The specific activity was determined to be > 5 nmol/min/mg using casein as substrate.

ALK-5 Protein, Human, Recombinant (aa 200-503, His & GST) is expressed in Baculovirus insect cells with His and GST tag. The predicted molecular weight is 62.6 kDa and the accession number is P36897-1.

Human

Baculovirus Insect Cells

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

The Human ALK5 (P36897-1) (Thr200-Mey503) was fused with the N-terminal polyhistidine-tagged GST tag at the N-terminus.

> 90 % 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 the product under sterile conditions at -20°C to -80°C. Samples are stable for up to 12 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).