Emerging Roles of RAD52 in Genome Maintenance

Cancers

Manisha Jalan¹  SimonN. Powell¹  KyrieS. Olsen¹ 

[1] Department of Radiation Oncology, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA;

关键词: RAD52;    RNA:DNA hybrids;    R-loops;    DNA repair;    double-strand break repair;    BRCA1;    BRCA2;    RAD51;    synthetic lethality;    genome instability;   

DOI  :  10.3390/cancers11071038

来源: DOAJ

【 摘 要 】

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.

【 授权许可】

Unknown