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Recombinant Rat TGFBR1 Protein (His tag)– MSE Supplies LLC

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Recombinant Rat TGFBR1 Protein (His tag)

SKU: PDER100074-100

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Recombinant Rat TGFBR1 Protein (His tag)

 

SKU # PDER100074
Expression Host E. coli

 

Description    

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 Leu 311-Met 501
Accession P80204
Calculated Molecular Weight 20.9 kDa
Observed Molecular Weight 28 kDa
Tag N-His
Bio-activity Not validated for activity
  

 

Properties

Purity > 95 % as determined by reducing SDS-PAGE.
Endotoxin Please contact us for more information.
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 sterile PBS, pH 7.4.
Normally 5% - 8% trehalose, mannitol and 0.01% Tween 80 are added as protectants before lyophilization.
Please refer to the specific buffer information in the printed manual.
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).