1. Capture Antibody 0.5 mg/mL of rabbit anti-OSMR monoclonal antibody, Dilute to a working concentration of 1 μg/mL in CBS before coating. (Catalog: # 11226-R002) 2. Detection Antibody 0.5 mg/mL mouse anti-OSMR monoclonal antibody conjugated to horseradish-peroxidase (HRP). Dilute to working concentration of 0.5 μg/mL in detection antibody dilution buffer before use. (Catalog: # 11226-MM01) 3. Standard Each vial contains 600 ng of recombinant OSMR. Reconstitute with 1 mL detection antibody dilution buffer. After reconstitution, store at -20℃ to -80℃ in a manual defrost freezer. A seven-point standard curve usi ng 2-fold serial dilutions in sample dilution buffer, and a high standard of 15,000 pg/mL is recommended.
This OSMR Matched ELISA Antibody Pair Set,Human is a solid phase sandwich ELISA for quantitative determination of Human OSMR . It contains Human OSMR capture antibody, Human OSMR detector antibody
and a highly purified
recombinant Human OSMR protein. This Pair Set is at affordable price for researchers.
This Matched ELISA Antibody Pair Set is shipped at ambient temperature.
Capture Antibody: Aliquot and store at -20℃ to -80℃ for up to 6 months from date of receipt. Avoid repeated freeze-thaw cycles. Detection Antibody: Store at 4℃ and protect it from prolonged exposure to light for up to 6 months from date of receipt. DO NOT FREEZE! Standard: Store lyophilized standard at -20℃ to -80℃ for up to 6 months from date of receipt. Aliquot and store the reconstituted Standard at -80℃ for up to 1 month. Avoid repeated freeze-thaw cycles.
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.
oncostatin M receptor
Arita K, et al.. (2008) Oncostatin M Receptor-β Mutations Underlie Familial Primary Localized Cutaneous Amyloidosis. Am J Hum. Genet. 82 (1): 73-80.
Malaval L, et al.. (2005) GP130/OSMR is the only LIF/IL-6 family receptor complex to promote osteoblast differentiation of calvaria progenitors. J Cell Physiol. 204(2): 585-93.
Lin MW, et al.. (2010) Novel IL31RA gene mutation and ancestral OSMR mutant allele in familial primary cutaneous amyloidosis. Eur J Hum Genet. 18(1): 26-32.