alk5

ALK-5 Protein, Human, Recombinant (His & hFc) is expressed in HEK293 mammalian cells with His and hFc tag. The predicted molecular weight is 38.1 kDa and the accession number is P36897-1.

ALK-5 Protein, Human, Recombinant (hFc) is expressed in HEK293 mammalian cells with hFc tag. The predicted molecular weight is 36.87 kDa and the accession number is P36897-1.

ALK-5 Protein, Human, Recombinant (aa 200-503, His & GST) is expressed in Baculovirus insect cells with His and GST tag. The predicted molecular weight is 62.6 kDa and the accession number is P36897-1.

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.

TMED10 disrupts the complex formation between TGF-beta type I (also termed ALK5) and type II receptors (TbetaRII). Misexpression studies revealed that TMED10 attenuated TGF-beta-mediated signaling. A 20-amino acid-long region from Thr(91) to Glu(110) within the extracellular region of TMED10 was found to be crucial for TMED10 interaction with both ALK5 and TbetaRII. Synthetic peptides corresponding to this region inhibit both TGF-beta-induced Smad2 phosphorylation and Smad-dependent transcriptional reporter activity. In a xenograft cancer model, where previously TGF-beta was shown to elicit tumor-promoting effects, gain-of-function and loss-of-function studies for TMED10 revealed a decrease and increase in the tumor size, respectively. That TMED10 expression levels are the key determinant for efficiency of TGF-beta receptor complex formation and signaling.

transforming growth factor beta receptor 1 (TGFBR1), a key stimulator of tumor proliferation and metastasis, was a direct target of miR‑98‑5p. miR‑98‑5p overexpression resulted in the downregulation of TGFBR1 and the suppression of the viability, proliferation, migration and invasion of A549 and H1299 cells. TGFBR1 Protein, Human, Recombinant (mFc & Avi) is expressed in HEK293 mammalian cells with C-mFc-Avi tag. The predicted molecular weight is 38.2 kDa and the accession number is P36897-1.

transforming growth factor beta receptor 1 (TGFBR1), a key stimulator of tumor proliferation and metastasis, was a direct target of miR‑98‑5p. miR‑98‑5p overexpression resulted in the downregulation of TGFBR1 and the suppression of the viability, proliferation, migration and invasion of A549 and H1299 cells. TGFBR1 Protein, Human, Recombinant (mFc & Avi), Biotinylated is expressed in HEK293 mammalian cells with C-mFc-Avi tag. The predicted molecular weight is 38.2 kDa and the accession number is P36897-1.