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Sigma-Aldrich

Anti-BRCA1 (Ab-1) Mouse mAb (MS110)

liquid, clone MS110, Calbiochem®

Synonym(s):

Anti-Breast Cancer Susceptibility Protein

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About This Item

UNSPSC Code:
12352203
NACRES:
NA.41

biological source

mouse

Quality Level

antibody form

purified antibody

antibody product type

primary antibodies

clone

MS110, monoclonal

form

liquid

contains

≤0.1% sodium azide as preservative

species reactivity

human

manufacturer/tradename

Calbiochem®

storage condition

do not freeze

isotype

IgG1

shipped in

wet ice

storage temp.

2-8°C

target post-translational modification

unmodified

Gene Information

human ... BRCA1(672)

General description

Anti-BRCA1 (Ab-1), mouse monoclonal, clone MS110, recognizes the ~220 kDa BRCA1 protein in MCF-7 cells. It is validated for WB, IF, IP, and frozen and paraffin sections.
Purified mouse monoclonal antibody generated by immunizing mice with the specified immunogen and fusing splenocytes with NS1 mouse myeloma cells. Recognizes the ~220 kDa BRCA1 protein.
Recognizes the ~220 kDa BRCA1 protein in MCF-7 cells. Does not cross-react with blood group antigens or growth factor receptors such as EGFR. Sold under license of U.S. Patent 5,753,441 and 6,162,897.

Immunogen

Epitope: within the N-terminal 304 amino acids of BRCA1
Human
recombinant human BRCA1

Application

Frozen Sections (see application reference)

Immunoblotting (2 µg/ml)

Immunofluorescence (see application reference)

Immunoprecipitation (see application reference)

Paraffin Sections (see application reference)

Packaging

Please refer to vial label for lot-specific concentration.

Warning

Toxicity: Standard Handling (A)

Physical form

In 50 mM sodium phosphate buffer, 0.2% gelatin, pH 7.5.

Analysis Note

Positive Control
MCF7 cells

Other Notes

Antibody should be titrated for optimal results in individual systems.
Scully, R., et al. 1996. Science272, 123.
Gudas, J.M., et al. 1996. Cell Growth Differ.7, 717.
Vaughn, J.P., et al. 1996. Cell Growth Differ.7, 711.
Goldgar, D.E. and Reilly, P.R. 1995. Nat. Genet.11, 113.
Merajver, S.D., et al. 1995. Clin. Can. Res.1, 539.
Merajver, S.D., et al. 1995. Nat. Genet.9, 439.
Struewing, J.P., et al. 1995. Nat. Genet.11, 198.
Thompson, M.E., et al. 1995. Nat. Genet.9, 444.
Futreal, P.A., et al. 1994. Science266, 120.
Miki, Y., et al. 1994. Science266, 66.
Wilson, C.A., et al. 1999. Nat. Genet.21, 236.

Legal Information

Sold under license of U.S. Patents 5,753,441 and 6,162,897.
CALBIOCHEM is a registered trademark of Merck KGaA, Darmstadt, Germany

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Storage Class Code

10 - Combustible liquids

WGK

nwg

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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Pierre Thouvenot et al.
Journal of cell science, 129(23), 4366-4378 (2016-11-02)
Understanding the effect of an ever-growing number of human variants detected by genome sequencing is a medical challenge. The yeast Saccharomyces cerevisiae model has held attention for its capacity to monitor the functional impact of missense mutations found in human
Drugging DNA repair to target T-ALL cells.
Yashodhara Dasgupta et al.
Leukemia & lymphoma, 59(7), 1746-1749 (2017-11-09)
Geon Kim et al.
Oncology letters, 17(6), 5023-5029 (2019-06-13)
Breast cancer type 1 susceptibility protein (BRCA1) is a tumor suppressor gene that encodes a nuclear phosphoprotein, which is involved in homologous recombination to repair DNA double strand breaks and maintain genome stability. When BRCA1 is mutated or altered, DNA
J Xu et al.
International journal of oncology, 34(4), 939-949 (2009-03-17)
BRCA1 dysfunction is associated with hormone-responsive cancers. We have identified a consensus SUMO modification site in the amino-terminal region of BRCA1/1a/1b proteins and the mutation in this potential SUMO acceptor site (K 109 to R) impaired their ability to bind
Lucie Portier et al.
International journal of molecular sciences, 22(3) (2021-01-31)
Tumor progression begins when cancer cells recruit tumor-associated stromal cells to produce a vascular niche, ultimately resulting in uncontrolled growth, invasion, and metastasis. It is poorly understood, though, how this process might be affected by deletions or mutations in the

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