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N3162

Sigma-Aldrich

Anti-NBS1 (Nibrin) antibody produced in rabbit

affinity isolated antibody, buffered aqueous solution

Synonym(s):

Anti-p95 Protein of the MRE11/RAD50 Complex

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About This Item

MDL number:
MFCD07784851
UNSPSC Code:
12352203
NACRES:
NA.41

biological source

rabbit

conjugate

unconjugated

antibody form

affinity isolated antibody

antibody product type

primary antibodies

clone

polyclonal

form

buffered aqueous solution

mol wt

antigen 95 kDa (also recognizes 100 kDa band)

species reactivity

canine, human, rat, chimpanzee

technique(s)

immunoprecipitation (IP): 5-10 μg
indirect immunofluorescence: 5-10 μg/mL using Hela cells, fixed with paraformaldehyde/triton
microarray: suitable
western blot: 1-2 μg/mL using MCF7 nuclear extracts

UniProt accession no.

O60934

shipped in

dry ice

storage temp.

−20°C

target post-translational modification

unmodified

Gene Information

human ... NBN(4683)
mouse ... Nbn(27354)
rat ... Nbn(85482)

General description

NBS1 (Nibrin), also known as p95 protein of the meiotic recombination 11 homolog 1/DNA repair protein RAD50 (MRE11/RAD50) complex. NBS1 contains two domains found in the cell cycle checkpoint proteins forkhead-associated domain (FHA) and an adjacent breast cancer carboxyterminal domain (BRCT). NBS1 is one of the protein components of the double-strand break repair complex NBS1/MRE11/p50.
Nibrin (NBS1) is made up of 754 amino acids.

Immunogen

synthetic peptide corresponding to amino acids 692-706 of mouse NBS1 (nibrin), conjugated to KLH via an N-terminal added cysteine residue.

Application

Anti-NBS1 (Nibrin) antibody has been used:
  • in immunofluorence
  • in immunoblotting
  • in immunoprecipitation

Biochem/physiol Actions

NBS1 (Nibrin) was first isolated as a protein involved in DNA repair through analysis of mutations in patients with Nijmegen breakage syndrome (NBS). The majority of NBS patients bear a five base pairs deletion that leads to truncated NBS1, called 657del5. p95/NBS1 (nibrin) deficiency abrogates the formation of the MRE11/RAD50 ionizing radiation-induced foci, revealing a molecular link between DSB repair and cell cycle checkpoints activated by DNA damage.
Nibrin (NBS1) is involved in stabilizing genomes and has a role in development of cancers. It also takes part in the repair mechanism after double strand breaks in the DNA.

Physical form

Solution in 0.01 M phosphate buffered saline containing 15 mM sodium azide.

Disclaimer

Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.

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Storage Class Code

10 - Combustible liquids

WGK

WGK 3

Flash Point(F)

Not applicable

Flash Point(C)

Not applicable

Certificates of Analysis (COA)

Search for Certificates of Analysis (COA) by entering the products Lot/Batch Number. Lot and Batch Numbers can be found on a product’s label following the words ‘Lot’ or ‘Batch’.

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Nibrin, a novel DNA double-strand break repair protein, is mutated in Nijmegen breakage syndrome
Varon R, et al.
Cell, 93(3), 467-476 (1998)
Adel Alblihy et al.
Biomedicines, 9(1) (2021-01-14)
Platinum resistance seriously impacts on the survival outcomes of patients with ovarian cancers. Platinum-induced DNA damage is processed through DNA repair. NBS1 is a key DNA repair protein. Here, we evaluated the role of NBS1 in ovarian cancers. NBS1 expression
VRK1 phosphorylates and protects NBS1 from ubiquitination and proteasomal degradation in response to DNA damage
Monsalve D M, et al.
Biochimica et Biophysica Acta - Molecular Cell Research, 1863(4), 760-769 (2016)
Jana Suchánková et al.
Biology of the cell, 107(12), 440-454 (2015-10-21)
The DNA damage response is a fundamental, well-regulated process that occurs in the genome to recognise DNA lesions. Here, we studied kinetics of proteins involved in DNA repair pathways and their recruitment to DNA lesions during the cell cycle. In
Kelly Gray et al.
Circulation research, 116(5), 816-826 (2014-12-20)
DNA damage and the DNA damage response have been identified in human atherosclerosis, including in vascular smooth muscle cells (VSMCs). However, although double-stranded breaks (DSBs) are hypothesized to promote plaque progression and instability, in part, by promoting cell senescence, apoptosis
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