TGFBR3

Also known as BGCAN, betaglycan, transforming growth factor beta receptor 3

Gene data

TGFBR3

Name: transforming growth factor beta receptor 3
Type: protein-coding
Position: 91,680,343–91,906,335 (−)
Aliases: BGCAN, betaglycan
Ensembl: ENSG00000069702
RefSeq RNA: NM_001195683.2, NM_001195684.1, NM_003243.5, NR_036634.2, XM_006710867.3
RefSeq protein: NP_001182612.1, NP_001182613.1, NP_003234.2, XP_006710930.1, XP_047285203.1

This locus encodes the transforming growth factor (TGF)-beta type III receptor. The encoded 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. Alternatively spliced transcript variants encoding different isoforms have been identified for this gene.[provided by RefSeq, Sep 2010].

Gene Ontology

Biological process

response to hypoxia

Article

5 sections

Contents

Domains and function
See also
References
Further reading
External links

Betaglycan also known as Transforming growth factor beta receptor III (TGFBR3), is a cell-surface chondroitin sulfate / heparan sulfate proteoglycan >300 kDa in molecular weight. Betaglycan binds to various members of the TGF-beta superfamily of ligands via its core protein, and bFGF via its heparan sulfate chains. TGFBR3 is the most widely expressed type of TGF-beta receptor. Its affinity towards all individual isoforms of TGF-beta is similarly high and therefore it plays an important role as a coreceptor mediating the binding of TGF-beta to its other receptors - specifically TGFBR2. The intrinsic kinase activity of this receptor has not yet been described. In regard of TGF-beta signalling it is generally considered a non-signaling receptor or a coreceptor. By binding to various member of the TGF-beta superfamily at the cell surface it acts as a reservoir of TGF-beta.

Study of a mouse knock-out for the Tgfbr3 gene showed a fundamental effect on the correct development of organs and the overall viability of the animals used. Within the same study, no significant changes in Smad signalling (typical for TGF-beta cascade) were detected. This fact suggests that additional, as yet undescribed functions of betaglycan may be mediated by non-classical signalling pathways.