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Recombinant Anti-OSMR Antibody (APC)

  • Product Information
  • Description
Catalog: C-FC-4222A
Product Type: FCM Antibody
Size: 25 Tests/100 Tests
Concentration: 10 μl/Test, 0.1 mg/ml
Reactivity: Human
Specificity: Human OSMR
Analysis mode: FCM
Host: Rabbit
Clonality: Monoclonal
Isotype: IgG
Alternate names: oncostatin M receptor
Form: Liquid
Shipping: This antibody is shipped as liquid solution at ambient temperature. Upon receipt, store it immediately at the temperature recommended below.
Storage: This antibody can be stored at 2℃-8℃ for twelve months without detectable loss of activity. 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.
Purification method: Protein A
Conjugation: APC
Immunogen: Recombinant Human OSMR / IL-31RB protein
Buffer: Aqueous solution containing 0.5% BSA and 0.09% sodium azide

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 of familial cutaneous lichen amyloidosis. PLCA1 is 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.

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