Browse our anti-Oncostatin M Receptor (OSMR) Antibodies

Human Oncostatin M Receptor (OSMR) interaction partners

1. 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.

2. The PLAC1 (show PLAC1 Antibodies) expression has been demonstrated for the first time in cervical cancers. This preliminary study has further revealed a complex relationship between PLAC1 (show PLAC1 Antibodies) expression, cervical cancer histologic type, p53 (show TP53 Antibodies), and HPV type that requires further investigation.

3. OSMR-beta deficiency in macrophages improved high-fat diet-induced atherogenesis and plaque vulnerability

4. OSM and OSMR are highly expressed in inflammatory bowel disease intestinal mucosa compared to control mucosa. Intestinal stromal cells express abundant OSMR.

5. OSM:OSMR interactions are able to induce EMT (show ITK Antibodies), increased cancer stem cell-like properties and enhanced lung colonisation in SCC (show CYP11A1 Antibodies) cells

6. the RET (show RET Antibodies) p.S891A mutation combined with OSMR p.G513D may underlie a novel phenotype manifesting as familial medullary thyroid carcinoma and cutaneous amyloidosis

7. this study offers new findings on the molecular genetics and disease relevance of mutations in OSMR in Familial primary localized cutaneous amyloidosis.

8. Oncostatin M (show OSM Antibodies) and interleukin-31 (show IL31 Antibodies): Cytokines, receptors, signal transduction and physiology.

9. primary localized cutaneous amyloidosis has a missense mutation in oncostatin M receptor beta

10. The interleukin IL-31 (show IL31 Antibodies)/IL-31receptor axis contributes to tumor growth in human follicular lymphoma.

Mouse (Murine) Oncostatin M Receptor (OSMR) interaction partners

1. OSMR-beta deficiency in macrophages improved high-fat diet-induced atherogenesis and plaque vulnerability

2. 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.

3. Oncostatin M (show OSM Antibodies) and interleukin-31 (show IL31 Antibodies): Cytokines, receptors, signal transduction and physiology.

4. In astrocytes but not microglia, phosphorylation of STAT1 (show STAT1 Antibodies) and STAT3 (show STAT3 Antibodies) occurred in response to OSM (show OSM Antibodies), whereas both microglia and astrocytes responded to hyper-IL-6 (IL-6 (show IL6 Antibodies) linked to the soluble IL-6 (show IL6 Antibodies) receptor).

5. OSM (show OSM Antibodies) signaling via OSMR in synovial fibroblasts has the potential to contribute significantly to joint destruction in inflammatory arthritis.

6. defects in OSM (show OSM Antibodies) signaling promote the deterioration of high-fat diet-induced obesity and related metabolic disorders

7. Data indicate that OSM (show OSM Antibodies) receptor beta subunit (show POLG Antibodies)-deficient (OSMRbeta(-/-)) mice exhibited phenotypic changes in adipose tissue macrophages (ATMs) to M1, increased proinflammatory cytokines in the adipose tissue, and systemic insulin (show INS Antibodies) resistance.

8. These data indicate that the transient RANKL (show TNFSF11 Antibodies) induction by intermittent PTH (show PTH Antibodies) administration, which is associated with its anabolic action, is changed to a prolonged induction in OSMR-deficient osteoblasts, resulting in bone destruction.

9. Bone formation can be stimulated independently of bone resorption and provide new insights into OSMR signaling.

10. Expression of oncostatin M receptor beta in a specific subset of nociceptive sensory neurons.