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Western blot analysis of NBS1 on a Jurkat cell lysate (Human T-cell leukemia; ATCC TIB-152). Lane 1: 1:1000, lane 2: 1:2000, lane 3: 1:4000 dilution of the mouse anti-NBS1 antibody.
Immunofluorescence staining of L6 cells (Rat skeletal muscle myoblasts; ATCC CRL-1458).
BD Transduction Laboratories™ Purified Mouse Anti-NBS1
BD Transduction Laboratories™ Purified Mouse Anti-NBS1
Regulatory Statusの凡例
Any use of products other than the permitted use without the express written authorization of Becton, Dickinson and Company is strictly prohibited.
Preparation and Storage
推奨アッセイ手順
Western blot: Please refer to http://www.bdbiosciences.com/pharmingen/protocols/Western_Blotting.shtml
Product Notices
- Since applications vary, each investigator should titrate the reagent to obtain optimal results.
- Please refer to www.bdbiosciences.com/us/s/resources for technical protocols.
- Caution: Sodium azide yields highly toxic hydrazoic acid under acidic conditions. Dilute azide compounds in running water before discarding to avoid accumulation of potentially explosive deposits in plumbing.
- Source of all serum proteins is from USDA inspected abattoirs located in the United States.
関連製品
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.
Development References (4)
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Carney JP, Maser RS, Olivares H. The hMre11/hRad50 protein complex and Nijmegen breakage syndrome: linkage of double-strand break repair to the cellular DNA damage response. Cell. 1998; 93(3):477-486. (Biology). View Reference
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Dong Z, Zhong Q, Chen PL. The Nijmegen breakage syndrome protein is essential for Mre11 phosphorylation upon DNA damage. J Biol Chem. 1999; 274(28):19513-19516. (Biology). View Reference
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Kim JS, Krasieva TB, LaMorte V, Taylor AM, Yokomori K. Specific recruitment of human cohesin to laser-induced DNA damage. J Biol Chem. 2002; 277(47):45149-45153. (Biology: Western blot). View Reference
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Trujillo KM, Yuan SS, Lee EY, Sung P. Nuclease activities in a complex of human recombination and DNA repair factors Rad50, Mre11, and p95. J Biol Chem. 1998; 273(34):21447-21450. (Biology). View Reference
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