|Datasheet||Specific References||Reviews||Related Products||Protocols|
|Recombinant Human OSMR / IL-31RB protein (Catalog#11226-H08H)|
|10 μl/Test, 0.1 mg/ml|
|Aqueous solution containing 0.5% BSA and 0.09% sodium azide|
|This antibody was obtained from a rabbit immunized with purified, recombinant Human OSMR / IL-31RB (rh OSMR / IL-31RB; Catalog#11226-H08H; NP_003990.1; Met1-Met740) and conjugated with APC under optimum conditions, the unreacted APC was removed.|
|Human OSMR / IL-31RB|
|This antibody is stable for 12 months from date of receipt when stored at 2℃-8℃. Protected from prolonged exposure to light. Do not freeze !|
Sodium azide is toxic to cells and should be disposed of properly. Flush with large volumes of water during disposal.
Oncostatin-M specific receptor subunit beta also known as the oncostatin M receptor (OSMR) and Interleukin-31 receptor subunit beta (IL-31RB), is one of the receptor proteins for oncostatin M. OSMR is a member of the type I cytokine receptor family. IL-31RB/OSMR heterodimerizes with interleukin 6 signal transducer to form the type II oncostatin M receptor and with interleukin 31 receptor A to form the interleukin 31 receptor, and thus transduces oncostatin M and interleukin 31 induced signaling events. Mutations in IL-31RB/OSMR have been associated with familial primary localized cutaneous amyloidosis. Defects in IL-31RB/OSMR are the cause of amyloidosis primary localized cutaneous type 1 (PLCA1), also known as familial lichen amyloidosis or familial cutaneous lichen amyloidosis. PLCA1 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.