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Merck

C2363

Sigma-Aldrich

Monoclonal Anti-phospho-β-Catenin (pSer33) antibody produced in mouse

clone BC-76, purified immunoglobulin, buffered aqueous solution

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About This Item

MDL-Nummer:
UNSPSC-Code:
12352203
NACRES:
NA.41
Konjugat:
unconjugated
application:
ARR
WB
Klon:
BC-76, monoclonal
Speziesreaktivität:
human
citations:
5
Methode(n):
microarray: suitable
western blot: 5 μg/mL using total cell extracts of cultured HEK-293T cells treated with MG132

Biologische Quelle

mouse

Qualitätsniveau

Konjugat

unconjugated

Antikörperform

purified immunoglobulin

Antikörper-Produkttyp

primary antibodies

Klon

BC-76, monoclonal

Form

buffered aqueous solution

Speziesreaktivität

human

Methode(n)

microarray: suitable
western blot: 5 μg/mL using total cell extracts of cultured HEK-293T cells treated with MG132

Isotyp

IgM

UniProt-Hinterlegungsnummer

Versandbedingung

dry ice

Lagertemp.

−20°C

Posttranslationale Modifikation Target

phosphorylation (pSer33)

Angaben zum Gen

human ... CTNNB1(1499)

Verwandte Kategorien

Allgemeine Beschreibung

Cateninβ is a multifunctional protein, coded by CTNNB1 (cateninβ 1) gene. It is present in the intracellular side of the cytoplasmic membrane. It is located on human chromosome 3p22.1.

Immunogen

synthetic phosphopeptide corresponding to the region that contains serine 33 of human β-catenin.

Anwendung

Monoclonal Anti-phospho-β-Catenin (pSer33) antibody produced in mouse is suitable for microarray and western blotting at a concentration of 5μg/mL using total cell extracts of cultured HEK-293T cells treated with MG132.

Biochem./physiol. Wirkung

Catenin (cadherin-associated protein), β 1 (88kDa) protein is encoded by CTNNB1 gene in humans. It is also called as β-catenin. It is a dual function protein that regulates the coordination of cell-cell adhesion and gene transcription. Human β-catenin is located at band p21 on chromosome 3.
Mutations in β-catenin results in retinal vascular condition FEVR (familial exudative vitreoretinopathy). It participates in stimulating disease progression, providing BCR–ABL (fusion gene) kinase-independent resistance and LSC (leukemic stem cell) self-renewal. CTNNB1 plays an important role in cell-to-cell adhesion and transcriptional modulation in the Wnt signalling pathway.

Physikalische Form

Solution in 0.01 M phosphate buffered saline, pH 7.4, containing 1% bovine serum albumin and 15 mM sodium azide.

Haftungsausschluss

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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In der Dokumentenbibliothek finden Sie die Dokumentation zu den Produkten, die Sie kürzlich erworben haben.

Die Dokumentenbibliothek aufrufen

Combined inhibition of β-catenin and Bcr?Abl synergistically targets tyrosine kinase inhibitor-resistant blast crisis chronic myeloid leukemia blasts and progenitors in vitro and in vivo.
Zhou H, et al.
Leukemia, 31(10), 2065?2074-2065?2074 (2017)
P D McCrea et al.
Science (New York, N.Y.), 254(5036), 1359-1361 (1991-11-29)
Three cytoplasmic proteins, called catenins, bind to the cytoplasmic tail of the epithelial cell-cell adhesion molecule E-cadherin. The complementary DNA sequence was determined for the 92-kilodalton beta catenin of Xenopus laevis. The sequence is homologous to mammalian plakoglobin, a protein
β-Catenin pathway activation in breast cancer is associated with triple-negative phenotype but not with CTNNB1 mutation.
Geyer FC, et al.
Modern Pathology, 24(2), 209?231-209?231 (2011)
Defects in the Cell Signaling Mediator ?-Catenin Cause the Retinal Vascular Condition FEVR
Panagiotou ES, et al.
American Journal of Human Genetics, 100(6), 960-968 (2017)
Wnt signaling in oncogenesis and embryogenesis--a look outside the nucleus.
M Peifer et al.
Science (New York, N.Y.), 287(5458), 1606-1609 (2000-03-25)

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