TGFBR1 / ALK-5 Protein

Transforming Growth Factor, Beta Receptor 1 / Activin receptor-like kinase 5

TGFBR1 / ALK-5 Products

TGFBR1 / ALK-5 Protein, Recombinant

Molecule	Species	Description //For Detailed Info. and Price------CLICK!	Cat. No
TGFBR1/ALK-5	Human	TGFBR1/ALK-5/Fc Protein, Recombinant	10459-H03H
TGFBR1/ALK-5	Human	TGFBR1 / ALK-5 / SKR4 (aa 200-503) Protein, Recombinant, with GST Tag	10459-H20B

10459-H03H:

1. Immobilized mouse CD105 at 10 µg/ml (100 µl/well) can bind human TGFRB1 with a linear ranger of 6.4-800 ng/ml. Measured by its binding ability in a functional ELISA.

2. Measured by its ability to bind human CD105 in a functional ELISA.

TGFBR1 / ALK-5 cDNA Clone

Molecule	Species	Description //For Detailed Info. and Price------CLICK!	Cat. No
TGFBR1/ALK-5	Human	Homo sapiens TGFBR1/ALK-5 cDNA Clone(NM_004612.2)	HG10459-M
TGFBR1/ALK-5	Mouse	Mus musculus TGFBR1/ALK-5 cDNA Clone	MG50238-M
TGFBR1/ALK-5	Canine	Canine TGFBR1 Gene cDNA Clone / ORF Clone	DG70047-G

TGFBR1 / ALK-5 Related Areas

Neuroscience>>Axon Guidance>>TGF-beta Family>>TGFBR1/ALK-5

Cancer>>Cancer Biomarkers>>TGFBR1/ALK-5

Cancer>>Growth Factor & Receptor>>TGF-beta Superfamily>>TGF-beta Family>>TGFBR1/ALK-5

Immunology>>Cytokine & Receptor>>TGF-beta Superfamily>>TGF-beta Superfamily Receptors>>TGFBR1/ALK-5

Immunology>>Adaptive Immunity>>T Cell>>Helper T Cell>>TGFBR1/ALK-5

TGFBR1 / ALK-5 Alternative Names

TGFBR1, ALK-5, ALK5, AAT5, ACVRLK4, LDS1A, LDS2A, SKR4, TGFR-1 [Homo sapiens]

Tgfbr1, Alk-5, ALK5, RP23-457P12.1, AU017191, TbetaR-I, TbetaRI, ESK2, TGFR-1 [Mus musculus]

TGFBR1 / ALK-5 Background

Transforming growth factor, beta receptor I, also known as Transforming growth factor-beta receptor type I , Serine / threonine-protein kinase receptor R4, Activin receptor-like kinase 5, SKR4, ALK-5, and TGFBR1, is a single-pass type I membrane protein which belongs to the protein kinase superfamily and TGFB receptor subfamily. TGFBR1 / ALK-5 is found in all tissues examined. It is most abundant in placenta and least abundant in brain and heart. TGF-beta functions as a tumor suppressor by inhibiting the cell cycle in the G1 phase. Administration of TGF-beta is able to protect against mammary tumor development in transgenic mouse models in vivo. Disruption of the TGF-beta/SMAD pathway has been implicated in a variety of human cancers, with the majority of colon and gastric cancers being caused by an inactivating mutation of TGF-beta RII. On ligand binding, TGFBR1 / ALK-5 forms a receptor complex consisting of two type I I and two type I transmembrane serine/threonine kinases. Type II receptors phosphorylate and activate type I receptors which auto-phosphorylate, then bind and activate SMAD transcriptional regulators. TGF-beta signaling via TGFBR1 / ALK-5 is not required in myocardial cells during mammalian cardiac development, but plays an irreplaceable cell-autonomous role regulating cellular communication, differentiation and proliferation in endocardial and epicardial cells. Defects in TGFBR1 / ALK-5 are the cause of Loeys-Dietz syndrome type 1A (LDS1A), Loeys-Dietz syndrome type 2A (LDS2A), and aortic aneurysm familial thoracic type 5 (AAT5).

TGFBR1 / ALK-5 Related Studies

Seki T, et al. (2006) Nonoverlapping expression patterns of ALK1 and ALK5 reveal distinct roles of each receptor in vascular development. Lab Invest. 86(2): 116-29. et al.
Piek E, et al. (1999) TGF-(beta) type I receptor/ALK-5 and Smad proteins mediate epithelial to mesenchymal transdifferentiation in NMuMG breast epithelial cells. J Cell Sci. 112 (24): 4557-68. et al.
Dudas M, et al. (2004) Tgf-beta3-induced palatal fusion is mediated by Alk-5/Smad pathway. Dev Biol. 266(1): 96-108.