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OSMR / IL-31RB Antibody (PE), Rabbit MAb

DatasheetSpecific ReferencesReviewsRelated ProductsProtocols
Human OSMR Antibody Product Information
Immunogen:Recombinant Human OSMR / IL-31RB protein (Catalog#11226-H08H)
Clone ID:002
Ig Type:Rabbit IgG
Concentration:10 μl/Test, 0.1 mg/ml
Formulation:Aqueous solution containing 0.5% BSA and 0.09% sodium azide
Preparation: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 PE under optimum conditions, the unreacted PE was removed.
Human OSMR Antibody Usage Guide
Specificity:Human OSMR / IL-31RB
Application:FCM
Storage: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.
Human OSMR Antibody FC Application Image
[Click to enlarge image]
Caption:
Flow cytometric analysis of Human OSMR expression in HeLa cells.
OSMR / IL-31RB Antibody (PE), Rabbit MAb, Flow cytometric
Other OSMR Antibody Products
OSMR/IL-31RB Background

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.

Human OSMR/IL-31RB References
  • 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.
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