Recombinant Human TGFBR1/ALK-5 Protein (His & Fc Tag)(Active) | PKSH031596

Recombinant Human TGFBR1/ALK-5 Protein (His & Fc Tag)(Active) | PKSH031596 | Gentaur US, UK & Europe Disrtribition

Synonyms: AAT5;ACVRLK4;ALK-5;ALK5;ESS1;LDS1;LDS1A;LDS2A;MSSE;SKR4;tbetaR-I;TGFR-1

Active Protein: Active protein

Activity: A DNA sequence encoding 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.

Protein Construction: A DNA sequence encoding 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.

Fusion Tag: C-His & Fc

Species: Human

Expressed Host: HEK293 Cells

Shipping: This product is provided as lyophilized powder which is shipped with ice packs.

Purity: > 85 % as determined by reducing SDS-PAGE.

Endotoxin: < 1.0 EU per µg as determined by the LAL method.

Stability and Storage: Generally, lyophilized proteins are stable for up to 12 months when stored at -20 to -80℃. Reconstituted protein solution can be stored at 4-8℃ for 2-7 days. Aliquots of reconstituted samples are stable at < -20℃ for 3 months.

Molecular Mass: 38.8 kDa

Formulation: Lyophilized from sterile PBS, pH 7.4

Reconstitution: Please refer to the printed manual for detailed information.

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).

Research Area: Signal Transduction, Cardiovascular, Cancer, metabolism, Stem cells