes, making RAD52 an attractive therapeutic target, particularly in the context of BRCA-deficient tumors.
Highlights
The maintenance of genome integrity is critical for cell survival
Human RAD52 consists of a C-terminal domain (CTD) which contains its nuclear localization signal (NLS) as well as its RAD51- and RPA-binding regions, and an N-terminal domain (NTD) which has been shown to be responsible for its multimerization and DNA-binding activity [16,31,32,33,34,35]
While RAD52 is evolutionarily conserved across species, it was long thought to be largely dispensable in humans
Summary
Double-strand breaks (DSBs) are the greatest threat to genomic integrity and can result from endogenous sources such as reactive oxygen species (ROS) and replication stress or exogenous insults such as UV, ionizing radiation (IR), and chemotherapeutic compounds. Whilein thebudding pattern ofyeast resection annealing of complementary sequences are similar, Alt-EJ and SSA have been shown to require different protein would inhibit repair of IR-induced DSBs, resulting in radio-sensitization [16,17]. Responsible for annealing the resected ends [9,11,12,13,14]; recent work by the Hendrickson lab Of this group, most proteins wereplasmid foundreporter to play similar rolesthat in HR, yeast andand human while Rad using previously established assays has shown. Several other and on RAD52 for annealing ssDNA ends, in yeast, both of these functions are performed by Rad, as DNA repair proteins were identified in this screen and are referred to as the Rad epistasis they lack agroup. Pathways are categorized by the cell cycle phase in which they are predominately active [24,25,26,27,28,29,30]
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