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Pack Size | Price | Availability | Quantity |
---|---|---|---|
50 μg | $498 | 7-10 days |
Biological Information | The specific activity was determined to be > 5 nmol/min/mg using casein as substrate. |
Description | 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. |
Species | Human |
Expression System | Baculovirus Insect Cells |
Tag | His, GST |
Accession Number | P36897-1 |
Synonyms | 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 |
Construction | The Human ALK5 (P36897-1) (Thr200-Mey503) was fused with the N-terminal polyhistidine-tagged GST tag at the N-terminus. |
Protein Purity | > 90 % as determined by SDS-PAGE |
Molecular Weight | 62.6 kDa (predicted) |
Endotoxin | < 1.0 EU/μg of the protein as determined by the LAL method. |
Formulation | Supplied as sterile 20 mM Tris, 500 mM Nacl, pH 8.5, 10% glycerol. |
Reconstitution | A Certificate of Analysis (CoA) containing reconstitution instructions is included with the products. Please refer to the CoA for detailed information. |
Stability & Storage | 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. |
Shipping | Kinases are highly recommended to be shipped at frozen temperature with blue ice or dry ice. |
Research 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 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). |
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