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Key Documents

NA26

Sigma-Aldrich

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

liquid, clone GB12, Calbiochem®

Sinónimos:

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

10 - Combustible liquids

wgk_germany

nwg

flash_point_f

Not applicable

flash_point_c

Not applicable


Certificados de análisis (COA)

Busque Certificados de análisis (COA) introduciendo el número de lote del producto. Los números de lote se encuentran en la etiqueta del producto después de las palabras «Lot» o «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
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
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
M B Weiss et al.
Cancer gene therapy, 14(1), 98-104 (2006-11-04)
The use of gene therapy to correct mutated or lost gene function for the treatment of human cancers has been an active, yet problematic area of biomedical research. Many technical difficulties, including efficient tissue-specific delivery, integration site specificity and general
Norma Keogh et al.
Nucleic acids research, 45(17), 10068-10078 (2017-10-04)
CTG•CAG repeat expansions cause at least twelve inherited neurological diseases. Expansions require the presence, not the absence, of the mismatch repair protein MutSβ (Msh2-Msh3 heterodimer). To evaluate properties of MutSβ that drive expansions, previous studies have tested under-expression, ATPase function

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