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Key Documents

NA26

Sigma-Aldrich

Anti-MSH2 (Ab-1) Mouse mAb (GB12)

liquid, clone GB12, Calbiochem®

Synonym(s):

Anti-Mismatch Repair Protein 2

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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

GB12, monoclonal

form

liquid

contains

≤0.1% sodium azide as preservative

species reactivity

human

should not react with

mouse

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 ... MSH2(4436)

General description

Purified mouse monoclonal antibody generated by immunizing BALB/c mice with the specified immunogen and fusing splenocytes with SP20 mouse myeloma cells. Recognizes the ~100 kDa MSH2 protein.
Recognizes the ~100 kDa MSH2 protein in HCT116 and SW480 cells and colon tissue.
This Anti-MSH2 (Ab-1) Mouse mAb (GB12) is validated for use in Frozen Sections, Immunoblotting, Immunoprecipitation, Paraffin Sections for the detection of MSH2 (Ab-1).

Immunogen

Human
an N-terminal fragment of human MSH2

Application

Frozen Sections (5 µg/ml)

Immunoblotting (1 µg/ml)

Immunoprecipitation (1 µg/reaction)

Paraffin Sections (3 µg/ml, heat pre-treatment required)

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

Negative Control
LoVo cells
Positive Control
HCT116 or SW480 cells or colon tissue

Other Notes

Bronner, C. E., et al. 1994. Nature368, 258.
Papadopoulos, N., et al. 1994. Science263, 1625.
Peltomäki, P. T. 1994. Annals of Medicine26, 215.
Fishel, R., et al. 1993. Cell75, 1027-1038, 1993.
Leach, F. S., et al. 1993. Cell75, 1215.
Lindbolm, A., et al. 1993. Nature Genetics5, 279.
For paraffin sections, pre-treat with heat for 20 min. Antibody should be titrated for optimal results in individual systems.

Legal Information

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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Leah C Young et al.
The American journal of pathology, 179(1), 411-421 (2011-06-28)
The fusion tyrosine kinase NPM-ALK is central to the pathogenesis of ALK-positive anaplastic large cell lymphoma (ALK(+)ALCL). We recently identified that MSH2, a key DNA mismatch repair (MMR) protein integral to the suppression of tumorigenesis, is an NPM-ALK-interacting protein. In
Laure Droy-Dupré et al.
United European gastroenterology journal, 2(4), 307-314 (2014-08-02)
Villous tumours of the rectosigmoid are historically defined as broad-based lesions associated with secretory diarrhoea. This study aimed to perform a reappraisal of these tumours, on the basis of newly introduced histological, immunohistochemical and molecular parameters. For this study, 22
Myrella Vlenterie et al.
Oncotarget, 6(33), 34680-34690 (2015-09-29)
Over 95% of all synovial sarcomas (SS) share a unique translocation, t(X;18), however, they show heterogeneous clinical behavior. We analyzed multiple SS to reveal additional genetic alterations besides the translocation. Twenty-six SS from 22 patients were sequenced for 409 cancer-related
Yasmijn J van Herwaarden et al.
Histopathology, 78(5), 749-758 (2020-10-25)
RNF43 is suggested to be involved in the serrated pathway towards colorectal cancer and encodes a transmembrane Ring-type E3 ubiquitin ligase that negatively regulates the Wnt pathway. This study aimed to elucidate the role of RNF43 gene variants in serrated
Gregory M Williams et al.
Proceedings of the National Academy of Sciences of the United States of America, 117(38), 23597-23605 (2020-09-10)
Trinucleotide repeat (TNR) expansions cause nearly 20 severe human neurological diseases which are currently untreatable. For some of these diseases, ongoing somatic expansions accelerate disease progression and may influence age of onset. This new knowledge emphasizes the importance of understanding

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