Recombinant Mouse ALK-5/TGFBR1 (C-Fc) | PKSM041408

Recombinant Mouse ALK-5/TGFBR1 (C-Fc) | PKSM041408 | Gentaur US, UK & Europe Disrtribition

Synonyms: AAT5; activin A receptor type II-like kinase, 53kD; ACVRLK4; ALK-5; ALK-5ALK5; LDS1A; LDS2A; SKR4; tbetaR-I; TGFB1R1; TGF-beta receptor type I; TGFbetaRI; TGFBR1; TGF-bRI; TGFR-1

Active Protein: N/A

Activity: Recombinant Mouse TGF-beta Receptor Type-1 is produced by our Mammalian expression system and the target gene encoding Leu30-Glu125 is expressed with a Fc tag at the C-terminus.

Protein Construction: Recombinant Mouse TGF-beta Receptor Type-1 is produced by our Mammalian expression system and the target gene encoding Leu30-Glu125 is expressed with a Fc tag at the C-terminus.

Fusion Tag: C-Fc

Species: Mouse

Expressed Host: Human Cells

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

Purity: > 95 % 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: 37.6 kDa

Formulation: Lyophilized from a 0.2 μm filtered solution of PBS, pH 7.4.

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

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.

Research Area: N/A