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Mouse Anti-OSMR Recombinant Antibody (3E12) (CBMAB-A6250-LY)

The product is antibody recognizes OSMR. The antibody 3E12 immunoassay techniques such as: WB, ELISA.
See all OSMR antibodies
Published Data
Fig.1 OSM induces EMT in OSMR overexpressing cervical SCC cells.
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Summary

Host Animal
Mouse
Specificity
Human
Clone
3E12
Antibody Isotype
IgG2b, κ
Application
WB, ELISA

Basic Information

Immunogen
OSMR (NP_003990.1, 141 a.a. ~ 240 a.a) partial recombinant protein with GST tag. MW of the GST tag alone is 26 KDa.
Specificity
Human
Antibody Isotype
IgG2b, κ
Clonality
Monoclonal
Application Notes
The COA includes recommended starting dilutions, optimal dilutions should be determined by the end user.

Formulations & Storage [For reference only, actual COA shall prevail!]

Format
Liquid
Purity
> 95% Purity determined by SDS-PAGE.
Storage
Store at +4°C short term (1-2 weeks). Aliquot and store at -20°C long term. Avoid repeated freezethaw cycles.

Target

Full Name
Oncostatin M Receptor
Introduction
Oncostatin M is a member of the IL6 family of cytokines. Functional receptors for IL6 family cytokines are multisubunit complexes involving members of the hematopoietin receptor superfamily. Many IL6 cytokines utilize gp130 as a common receptor subunit. OSM binds to the gp130 receptor subunit and, in association with the leukemia inhibitory factor receptor, induces a proliferative response in permissive cells. OSMR is an alternative subunit (for an OSM receptor complex (a heterodimer of gp130 and OSMR) that is activated by OSM but not by LIF [provided by RefSeq]
Entrez Gene ID
9180
UniProt ID
Q99650
Alternative Names
MGC150626; MGC150627; MGC75127; OSMRB
Function
Associates with IL31RA to form the IL31 receptor. Binds IL31 to activate STAT3 and possibly STAT1 and STAT5. Capable of transducing OSM-specific signaling events.
Biological Process
Cytokine-mediated signaling pathwayManual Assertion Based On ExperimentIBA:GO_Central
Oncostatin-M-mediated signaling pathwayManual Assertion Based On ExperimentIMP:BHF-UCL
Positive regulation of acute inflammatory response1 PublicationIC:BHF-UCL
Positive regulation of cell population proliferationManual Assertion Based On ExperimentIGI:BHF-UCL
Response to cytokineManual Assertion Based On ExperimentIDA:BHF-UCL
Cellular Location
Membrane
Involvement in disease
Amyloidosis, primary localized cutaneous, 1 (PLCA1):
A 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 that may be exacerbated by chronic scratching and rubbing. Primary localized cutaneous amyloidosis is often divided into macular and lichen subtypes although many affected individuals often show both variants coexisting. Lichen amyloidosis characteristically presents as a pruritic eruption of grouped hyperkeratotic papules with a predilection for the shins, calves, ankles and dorsa of feet and thighs. Papules may coalesce to form hyperkeratotic plaques that can resemble lichen planus, lichen simplex or nodular prurigo. Macular amyloidosis is characterized by small pigmented macules that may merge to produce macular hyperpigmentation, sometimes with a reticulate or rippled pattern. In macular and lichen amyloidosis, amyloid is deposited in the papillary dermis in association with grouped colloid bodies, thought to represent degenerate basal keratinocytes. The amyloid deposits probably reflect a combination of degenerate keratin filaments, serum amyloid P component, and deposition of immunoglobulins.
Topology
Extracellular: 28-740
Helical: 741-761
Cytoplasmic: 762-979

Polak, K. L., Tamagno, I., Parameswaran, N., Smigiel, J., Chan, E. R., Yuan, X., ... & Jackson, M. W. (2023). Oncostatin-M and OSM-Receptor feed-forward activation of MAPK induces separable stem-like and mesenchymal programs. Molecular Cancer Research, 21(9), 975-990.

Geng, Q., Wang, J., Zhang, W., Zhou, W., Tang, G., & Gu, M. (2023). Oncostatin M receptor is overexpressed in oral squamous cell carcinoma and connected to poor prognosis. Journal of Oral Pathology & Medicine, 52(2), 136-144.

Geethadevi, A., Tsaih, S. W., Nair, A., Ku, Z., Kadamberi, I. P., Parashar, D., ... & Raghavan, P. C. (2023). Oncostatin m receptor signaling reprograms tumor microenvironment for chemoresistance. Cancer Research, 83(7_Supplement), 3653-3653.

Zhou, J., Yang, J., Dong, Y., Shi, Y., Zhu, E., Yuan, H., ... & Wang, B. (2022). Oncostatin M receptor regulates osteoblast differentiation via extracellular signal-regulated kinase/autophagy signaling. Stem Cell Research & Therapy, 13(1), 278.

Geethadevi, A., Nair, A., Parashar, D., Ku, Z., Xiong, W., Deng, H., ... & Chaluvally-Raghavan, P. (2021). Oncostatin M Receptor–Targeted Antibodies Suppress STAT3 Signaling and Inhibit Ovarian Cancer Growth. Cancer research, 81(20), 5336-5352.

Houben, E., Hellings, N., & Broux, B. (2019). Oncostatin M, an underestimated player in the central nervous system. Frontiers in immunology, 10, 455653.

Yu, Z., Li, Z., Wang, C., Pan, T., Chang, X., Wang, X., ... & Su, L. (2019). Oncostatin M receptor, positively regulated by SP1, promotes gastric cancer growth and metastasis upon treatment with Oncostatin M. Gastric Cancer, 22, 955-966.

Guo, Q., Guan, G. F., Cao, J. Y., Zou, C. Y., Zhu, C., Cheng, W., ... & Wu, A. H. (2019). Overexpression of oncostatin M receptor regulates local immune response in glioblastoma. Journal of Cellular Physiology, 234(9), 15496-15509.

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For research use only. Not intended for any clinical use.

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