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Recombinant Rat TGFBR1 protein (His Tag) (PDER100218)

All Size Price Qty
500μg $ 1440.00
100μg $ 488.00
20μg $ 158.00
1mg $ 2340.00
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For research use only.

Synonyms AAT5, ACVRLK4, ALK-5, Activin receptor like kinase 5, LDS1A, LDS2A, MSSE, SKR4, TGF-beta receptor type-1, TGFBR1, TbetaR I, Transforming growth factor beta receptor 1
Species Rat
Expression Host E.coli
Sequence Leu311-Met501
Accession P80204
Calculated Molecular Weight 20.9 kDa
Observed Molecular Weight 28 kDa
Tag N-His
Bio-activity Not validated for activity
Purity > 95% as determined by reducing SDS-PAGE.
Endotoxin < 10 EU/mg of the protein as determined by the LAL method
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.
Shipping This product is provided as lyophilized powder which is shipped with ice packs.
Formulation Lyophilized from a 0.2 μm filtered solution in PBS with 5% Trehalose and 5% Mannitol.
Reconstitution It is recommended that sterile water be added to the vial to prepare a stock solution of 0.5 mg/mL. Concentration is measured by UV-Vis.
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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