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224M-1

Sigma-Aldrich

Beta-Catenin (14) Mouse Monoclonal Antibody

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About This Item

UNSPSC Code:
12352203
NACRES:
NA.41

Pricing and availability is not currently available.

biological source

mouse

Quality Level

conjugate

unconjugated

antibody form

culture supernatant

antibody product type

primary antibodies

clone

14, monoclonal

description

For In Vitro Diagnostic Use in Select Regions (See Chart)

form

buffered aqueous solution

species reactivity

human

packaging

vial of 0.1 mL concentrate (224M-14)
vial of 0.5 mL concentrate (224M-15)
bottle of 1.0 mL predilute (224M-17)
vial of 1.0 mL concentrate (224M-16)
bottle of 7.0 mL predilute (224M-18)

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This Item
420M-1MABF316104-958
conjugate

unconjugated

conjugate

unconjugated

conjugate

unconjugated

conjugate

-

antibody form

culture supernatant

antibody form

culture supernatant

antibody form

purified antibody

antibody form

purified immunoglobulin

biological source

mouse

biological source

mouse

biological source

mouse

biological source

mouse

species reactivity

human

species reactivity

human

species reactivity

human

species reactivity

rat, mouse, human

clone

14, monoclonal

clone

MRQ-5, monoclonal

clone

12F7, monoclonal

clone

7F7.2, monoclonal

storage temp.

2-8°C

storage temp.

2-8°C

storage temp.

-

storage temp.

-

General description

Beta-Catenin is a 92 kD protein normally found in the cytoplasm of the cell in the submembranous location. This protein is associated with E-Cadherin and may be essential for the function of E-Cadherin. Mutations in the Beta-Catenin gene result in nuclear accumulation of this protein. Nuclear accumulation of this protein has been demonstrated in fibromatosis lesions of the breast and abdomen and therefore is useful in differentiating this lesion from other spindle cell lesions that may occur in these locations. Nuclear accumulation of Beta-Catenin has also been demonstrated in colorectal carcinoma.

Quality


IVD

IVD

IVD

RUO

Linkage

Beta-Catenin Positive Control Slides, Product No. 224S, are available for immunohistochemistry (formalin-fixed, paraffin-embedded sections).

Physical form

Solution in Tris Buffer, pH 7.3-7.7, with 1% BSA and <0.1% Sodium Azide

Preparation Note

Download the IFU specific to your product lot and formatNote: This requires a keycode which can be found on your packaging or product label.

Other Notes

For Technical Service please contact: 800-665-7284 or email: service@cellmarque.com

Legal Information

Cell Marque is a registered trademark of Merck KGaA, Darmstadt, Germany

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Wei Min et al.
The American journal of Chinese medicine, 42(3), 709-727 (2014-05-30)
Ultraviolet A (UVA) radiation contributes to skin photoaging. Baicalin, a plant-derived flavonoid, effectively absorbs UV rays and has been shown to have anti-oxidant and anti-inflammatory properties that may delay the photoaging process. In the current study, cultured human skin fibroblasts
Jia-Ming Xie et al.
Cancer research, 74(18), 5127-5138 (2014-08-03)
The p53-induced glycolysis and apoptosis regulator (TIGAR) inhibits glycolysis, resulting in higher intracellular NADPH, lower reactive oxygen species (ROS) and autophagy activity. In this study, we investigated whether TIGAR might exert dual impacts on cancer cell survival based on its
Timothy S Pardee et al.
Oncotarget, 5(12), 4170-4179 (2014-06-26)
F10 is an oligonucleotide based on the thymidylate synthase (TS) inhibitory 5-fluorouracil (5-FU) metabolite, 5-fluoro-2'-deoxyuridine-5'-O-monophosphate. We sought to determine the activity of F10 against preclinical models of acute lymphoblastic leukemia (ALL). F10 treatment resulted in robust induction of apoptosis that
C Leufke et al.
Oncogene, 33(27), 3506-3518 (2013-08-21)
The incidence of skin cancer is increasing worldwide and cutaneous squamous cell carcinomas (SCCs) are associated with considerable morbidity and mortality, particularly in immunosuppressed individuals ('carcinomatous catastrophy'). Yet, molecular mechanisms are still insufficiently understood. Besides ultraviolet (UV)-indicative mutations, chromosomal aberrations
Maja T Tomicic et al.
Cancer research, 74(19), 5585-5596 (2014-08-16)
DNA repair processes are a key determinant of the sensitivity of cancer cells to DNA-damaging chemotherapeutics, which may induce certain repair genes as a mechanism to promote resistance. Here, we report the results of a screen for repair genes induced

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