Browse our anti-RAD52 (RAD52) Antibodies

Human RAD52 Homolog (S. Cerevisiae) (RAD52) interaction partners

1. 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.

2. inhibition of ataxia telangiectasia mutated (ATM (show ATM Antibodies)) protein by siRNA or inhibitor treatment demonstrated that the acetylation of RAD52 at DSB sites is dependent on the ATM (show ATM Antibodies) protein kinase (show CDK7 Antibodies) activity, through the formation of RAD52, p300/CBP (show CREBBP Antibodies), SIRT2 (show SIRT2 Antibodies), and SIRT3 (show SIRT3 Antibodies) foci at DSB sites

3. 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

4. RAD52 gene polymorphism is associated with colorectal cancer.

5. our study demonstrated that RAD52 polymorphisms were associated with colorectal cancer in a Chinese Han cohort

6. DNA-bound RAD52 is efficient at capturing ssDNA in trans.

7. Structure of the human DNA-repair protein RAD52 containing surface mutations has been reported.

8. Rad52 inverse strand exchange plays an important role in RNA-templated double strand break repair in vivo.

9. The mitotic DNA synthesis is RAD52 dependent, and RAD52 is required for the timely recruitment of MUS81 (show MUS81 Antibodies) and POLD3 (show POLD3 Antibodies) to common fragile sites in early mitosis.

10. Human RAD52-null cells retain a significant level of single-strand annealing (SSA (show TRIM21 Antibodies)) activity demonstrating perforce that additional SSA (show TRIM21 Antibodies)-like activities must exist in human cells. Moreover, the SSA (show TRIM21 Antibodies) activity associated with RAD52 is involved in, but not absolutely required for, most homology-directed repair (HDR (show GATA3 Antibodies)) subpathways. Specifically, a deficiency in RAD52 impaired the repair of DNA DSBs.

Mouse (Murine) RAD52 Homolog (S. Cerevisiae) (RAD52) interaction partners

1. Results demonstrate that Rad52 depletion increased cell death, decreased myeloid cell frequency, and augmented the activity of CD8 (show CD8A Antibodies)+ 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 (show RAB1A Antibodies), implicating a major role for the combined processes of recombinational repair and host immunity in determining risk for Squamous Cell.

2. In cancer-prone, heterozygous APC (show APC Antibodies) mutant mice, homozygous deletion of the Rad52 gene suppressed tumor growth and prolonged lifespan.

3. Rad54 (show RAD54L Antibodies) has a key function in maintaining genomic integrity of the developing germ cells.

4. Loss of Rad52 partially rescues tumorigenesis and T-cell maturation in Atm (show ATM Antibodies)-deficient mice.

5. RAD52 modulates the outcome of recombinant HIV-l vector infection by markedly reducing the efficiency of productive integration events

6. Inactivation of RAD52 aggravates X-ray and mitomycine C sensitivity in mice with RAD54 (show RAD54L Antibodies) gene degect.

7. Cells expressing Rad52 splice variants favor sister chromatid repair.

8. Results indicate that RAD52 cooperates with OGG1 (show OGG1 Antibodies) to repair oxidative DNA damage and enhances the cellular resistance to oxidative stress.

Pig (Porcine) RAD52 Homolog (S. Cerevisiae) (RAD52) interaction partners

1. The complete cDNA sequences of the pig RAD51 (show RAD51 Antibodies), RAD52, and RAD54 (show RAD54L Antibodies) genes, which are closely related to homologous recombination events, arae identified using molecular cloning technique in pigs.

Candida albicans RAD52 Homolog (S. Cerevisiae) (RAD52) interaction partners

1. Rad51 (show RAD51 Antibodies) and Rad52 physically interact with CENP-ACaCse4 in vivo.

2. Rad52 prevents chromosome loss and truncation.