抗Human Oncostatin M Receptor 抗体:
抗Mouse (Murine) Oncostatin M Receptor 抗体:
抗Rat (Rattus) Oncostatin M Receptor 抗体:
Mouse (Murine) Monoclonal Oncostatin M Receptor Primary Antibody for CyTOF, FACS - ABIN4899852
Jung, Noh, Lee, Chun, Jeong, Park, Park, Kim, Yun, Shin, Park: Oncostatin M induces dendritic cell maturation and Th1 polarization. in Biochemical and biophysical research communications 2010
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Human Monoclonal Oncostatin M Receptor Primary Antibody for FACS - ABIN4897176
Maier, Mittermeir, Ess, Neuper, Schmiedlechner, Duschl, Horejs-Hoeck: Prerequisites for Functional Interleukin 31 Signaling and Its Feedback Regulation by Suppressor of Cytokine Signaling 3 (SOCS3). in The Journal of biological chemistry 2015
The present data indicate OSMR mutations as not only the main cause of fPLCA, but also the potential source of the pathogenesis of sPLCA, although the exact molecular mechanism remains unknown.
OSMR genotype frequencies were found to be associated with higher recurrence in bladder cancer, and it may serve as a biomarker candidate gene to predict prognosis of this disease.
substitution of the AB loop and D-helix in LIF with their OSM counterparts was sufficient for OSMR activation
The current study suggested that the OSMR gene is highly expressed in human chronic autoimmune urticaria (CAU) skin tissues, and cause the up-regulation of the JAK/STAT3 signaling pathway-related genes. OSMR gene silencing in mice inhibits the activation of the JAK/STAT3 signaling pathway, thereby suppressing the development of CAU.
Polymorphisms of the OSMR rs2292016 locus are related to the development and outcome of DCM.
Missense mutatios were found in exon 10 of the oncostatin-M specific receptor beta subunit (OSMR) gene in all of the six patients from family 1, and in exon 14 of the OSMR gene in all of the four patients from family 2.
The PLAC1 expression has been demonstrated for the first time in cervical cancers. This preliminary study has further revealed a complex relationship between PLAC1 expression, cervical cancer histologic type, p53, and HPV type that requires further investigation.
OSMR-beta deficiency in macrophages improved high-fat diet-induced atherogenesis and plaque vulnerability
OSM and OSMR are highly expressed in inflammatory bowel disease intestinal mucosa compared to control mucosa. Intestinal stromal cells express abundant OSMR.
OSM:OSMR interactions are able to induce EMT, increased cancer stem cell-like properties and enhanced lung colonisation in SCC cells
the RET p.S891A mutation combined with OSMR p.G513D may underlie a novel phenotype manifesting as familial medullary thyroid carcinoma and cutaneous amyloidosis
this study offers new findings on the molecular genetics and disease relevance of mutations in OSMR in Familial primary localized cutaneous amyloidosis.
Oncostatin M and interleukin-31: Cytokines, receptors, signal transduction and physiology.
OSMRBeta in neurons is critical for neuronal survival during cerebral ischemic/reperfusion.
primary localized cutaneous amyloidosis has a missense mutation in oncostatin M receptor beta
The interleukin IL-31/IL-31receptor axis contributes to tumor growth in human follicular lymphoma.
oncostatin M is a cytokine possessing vigorous antiviral and immunostimulatory properties which is released by APC upon interaction with CD40L present on activated CD4+ T cells.
The disease severity of rheumatoid arthritis and systemic lupus erythematosus can be partially affected by the OSMR promoter polymorphisms.
We conclude that an OSMR/TGM2/integrin-alpha5beta1/fibronectin pathway is of biological significance in cervical squamous cell carcinoma
A unique loop structure in oncostatin M determines binding affinity toward oncostatin M receptor and leukemia inhibitory factor receptor.
The results of the present study provide evidence that the overexpression of miR183 promotes the apoptosis of substantia nigra neurons by inhibiting the expression of OSMR.
The results suggest that BRG1 and STAT3 coordinately regulate gene clustering and up-regulate Gfap and Osmr transcription in astrocytes.
Osmr expression in healthy mouse colon tissue was detected in endothelial and stromal cells. In agreement with observations of increased OSMR expression in inflamed colon tissue, the number of cells expressing Osmr was markedly increased in the lamina propria of mice with colitis.
In astrocytes but not microglia, phosphorylation of STAT1 and STAT3 occurred in response to OSM, whereas both microglia and astrocytes responded to hyper-IL-6 (IL-6 linked to the soluble IL-6 receptor).
OSM signaling via OSMR in synovial fibroblasts has the potential to contribute significantly to joint destruction in inflammatory arthritis.
defects in OSM signaling promote the deterioration of high-fat diet-induced obesity and related metabolic disorders
Data indicate that OSM receptor beta subunit-deficient (OSMRbeta(-/-)) mice exhibited phenotypic changes in adipose tissue macrophages (ATMs) to M1, increased proinflammatory cytokines in the adipose tissue, and systemic insulin resistance.
These data indicate that the transient RANKL induction by intermittent PTH administration, which is associated with its anabolic action, is changed to a prolonged induction in OSMR-deficient osteoblasts, resulting in bone destruction.
Bone formation can be stimulated independently of bone resorption and provide new insights into OSMR signaling.
Expression of oncostatin M receptor beta in a specific subset of nociceptive sensory neurons.
regulates hematopoiesis in vivo by stimulating stromal cells as well as hematopoietic progenitors, in particular megakaryocytic and erythrocytic progenitors.
Mice deficient in OSM receptor showed impaired liver regeneration with persistent parenchymal necrosis after carbon tetrachloride exposure. Recovery of liver mass from partial hepatectomy was also significantly delayed in OSMR(-/-) mice.
the up-regulation of p-STAT3 and p-CREB may be induced possibly through OSMR in inflammation
These findings suggest that IL-31 and OSM may thus have redundant functions in the development of OSMRbeta-expressing neurons.
Bone marrow progenitor cells involved in injured liver regeneration express OSMRB.
murine OSMR initiates STAT5 activation directly via the receptor bound Janus kinases. Intriguingly, the murine receptor preferentially recruits JAK2, whereas the human receptor seems to have a higher affinity for JAK1.
IL-6 and Oncostatin M individually affect the profile of leukocyte trafficking
These findings provide the first evidence that OSM receptor (OSMR) is regulated during follicle atresia, ovulation and luteolysis, and that OSM from other cells may mediate granulosa and luteal cell function, regulating the expression of genes involved in cell's viability.
This gene encodes a member of the type I cytokine receptor family. The encoded protein 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 this gene have been associated with familial primary localized cutaneous amyloidosis. Alternatively spliced transcript variants encoding different isoforms have been found for this gene.
IL-31 receptor subunit beta
, IL-31R subunit beta
, interleukin-31 receptor subunit beta
, oncostatin-M specific receptor beta subunit
, oncostatin-M-specific receptor subunit beta
, oncostatin receptor
, oncostatin-M specific receptor subunit beta
, oncostatin M specific receptor