Characterization of the murine gene encoding the hyaluronan receptor RHAMM

The Hyaluronan Receptor RHAMM Regulates Extracellular-regulated Kinase

“…RHAMM has been reported to occur on the cell surface, intracellularly, and in the extracellular milieu (29 -31). This glycoprotein is encoded by a single gene (32) that is expressed as at least five isoforms in murine 10T1/2 fibroblasts (33,34). We report here that cell surface and intracellular RHAMM isoforms are required for the activation of ERK by PDGF and by mutant active Ras, respectively.…”

Toll-like Receptor 2 (TLR2), Transforming Growth Factor-β, Hyaluronan (HA), and Receptor for HA-mediated Motility (RHAMM) Are Required for Surfactant Protein A-stimulated Macrophage Chemotaxis

“…Highly purified and defined HA oligosaccharides, including HA, a six sugar oligosaccharide of HA, 8-, 14-, and 34-mer and a 900-kDa HA (HA900, HMW HA) that were free of endotoxin, protein, or nucleic acid, were the kind gifts of Seikagaku Corp. (Tokyo, Japan). Anti-RHAMM antibody (R36), generated in rabbits against amino acids 585-605 encoded in the full-length RHAMM cDNA (22,23), has been described previously (24). CD44 antibodies included KM81 (generously provided by Ellen Puré, Wistar Institute, University of Pennsylvania), CD44v3 (Calbiochem), and IM-7 (BD Biosciences).…”

Functional Aspects of the Hyaluronan and Chondroitin Sulfate Receptors

“…Receptor for hyaluronic acid mediated motility (RHAMM) is present as both a plasma membrane GPI-anchored HA receptor and an intracellular HA-binding protein lacking both transmembrane and cytoplasmic signal sequences [41]. Consequently, it is also called intracellular hyaluronic acidbinding protein (IHABP) or CD168.…”

“…Likewise, the mouse gene contains 14 exons and Western analyses of fibroblast cell lysates revealed two bands, a major 70 kDa band and a minor larger 73 kDa band encoding exon 4 [41]. An analysis of both breast and cervical cancers versus normal tissue revealed the expression of RHAMM splice variants lacking sequences encoded by only exon 4, only exon 13, and both exons 4 and 13, suggesting that increased expression of RHAMM-like splice variants contribute to an oncogenic phenotype [51,68].…”

“…It is thought that tumor necrosis factor-alpha (TNF-) induces sialidase activity to remove sialic acid from the N-glycans, which then allows HA-binding to the receptor [84]. The critical residues involved with HA binding include Arg 41 …”