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.
| 説明 |
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 Host |
HEK293 Cells
|
| Tag |
C-hFc
|
| Accession Number |
Q64729
|
| 別名 |
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)
|
| 分子量 |
40-60 KDa (reducing condition)
|
| Endotoxin |
< 0.1 ng/µg (1 EU/µg) as determined by LAL test.
|
| Formulation |
Lyophilized 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℃. For reconstituted proteinsolutions, 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.
|
| Shipping |
In 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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