Transforming growth factor-β (TGF-β) is an essential regulator in the processes of development, cell proliferation, and extracellular matrix deposition. TGF-β regulates cellular processes by binding to three high-affinity cell surface receptors: TGF-β receptor type I (TGF-β-RI), TGF-β receptor type II (TGF-β-RII), and TGF-ββ receptor type III (TGF-β-RIII). TGF-β RII is consists of a C-terminal protein kinase domain and an N-terminal ectodomain and belongs to transforming growth factor-beta (TGF-β) receptor subfamily. TGF-β RII has a protein kinase domain which can form a heterodimeric complex with another receptor protein and bind TGF-beta. This receptor/ligand complex phosphorylates protein will enter the nucleus and regulate the transcription of a subset of genes related to cell proliferation.
Betaglycan also known as transforming growth factor beta receptor III (TGFBR3), is a cell-surface chondroitin sulfate / heparan sulfate proteoglycan. TGFBR3 is a transforming growth factor (TGF)-beta type III receptor. This receptor is a membrane proteoglycan that often functions as a co-receptor with other TGF-beta receptor superfamily members. Ectodomain shedding produces soluble TGFBR3, which may inhibit TGFB signaling. Decreased expression of this receptor has been observed in various cancers. TGFBR3 is the TGF-β component most commonly downregulated among localized human prostate cancer studies. TGFBR3 knockdown led to focus formation and enhanced expression of CD133, a marker found on prostate cancer stem cells. TGFBR3 is an accessory receptor that binds to and modulates the activities of both transforming growth factor-beta (TGFβ) and inhibin, two members of the TGFβ superfamily of growth factors that regulate many aspects of reproductive biology. TGFBR3 is known to be expressed in adult testis and ovary, but little is known about this receptor during gonadogenesis.
Transforming growth factor beta receptor III (TGF-beta RIII; also betaglycan) is a ubiquitously expressed, 280 kDa type I transmembrane proteoglycan member of the TGF-beta superfamily of proteins. This receptor is a membrane proteoglycan that often functions as a co-receptor with other TGF-beta receptor superfamily members. TGF-beta RIII can enhance or inhibit cell signaling. TGF-beta RIII has been shown to play an essential role in the formation of the atrioventricular cushion and coronary vessels during development of the heart. TGF beta RIII also plays a role in many cancers. Increased expression of TGF beta RIII is found in higher grade lymphomas, and reduced expression of TGF beta RIII is found with advanced stage neuroblastomas and ovarian carcinomas. Low TGF-beta RIII expression also correlates with higher grade among a cohort of breast cancers. TGFBR3 is known to be expressed in adult testis and ovary, but little is known about this receptor during gonadogenesis.
Transforming growth factor beta 1 (TGFβ1) is the prototype of a growing superfamily of peptide growth factors and plays a prominent role in a variety of cellular processes, including cell-cycle progression, cell differentiation, reproductive function, development, motility, adhesion, neuronal growth, bone morphogenesis, wound healing, and immune surveillance. TGF-β1, TGF-β2 and TGF-β3 signal via the same heteromeric receptor complex, consisting of a ligand binding TGF-β receptor type II (TβR-II), and a TGF-β receptor type I (TβR-I). Signal transduction from the receptor to the nucleus is mediated via SMADs. TGF-β expression is found in cartilage, bone, teeth, muscle, heart, blood vessels, haematopoitic cells, lung, kidney, gut, liver, eye, ear, skin, and the nervous system.
Protein-glutamine gamma-glutamyltransferase 2 (TGM2) is a 78-kDa, calcium dependent enzyme,It belongs to the transglutaminase superfamily and transglutaminase family. The protein encoded by this TGM2 gene acts as a monomer, is induced by retinoic acid, and appears to be involved in apoptosis. TGM2 is the autoantigen implicated in celiac disease. Two transcript variants encoding different isoforms have been found for this gene.
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