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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.
This study found that only the RAD52 rs7963551 single nucleotide polymorphism was significantly associated with hepatitis B virus related - hepatocellular carcinoma risk.
Suppression of Rad52 expression in combination with FANCM knockout drastically reduces cell and tumor growth, suggesting a synthetic lethality interaction between these two genes.
Results demonstrate that Rad52 depletion increased cell death, decreased myeloid cell frequency, and augmented the activity of CD8+ T cells and NK effectors that ultimately led to reduced tumor growth. These data provide support for the notion of RAD52 as a potential oncogene, implicating a major role for the combined processes of recombinational repair and host immunity in determining risk for Squamous Cell.
In cancer-prone, heterozygous APC mutant mice, homozygous deletion of the Rad52 gene suppressed tumor growth and prolonged lifespan.
Rad54 has a key function in maintaining genomic integrity of the developing germ cells.
Loss of Rad52 partially rescues tumorigenesis and T-cell maturation in Atm-deficient mice.
RAD52 modulates the outcome of recombinant HIV-l vector infection by markedly reducing the efficiency of productive integration events
Inactivation of RAD52 aggravates X-ray and mitomycine C sensitivity in mice with RAD54 gene degect.
Cells expressing Rad52 splice variants favor sister chromatid repair.
Results indicate that RAD52 cooperates with OGG1 to repair oxidative DNA damage and enhances the cellular resistance to oxidative stress.
The complete cDNA sequences of the pig RAD51, RAD52, and RAD54 genes, which are closely related to homologous recombination events, arae identified using molecular cloning technique in pigs.
Rad51 and Rad52 physically interact with CENP-ACaCse4 in vivo.
Rad52 prevents chromosome loss and truncation.
The protein encoded by this gene shares similarity with Saccharomyces cerevisiae Rad52, a protein important for DNA double-strand break repair and homologous recombination. This gene product was shown to bind single-stranded DNA ends, and mediate the DNA-DNA interaction necessary for the annealing of complementary DNA strands. It was also found to interact with DNA recombination protein RAD51, which suggested its role in RAD51 related DNA recombination and repair.
DNA repair protein RAD52 homolog
, recombination protein RAD52
, rhabdomyosarcoma antigen MU-RMS-40.23
, RAD52 homolog (S. cerevisiae)
, RAD52 homolog isoform alpha
, DNA repair protein RAD52
, DNA repair protein RAD52 homolog-like
, RAD52 homolog
, potential dsDNA break repair annealing factor
, DNA repair and recombination protein, putative
, RAD52 protein