disease:Defects in OSMR are the cause of amyloidosis type 9 (AMYL9) [MIM:105250]; also known as primary cutaneous amyloidosis (PCA), primary localized cutaneous amyloidosis (PLCA), familial lichen amyloidosis or familial cutaneous lichen amyloidosis. AMYL9 is a hereditary primary amyloidosis characterized by localized cutaneous amyloid deposition. This condition usually presents with itching (especially on the lower legs) and visible changes of skin hyperpigmentation and thickening (lichenification) that may be exacerbated by chronic scratching and rubbing. The amyloid deposits probably reflect a combination of degenerate keratin filaments, serum amyloid P component, and deposition of immunoglobulins.,domain:The box 1 motif is required for JAK interaction and/or activation.,domain:The WSXWS motif appears to be necessary for proper protein folding and thereby efficient intracellular transport and cell-surface receptor binding.,function:Associates with IL31RA to form the IL31 receptor. Binds IL31 to activate STAT3 and possibly STAT1 and STAT5. Capable of transducing OSM-specific signaling events.,induction:Activated by oncostatin-M. Up-regulated by IFNG and lipopolysaccharide.,similarity:Belongs to the type I cytokine receptor family. Type 2 subfamily.,similarity:Contains 4 fibronectin type-III domains.,subunit:Heterodimer composed of OSMR and IL6ST (type II OSM receptor). Heterodimer with IL31RA to form the IL31 receptor.,tissue specificity:Expressed at relatively high levels in all neural cells as well as fibroblast, epithelial and a variety of tumor cell lines.,