Product Pathways - DNA Damage
Rad52 Antibody #3425
PhosphoSitePlus® protein, site, and accession data: Rad52
| Applications | Reactivity | Sensitivity | MW (kDa) | Source |
|---|---|---|---|---|
| W IF-IC | H M R Mk (Hm) | Endogenous | 40 | Rabbit |
Applications Key:
W=Western Blotting
IF-IC=Immunofluorescence (Immunocytochemistry)
Reactivity Key:
H=Human
M=Mouse
R=Rat
Hm=Hamster
Mk=Monkey
Species cross-reactivity is determined by western blot. Species enclosed in parentheses are predicted to react based on 100% sequence homology.
Protocols
Specificity / Sensitivity
Rad52 Antibody detects endogenous levels of total Rad52 protein.
Source / Purification
Polyclonal antibodies are produced by immunizing animals with a synthetic peptide corresponding to the central sequence of human Rad52. Antibodies are purified by protein A and peptide affinity chromatography.
Background
Repair of DNA double-stranded breaks (DSBs) can occur via nonhomologous end joining (NHEJ), homologous recombination (HR), or other DSB repair pathways (1). In yeast, one family of proteins involved in HR is the Rad52 group, which includes Rad52 itself, Rad51, and Rad54 (1). Vertebrate cells lacking Rad51, Rad52, or Rad54 often show enhanced sensitivity to ionizing radiation (IR) or chromosomal abnormatlities (2-4). In response to IR-induced DNA damage, ATM activates the kinase c-Abl, which phosphorylates Rad51 at Tyr54 and Tyr315, and Rad52 at Tyr104, causing translocation of these proteins to sites of DNA strand breaks/subnuclear foci (5-7).
- Paques, F. and Haber, J.E. (1999) Microbiol. Mol. Biol. Rev. 63, 349-404.
- Bezzubova, O. et al. (1997) Cell 89, 185-193.
- Takata, M. et al. (2000) Mol. Cell. Biol. 20, 6476-6482.
- Fujimori, A. et al. (2001) EMBO J. 20, 5513-5520.
- Chen, G. et al. (1999) J. Biol. Chem. 274, 12748-12752.
- Yuan, Z. M. et al. (1998) J. Biol. Chem. 273, 3799-3802.
- Kitao, H. and Yuan, Z.M. (2002) J. Biol. Chem. 277, 48944-48948.
Application References
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For Research Use Only. Not For Use In Diagnostic Procedures.