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Merck

SAB5500002

Sigma-Aldrich

Anti-SMA antibody, Rabbit monoclonal

clone SP171, recombinant, expressed in proprietary host, affinity isolated antibody

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About This Item

UNSPSC-Code:
12352203
NACRES:
NA.41

Biologische Quelle

rabbit

Qualitätsniveau

Rekombinant

expressed in proprietary host

Konjugat

unconjugated

Antikörperform

affinity isolated antibody

Antikörper-Produkttyp

primary antibodies

Klon

SP171, monoclonal

Speziesreaktivität

human (tested)

Speziesreaktivität (Voraussage durch Homologie)

rabbit, rat, bovine, chicken, mouse, pig

Methode(n)

immunoblotting: 1:50
immunohistochemistry: 1:200

Isotyp

IgG

UniProt-Hinterlegungsnummer

Versandbedingung

wet ice

Lagertemp.

2-8°C

Posttranslationale Modifikation Target

unmodified

Angaben zum Gen

human ... ACTA2(59)

Allgemeine Beschreibung

Smooth muscle actin-α (SMA), also known as α2-smooth muscle actin (ACTA2), is a cytoskeleton protein in smooth muscle cells. It is encoded by the gene mapped to human chromosome 10q23.31. SMA is a vascular smooth muscle specific isoform,
Smooth muscle actin-alpha (SMA) is a cytoskeleton protein in smooth muscle cells and their derived tumors such as leiomyoma and leiomyosarcoma. It is also expressed in myoepithelial cells of the breast and salivary gland, but not in fibroblasts, striated muscle, and myocardium.

Immunogen

Synthetic peptide near the N-terminus of human SMA protein.

Anwendung

Anti-SMA antibody, Rabbit monoclonal has been used in:
  • western blotting
  • immunohistochemistry
  • immunofluorescence

Biochem./physiol. Wirkung

Smooth muscle actin-α (SMA)/ α2-smooth muscle actin (ACTA2) interacts with β-myosin heavy chain and facilitates vascular smooth muscle cell contraction. The encoded protein regulates c-MET (tyrosine-protein kinase Met) and focal adhesion kinase (FAK) expression in human lung adenocarcinoma cells, which positively and selectively mediates tumor progression. Thus, SMA can be used as a potential prognostic biomarker and/or target for treating metastatic lung adenocarcinoma. Mutation in the gene is associated with the development of patent ductus arteriosus (PDA), bicuspid aortic valve (BAV), iris flocculi, livedo reticularis, cerebrovascular accident (CVA) and stenosis of the aortic vasa vasorum. In addition, variation in the gene expression leads to thoracic aortic aneurysms and dissections (TAAD).

Leistungsmerkmale und Vorteile

Evaluate our antibodies with complete peace of mind. If the antibody does not perform in your application, we will issue a full credit or replacement antibody. Learn more.

Physikalische Form

0.1 ml rabbit monoclonal antibody purified by protein A/G in PBS/1% BSA buffer pH 7.6 with less than 0.1% 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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Lagerklassenschlüssel

10 - Combustible liquids

WGK

WGK 2

Flammpunkt (°F)

Not applicable

Flammpunkt (°C)

Not applicable


Analysenzertifikate (COA)

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

Die Dokumentenbibliothek aufrufen

Macrophage-derived MCPIP1 mediates silica-induced pulmonary fibrosis via autophagy.
Liu H, et al.
Particle and Fibre Toxicology, 13(1), 55-55 (2016)
BBC3 in macrophages promoted pulmonary fibrosis development through inducing autophagy during silicosis.
Liu H, et al.
Cell Death & Disease, 8(3), e2657-e2657 (2017)
Ying-Chun Zhu et al.
International journal of molecular medicine, 40(4), 1165-1171 (2017-08-30)
Transforming growth factor-β (TGF-β) induces epithelial-mesenchymal transition (EMT) primarily via a Smad‑dependent mechanism. However, there are few studies available on TGF-β-induced EMT through the activation of non‑canonical pathways. In this study, the Cdc42-interacting protein-4 (CIP4)/partitioning-defective protein 6 (Par6) pathway was investigated in TGF-β1‑stimulated NRK-52E cells. Rat
The genetics and genomics of thoracic aortic disease.
Pomianowski P and John A E
Journal of Cardiothoracic Surgery, 2(3), 271-271 (2013)
Suppression of CIP4/Par6 attenuates TGF-β1-induced epithelial-mesenchymal transition in NRK-52E cells.
Zhu Y-C, et al.
International Journal of Molecular Medicine, 40(4), 1165-1171 (2017)

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