High impact information on Tgfbr3

• Recently, betaglycan and inhibin binding protein (InhBP/p120, also known as the product of immunoglobulin superfamily gene 1 [IGSF1]) were identified as candidate inhibin coreceptors, shedding light on the molecular basis of how inhibins may affect target cells [1].
• Betaglycan promoter activity was increased by RA and inhibited by the three isoforms of TGF-beta [2].
• These results indicate that betaglycan expression is up-regulated during myogenesis and that MyoD and RA modulate its expression by a mechanism that is independent of myogenin [2].
• Betaglycan is a membrane-anchored proteoglycan co-receptor that binds transforming growth factor beta (TGF-beta) via its core protein and basic fibroblast growth factor through its glycosaminoglycan chains [2].
• Forced expression of betaglycan in C(2)C(12) myoblasts increases their responsiveness to TGF-beta2, suggesting that it performs a TGF-beta presentation function in this cell lineage [2].

Biological context of Tgfbr3

• Betaglycan gene expression was detected in embryonic murine lungs undergoing branching morphogenesis in ex vivo culture [3].
• We therefore conclude that the abrogation of endogenous betaglycan attenuates endogenous autocrine and/or paracrine TGF-beta-mediated negative regulation of lung organogenesis [3].
• The primary structure of murine betaglycan, also known as transforming growth factor beta (TGF-beta) type III receptor, was deduced from the nucleotide sequence of a cDNA clone isolated from a heart library [4].
• Transfection of this cDNA into COS1 cells resulted in the expression of a membrane proteoglycan that binds TGF-beta and is recognized by antibodies raised against rat betaglycan [4].
• The KETc7 cDNA was cloned into the pcDNA3 plasmid alone or with the betaglycan signal peptide sequence (pTc-7 and pTc-sp7, respectively) [5].

Anatomical context of Tgfbr3

• Betaglycan was immunolocalized mainly to the epithelial cells in developing airways, a spatial distribution which overlaps with that of TGF-beta type II receptor [3].
• In this study we evaluated the expression of betaglycan during the C(2)C(12) skeletal muscle differentiation [2].
• Betaglycan expression, as determined by Northern and Western blot, was up-regulated during the conversion of myoblasts to myotubes [2].
• We report here that the apparent molecular mass of betaglycan from an osteoblast-enriched primary culture of fetal rat calvaria is decreased in response to bFGF, as detected by an increased electrophoretic migration of betaglycan [6].
• A similar dexamethasone enhancement of betaglycan mRNA expression was also observed in a preosteoblast-like cell line, RCT1 [7].

Associations of Tgfbr3 with chemical compounds

• Betaglycan expression is transcriptionally up-regulated during skeletal muscle differentiation. Cloning of murine betaglycan gene promoter and its modulation by MyoD, retinoic acid, and transforming growth factor-beta [2].
• The effect of dexamethasone on the betaglycan mRNA level was observed within 9 h and was sustained at least up to 48 h [7].
• Dexamethasone enhancement of betaglycan mRNA expression was blocked by actinomycin D, but it was not blocked by cycloheximide [7].
• Betaglycan (type III transforming growth factor-beta (TGF-beta) receptor) is a cell surface heparan/chondroitin sulfate proteoglycan that binds TGF-beta via its core protein and is abundantly expressed in osteoblastic cells [7].

Other interactions of Tgfbr3

• Abrogation of betaglycan attenuates TGF-beta-mediated inhibition of embryonic murine lung branching morphogenesis in culture [3].

Analytical, diagnostic and therapeutic context of Tgfbr3

• In myotubes, up-regulated betaglycan was also detectable by TGF-beta affinity labeling and immunofluorescence microscopy studies [2].

References