|Positive WB detected in||HeLa cells, human testis tissue, HepG2 cells, HEK-293 cells, mouse brain tissue|
|Positive IP detected in||HeLa cells|
|Positive IF detected in||HepG2 cells, A549 cells|
|Western Blot (WB)||WB : 1:500-1:2400|
|Immunoprecipitation (IP)||IP : 0.5-4.0 ug for IP and 1:500-1:1000 for WB|
|Immunofluorescence (IF)||IF : 1:50-1:500|
|Sample-dependent, check data in validation data gallery|
55025-1-AP targets NBS1 in WB, IP, IF,ELISA applications and shows reactivity with human, mouse, rat samples.
|Tested Reactivity||human, mouse, rat|
|Cited Reactivity||human, mouse|
|Host / Isotype||Rabbit / IgG|
|Calculated molecular weight||85 kDa|
|Observed molecular weight||90-95 kDa|
|GenBank accession number||NM_002485|
|Gene ID (NCBI)||4683|
|Purification Method||Antigen affinity purification|
|Storage Buffer||PBS with 0.02% sodium azide and 50% glycerol pH 7.3.|
|Storage Conditions||Store at -20°C. Aliquoting is unnecessary for -20oC storage.|
NBN, also named as NBS, NBS1 and P95, is a component of the MRE11/RAD50/NBN (MRN complex) which plays a critical role in the cellular response to DNA damage and the maintenance of chromosome integrity. The complex is involved in double-strand break (DSB) repair, DNA recombination, maintenance of telomere integrity, cell cycle checkpoint control and meiosis. The complex possesses single-strand endonuclease activity and double-strand-specific 3'-5' exonuclease activity, which are provided by MRE11A. NBN modulate the DNA damage signal sensing by recruiting PI3/PI4-kinase family members ATM, ATR, and probably DNA-PKcs to the DNA damage sites and activating their functions. NBN also functions in telomere length maintenance by generating the 3' overhang which serves as a primer for telomerase dependent telomere elongation. NBN is a major player in the control of intra-S-phase checkpoint and there is some evidence that NBN is involved in G1 and G2 checkpoints. Defects in NBN are the cause of Nijmegen breakage syndrome (NBS). Defects in NBN are a cause of genetic susceptibility to breast cancer (BC). Defects in NBN may be associated with aplastic anemia. Defects in NBN might play a role in the pathogenesis of childhood acute lymphoblastic leukemia (ALL). The antibody is specific to NBN. The full-length NBN protein, with an apparent molecular weight of 95 kDa and the two protein fragments of 26 and 70 kDa arising from the c.657_661del5 (p.K219fsX19) mutation, and the 80 kDa protein found in patient RR with the mutation c.742_743insGG leading to excision of exons 6 and 7 from the NBN mRNA are shown. (PMID: 26265251) The predicted molecular weight of NBN protein (p95) is 85kDa, actually detection result is about 95kDa(PMID: 23762398).
Arch Biochem Biophys
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