-
RAD52 limits excessive remodelling of stalled replication forks, thus indirectly assisting RAD51 and BRCA2 in protecting forks from unscheduled degradation and preventing genome instability.
-
RAD52 and SLX4 mediate distinct postreplicative DNA repair processes that maintain ALT telomere stability and cancer cell viability
-
Rad52 competes with Ku for binding to S-region double-strand DNA breaks (DSB) free ends, where it facilitates a DSB synaptic process, which favours intra-S region recombination.
-
Due to its similarity to RAD52, we hypothesized that RDM1 potentially repairs DNA doublestrand breaks arising through DNA replication.
-
The mechanism by which RAD52 depletion causes synthetic lethality in BRCA1 mutant cancer cells depends on the 5' endonuclease EEPD1, which normally functions to cleave stressed replication forks to initiate HR repair.
-
inhibition of ataxia telangiectasia mutated (ATM) protein by siRNA or inhibitor treatment demonstrated that the acetylation of RAD52 at DSB sites is dependent on the ATM protein kinase activity, through the formation of RAD52, p300/CBP, SIRT2, and SIRT3 foci at DSB sites
-
n a cohort of patients with typical symptoms of ischemic heart disease, a common single nucleotide polymorphism of the human RAD52 gene has a role in increased hazard of death, showing that it may influence aging
-
RAD52 gene polymorphism is associated with colorectal cancer.
-
our study demonstrated that RAD52 polymorphisms were associated with colorectal cancer in a Chinese Han cohort
-
DNA-bound RAD52 is efficient at capturing ssDNA in trans.
-
Structure of the human DNA-repair protein RAD52 containing surface mutations has been reported.
-
Rad52 inverse strand exchange plays an important role in RNA-templated double strand break repair in vivo.
-
The mitotic DNA synthesis is RAD52 dependent, and RAD52 is required for the timely recruitment of MUS81 and POLD3 to common fragile sites in early mitosis.
-
Human RAD52-null cells retain a significant level of single-strand annealing (SSA) activity demonstrating perforce that additional SSA-like activities must exist in human cells. Moreover, the SSA activity associated with RAD52 is involved in, but not absolutely required for, most homology-directed repair (HDR) subpathways. Specifically, a deficiency in RAD52 impaired the repair of DNA DSBs.
-
Data suggest RAD52 binds tightly to RPA/ssDNA complex in presynaptic complex and inhibits RPA turnover; during presynaptic complex assembly, most of RPA and RAD52 is displaced from ssDNA, but some RAD52/RPA/ssDNA complexes persist as interspersed clusters surrounded by RAD51 filaments. (RAD52 = Rad52 DNA repair/recombination protein; RPA = replication protein A; ssDNA = single-stranded DNA; RAD51 = Rad51 recombinase)
-
The C-terminal region of yRad52, but not of hRAD52, is involved in ssDNA annealing. This suggests that the second DNA binding site is required for the efficient ssDNA annealing by yRad52. We propose an updated model of Rad52-mediated ssDNA annealing.
-
Study discovered two cis-expression quantitative trait loci SNPs in the RAD52 gene that are associated with its expression and are also associated with lung squamous cell carcinomas (LUSC) risk.
-
BRG1-RAD52 complex mediates the replacement of RPA with RAD51 on single-stranded DNA (ssDNA) to initiate DNA strand invasion. Loss of BRG1 results in a failure of RAD51 loading onto ssDNA, abnormal homologous recombination repair
-
these results implicate increased RAD52 expression in both genetic susceptibility and tumorigenesis of upper aerodigestive tract and lung squamous cell carcinoma tumors.
-
RAD52 rs7963551 single nucleotide polymorphism was significantly associated with glioma risk.
