Recombinant Human Transforming Growth Factor Receptor Type II/TGFBR2 (C-Fc)

Source: Human Cells. MW :42.6kD. Recombinant Human TGF beta receptor II is produced by our Mammalian expression system and the target gene encoding Thr23-Asp159 is expressed with a Fc tag at the C-terminus. TGFBR2 is a single-pass type I membrane protein and contains one protein kinase domain. TGFBR2 exsits as a heterodimeric complex with another receptor protein and binds TGF-beta. Signals triggered through the TGF-beta receptor complex prompt various responses by the cell. One such response is to inhibit cell growth and division. Based on this action, the TGF-beta receptor type 2 is sometimes called a tumor suppressor. Defects in TGFBR2 have been associated with Marfan syndrome, Loeys-Deitz aortic aneurysm syndrome, Osler-Weber-Rendu syndrome and the development of various types of tumors. Protein function: Transmembrane serine/threonine kinase forming with the TGF-beta type I serine/threonine kinase receptor, TGFBR1, the non- promiscuous receptor for the TGF-beta cytokines TGFB1, TGFB2 and TGFB3. Transduces the TGFB1, TGFB2 and TGFB3 signal from the cell surface to the cytoplasm and is thus regulating a plethora of physiological and pathological processes including cell cycle arrest in epithelial and hematopoietic cells, control of mesenchymal cell proliferation and differentiation, wound healing, extracellular matrix production, immunosuppression and carcinogenesis. The formation of the receptor complex composed of 2 TGFBR1 and 2 TGFBR2 molecules symmetrically bound to the cytokine dimer results in the phosphorylation and the activation of TGFRB1 by the constitutively active TGFBR2. Activated TGFBR1 phosphorylates SMAD2 which dissociates from the receptor and interacts with SMAD4. The SMAD2-SMAD4 complex is subsequently translocated to the nucleus where it modulates the transcription of the TGF-beta-regulated genes. This constitutes the canonical SMAD-dependent TGF-beta signaling cascade. Also involved in non- canonical, SMAD-independent TGF-beta signaling pathways. [The UniProt Consortium]