OSMR Protein & Antibody (IL-31RB)

Oncostatin M Receptor (Interleukin-31 receptor subunit beta)

OSMR Protein Products

OSMR Protein, Recombinant

Molecule	Species	Description	Cat. No
OSMR/IL-31RB	Human	OSMR/IL-31RB Protein, Recombinant	11226-H08H
OSMR/IL-31RB	Mouse	OSMR/IL-31RB Protein, Recombinant	50500-M08H

OSMR Antibody

Molecule	Application	Description	Cat. No
Human OSMR/IL-31RB	WB, ELISA	OSMR/IL-31RB Antibody, Mouse MAb	11226-MM01
Human OSMR/IL-31RB	WB, ELISA	Rabbit Polyclonal Antibody	11226-RP01
Human OSMR/IL-31RB	WB, ELISA	Rabbit Polyclonal Antibody (Antigen Affinity Purified)	11226-RP02

OSMR cDNA Clone

Molecule	Species	Description	Cat. No
OSMR/IL-31RB	Human	Homo sapiens OSMR/IL-31RB DNA ORF clone(NM_003999.1)	HG11226-M
OSMR/IL-31RB	Mouse	Mus musculus OSMR/IL-31RB cDNA Clone	MG50500-M

OSMR Related Areas

Immunology>>Cytokine & Receptor>>Interleukin & Receptor>>Other>>OSMR/IL-31RB

OSMR Alternative Names

OSMR, IL-31RB, OSMRB, IL-31R-beta, IL-31R subunit beta, MGC150626, MGC150627, MGC75127 [Homo sapiens]

Osmr, IL-31RB, OSMRB, IL-31R-beta, IL-31R subunit beta [Mus musculus]

OSMR 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.

OSMR Related Studies

1. Arita K, et al.. (2008) Oncostatin M Receptor-β Mutations Underlie Familial Primary Localized Cutaneous Amyloidosis. Am J Hum. Genet. 82 (1): 73-80.
2. 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.
3. 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.