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TGFBR1 Protein, Mouse, Recombinant (hFc)

TGFBR1 Protein, Mouse, Recombinant (hFc)
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TGFBR1 Protein, Mouse, Recombinant (hFc)

Catalog No. TMPJ-01178
TGF-beta RI, also called ALK-5, is an approximately 55 kDa type I transmembrane serine/threonine receptor kinase. In the presence of TGF-beta, TGF-beta RI forms a complex with, and is phosphorylated by, TGF-beta RII. Phosphorylated TGF-beta RI can then transiently bind and phosphorylate Smad2 and Smad3. 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. TGF-beta RI is likely important during development, since mice deficient for TGF-beta RI die at midgestation with severe defects in vascular development of the yolk sac and placenta, and an absence of circulating red blood cells. Furthermore, TGF-beta RI appears to be involved in proper lymphatic network development.
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Pack SizePriceAvailabilityQuantity
10 μg$1407-10 days
50 μg$4237-10 days
500 μg$2,1207-10 days
1 mg$3,1707-10 days
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Biological Description

Biological Information
Activity has not been tested. It is theoretically active, but we cannot guarantee it. If you require protein activity, we recommend choosing the eukaryotic expression version first.
Description
TGF-beta RI, also called ALK-5, is an approximately 55 kDa type I transmembrane serine/threonine receptor kinase. In the presence of TGF-beta, TGF-beta RI forms a complex with, and is phosphorylated by, TGF-beta RII. Phosphorylated TGF-beta RI can then transiently bind and phosphorylate Smad2 and Smad3. 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. TGF-beta RI is likely important during development, since mice deficient for TGF-beta RI die at midgestation with severe defects in vascular development of the yolk sac and placenta, and an absence of circulating red blood cells. Furthermore, TGF-beta RI appears to be involved in proper lymphatic network development.
Species
Mouse
Expression System
HEK293 Cells
TagC-hFc
Accession NumberQ64729
Synonyms
ALK-5,ALK-5ALK5,TGFβRI,tβR-I,LDS1A,TGFbetaRI,TGFB1R1,activin A receptor type II-like kinase, 53kD,TGF-β receptor type I,LDS2A,TGF-bRI,ACVRLK4,TGFR-1,SKR4,TGFBR1,TGF-beta receptor type I,AAT5,tbetaR-I
Amino Acid
Leu30-Glu125
Construction
Leu30-Glu125
Protein Purity
Greater than 95% as determined by reducing SDS-PAGE. (QC verified)
Molecular Weight40-60 KDa (reducing condition)
Endotoxin< 0.1 ng/µg (1 EU/µg) as determined by LAL test.
FormulationLyophilized from a solution filtered through a 0.22 μm filter, containing PBS, pH 7.4.
Reconstitution
Reconstitute the lyophilized protein in distilled water. The product concentration should not be less than 100 μg/ml. Before opening, centrifuge the tube to collect powder at the bottom. After adding the reconstitution buffer, avoid vortexing or pipetting for mixing.
Stability & Storage
Lyophilized powders can be stably stored for over 12 months, while liquid products can be stored for 6-12 months at -80°C. For reconstituted protein solutions, the solution can be stored at -20°C to -80°C for at least 3 months. Please avoid multiple freeze-thaw cycles and store products in aliquots.
ShippingIn general, Lyophilized powders are shipping with blue ice. Solutions are shipping with dry ice.
Research Background
TGF-beta RI, also called ALK-5, is an approximately 55 kDa type I transmembrane serine/threonine receptor kinase. In the presence of TGF-beta, TGF-beta RI forms a complex with, and is phosphorylated by, TGF-beta RII. Phosphorylated TGF-beta RI can then transiently bind and phosphorylate Smad2 and Smad3. 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. TGF-beta RI is likely important during development, since mice deficient for TGF-beta RI die at midgestation with severe defects in vascular development of the yolk sac and placenta, and an absence of circulating red blood cells. Furthermore, TGF-beta RI appears to be involved in proper lymphatic network development.

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Keywords