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Key Documents

SAB4502958

Sigma-Aldrich

Anti-TGF β Receptor I antibody produced in rabbit

affinity isolated antibody

Synonym(s):

ADRB2, ALK-5, Activin receptor-like kinase 5, ESK2, SKR4

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About This Item

UNSPSC Code:
12352203
NACRES:
NA.41

biological source

rabbit

conjugate

unconjugated

antibody form

affinity isolated antibody

antibody product type

primary antibodies

clone

polyclonal

form

buffered aqueous solution

mol wt

antigen 55 kDa

species reactivity

mouse, human, rat

concentration

~1 mg/mL

technique(s)

ELISA: 1:10000
immunofluorescence: 1:100-1:500
western blot: 1:500-1:1000

NCBI accession no.

UniProt accession no.

shipped in

wet ice

storage temp.

−20°C

target post-translational modification

unmodified

Gene Information

human ... TGFBR1(7046)

Related Categories

General description

Anti-TGF β Receptor I Antibody detects endogenous levels of total TGF β Receptor I protein.
Transforming growth factor β receptor-1 (TGF-β R1), also known as activin receptor-like kinase 5 (ALK5) receptor, is encoded by the gene mapped to human chromosome 9q22.3. It is widely expressed in human tissues.

Immunogen

The antiserum was produced against synthesized peptide derived from human TGF beta Receptor I.

Immunogen Range: 131-180

Application

Anti-TGF β Receptor I antibody produced in rabbit has been used for:
  • Immunohistochemistry
  • Western blotting
  • Immunofluroscence

Biochem/physiol Actions

Transforming growth factor β receptor-1 (TGF-β R1) plays an essential role in carbon nanotube-induced fibrogenesis by enhancing collagen production in lung fibroblasts. TβR-dependent signals plays a crucial role in cell growth and differentiation, and polymorphism or mutation of TGF-β R1 leads to head and neck cancer. Activin receptor-like kinase 5 (ALK5) or TGF-β R1 promotes the phosphorylation of small mothers against decapentaplegic (Smad) 2 and Smad3. Activated ALK5 inhibits migration and proliferation of endothelial cells (ECs). ALK1 acts as an antagonist for ALK5/Smad signaling. Mutation of TGF-β R1 can also cause autosomal dominant skin cancer called multiple self-healing squamous epithelioma (MSSE) or Ferguson-Smith disease (FSD).

Features and Benefits

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.

Physical form

Rabbit IgG in phosphate buffered saline (without Mg2+ and Ca2+), pH 7.4, 150mM NaCl, 0.02% sodium azide and 50% glycerol.

Disclaimer

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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Storage Class

10 - Combustible liquids

wgk_germany

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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Rongfen Gao et al.
Oxidative medicine and cellular longevity, 2023, 5012474-5012474 (2023-02-15)
Both epithelial-to-mesenchymal (EMT) and endothelial-to-mesenchymal (EndMT) transitions have shown to contribute to the development and progression of kidney fibrosis. It has been reported that apelin, a regulatory peptide, alleviates EMT by inhibiting the transforming growth factor β (TGFβ) pathway in
Wenlong Yang et al.
Journal of molecular and cellular cardiology, 134, 119-130 (2019-07-13)
Trimethylamine N-oxide (TMAO), a gut microbe-derived metabolite of dietary choline and other trimethylamine-containing nutrients, has been associated with poor prognosis in coronary heart disease. However, the role and underlying mechanisms of TMAO in the cardiac fibrosis after myocardial infarction (MI)
Feng Zhang et al.
BMC medical genomics, 17(1), 56-56 (2024-02-21)
Liver fibrosis is a major global healths problem; nevertheless, its molecular mechanism are not completely clear. This study aimed to build a lncRNA-miRNA-mRNA network, identify potentially related lncRNAs, and explore the pathogenesis of liver fibrosis. We used the Gene Expression
T J Knobloch et al.
Mutation research, 479(1-2), 131-139 (2001-07-27)
Transforming growth factor-beta receptor (TbetaR)-dependent signals are critical for cell growth and differentiation and are often disrupted during tumorigenesis. The entire coding region of TbetaR-I and flanking intron sequences from 30 head and neck carcinomas were examined for alterations using
Marie José Goumans et al.
Molecular cell, 12(4), 817-828 (2003-10-29)
Transforming growth factor-beta (TGFbeta) regulates the activation state of the endothelium via two opposing type I receptor/Smad pathways. Activin receptor-like kinase-1 (ALK1) induces Smad1/5 phosphorylation, leading to an increase in endothelial cell proliferation and migration, while ALK5 promotes Smad2/3 activation

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