Mouse TGF-beta  RIII Alexa Fluor® 350-conjugated Antibody

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 (1). Mouse TGF-beta RIII is synthesized as an 850 amino acid (aa) precursor that consists of a 22 aa signal sequence, a 763 extracellular domain (ECD), a 23 aa transmembrane region, and a 42 aa cytoplasmic tail. The large ECD contains heparan sulfate and chondroitin sulfate glycosaminoglycans, five potential N-linked glycosylation sites, and a zona pellucida-like domain from residues 454‑731 (1, 2). The short cytoplasmic domain is rich in serine and threonine, but has no discernible signaling structure typical of receptor kinases (2). Proteolysis at one of two potential juxtamembrane cleavage sites (Lys743Lys and Leu750AlaValVal) allows cells to release TGF-beta RIII in a soluble form (1, 2). Mouse TGF-beta RIII shares 94%, 82%, 80%, and 67% aa sequence identity with rat, human, porcine, and chicken TGF-beta RIII, respectively (2). In all of these species, TGF beta RIII contains 17 cysteines that are 100% conserved (2). TGF-beta RIII binds with high affinity to TGF-beta 1, TGF-beta 2, and TGF-beta 3 isoforms (1). TGF-beta RIII functions by binding, and then "presenting" ligand to TGF-beta type II receptors (1, 3). It also functions to limit ligand availability to the receptor via proteolysis which releases the soluble form of TGF beta RIII along with any bound factors, making them inaccessible to cell-surface receptors (1, 3). TGF-beta RIII can therefore 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 (4‑6). 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 (4, 7‑9). Low TGF-beta RIII expression also correlates with higher grade among a cohort of breast cancers (4, 10). Additionally, overexpression of TGF-beta RIII in MDA-231 human breast cancer cells and DU145 prostate cancer cells results in decreased tumor invasion in vitro and in vivo (4, 11, 12).