1. Measured by its binding ability in a functional ELISA. Immobilized mouse CD105 at 10 μg/ml (100 μl/well) can bind human TGFRB1 with a linear range of 6.4-800 ng/ml. 2. Measured by its ability to bind human CD105 in a functional ELISA.

ALK-5 Protein, Human, Recombinant (His & hFc) is expressed in HEK293 mammalian cells with His and hFc tag. The predicted molecular weight is 38.1 kDa and the accession number is P36897-1.

Human

HEK293 Cells

tβR-I,ALK5,AAT5,TGFR-1,LDS2A,LDS1,transforming growth factor, beta receptor 1,ACVRLK4,SKR4,LDS1A,tbetaR-I,ALK-5,ESS1,MSSE,transforming growth factor, β receptor 1

The Human TGFBR1 (NP_004603.1) extracellular domain (Met 1-Glu 125) was fused with the C-terminal polyhistidine-tagged Fc region of Human IgG1 at the C-terminus.

> 85 % as determined by SDS-PAGE

A Certificate of Analysis (CoA) containing reconstitution instructions is included with the products. Please refer to the CoA for detailed information.

It is recommended to store recombinant proteins at -20°C to -80°C for future use. Lyophilized powders can be stably stored for over 12 months, while liquid products can be stored for 6-12 months at -80°C. For reconstituted protein solutions, the solution can be stored at -20°C to -80°C for at least 3 months. Please avoid multiple freeze-thaw cycles and store products in aliquots.

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 that 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).