NBS1 Mouse, Unlabeled, Clone: 34, BD
Mouse Monoclonal Antibody
Manufacturer: BD Biosciences 611871
Nijmegen Breakage Syndrome (NBS) is characterized by extreme radiation sensitivity and chromosomal instability. The NBS1 gene product, p95/nibrin/NBS1, forms a complex with Rad50 and Mre11. Cells deficient in this complex have problems with DNA double-strand break repair, cell cycle checkpoint control, and telomere length maintenance. NBS1 contains a forkhead-associated domain (FHA) and a breast cancer carboxy-terminal domain (BRCT) in the N-terminal region. Both of these domains have been found in DNA-damage responsive cell cycle checkpoint proteins. The complex containing NBS1, Rad50, and Mre11 possesses manganese-dependent single stranded DNA endonuclease and 3′ to 5′ exonuclease activities. In addition, NBS1 is required for DNA-damage dependent phosphorylation of Mre11. This phosphorylation may be required for proper nuclear localization of the NBS1-Rad50-Mre11 complex to sites of DNA double-strand breaks. NBS1 interacts directly with telomere repeat binding factor, TRF1, via its C-terminal region, and both NBS1 and Mre11 co-localize with TRF1 at promyelocytic leukemia nuclear bodies. Thus, the NBS1-Rad50-Mre11 complex may be important for both DNA damage repair, and telomere length maintenance.
Host Species: Mouse
Species Reactivity [for Features Main]: Human
Immunogen: Human NBS1 aa. 620-732
Immunofluorescence, Western Blotting
|Aqueous buffered solution containing BSA, glycerol, and ≤0.09% sodium azide.|
|Store undiluted at -20°C.|
|Nijmegen Breakage Syndrome-1|
|Human NBS1 aa. 620-732|
|Canine, Chicken, Human, Murine, Rat|
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