All alk5 reagents are produced in house and quality controlled, including 1 alk5 Antibody, 39 alk5 Gene, 2 alk5 Lysate, 2 alk5 Protein, 2 alk5 qPCR. All alk5 reagents are ready to use.
Recombinant alk5 proteins are expressed by HEK293 Cells, Baculovirus-Insect Cells with fusion tags as C-human IgG1-Fc & His, N-GST & His.
alk5antibodies are validated with different applications, which are WB, ELISA, IHC-P.
alk5cDNA clones are full length sequence confirmed and expression validated. There are 13 kinds of tags for each alk5 of different species, especially GFP tag, OFP tag, FLAG tag and so on. There are three kinds of vectors for choice, cloning vector, expression vector and lentivrial expression vector.
Expression host: Baculovirus-Insect Cells
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).