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Human Oncostatin M ELISA Kit for Sandwich ELISA - ABIN625069
Kanda, Hau, Tada, Sato, Watanabe: Decreased serum LL-37 and vitamin D3 levels in atopic dermatitis: relationship between IL-31 and oncostatin M. in Allergy 2012
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Mouse (Murine) Oncostatin M ELISA Kit for Sandwich ELISA - ABIN415531
Moidunny, Matos, Wesseling, Banerjee, Volsky, Cunha, Agostinho, Boddeke, Roy: Oncostatin M promotes excitotoxicity by inhibiting glutamate uptake in astrocytes: implications in HIV-associated neurotoxicity. in Journal of neuroinflammation 2016
Human Oncostatin M ELISA Kit for Sandwich ELISA - ABIN414913
Lee, Kil, Kwon, Kim, Yoo, Shin: Oncostatin M as a target biological molecule of preeclampsia. in The journal of obstetrics and gynaecology research 2010
Genistein (a specific Tyr (show TYR ELISA Kits) phosphorylation inhibitor) leads to the interaction of CHOP (C/EBP Homologous Protein (show DDIT3 ELISA Kits)) with C/EBP-beta (show CEBPB ELISA Kits), thus negatively regulating it. Knockdown of C/EBP-beta (show CEBPB ELISA Kits) also leads to inhibition of PMA-mediated OSM induction.
Data provide evidence that OSM regulates an epithelial-mesenchymal transition and cancer stem cell plasticity program that promotes tumorigenic properties in pancreatic cells.
OSM-induced plasticity was Signal Transducer and Activator of Transcription 3 (STAT3 (show STAT3 ELISA Kits))-dependent, and also required a novel intersection with transforming growth factor-beta (TGF-beta)/SMAD (show SMAD1 ELISA Kits) signaling. Removal of OSM or inhibition of STAT3 (show STAT3 ELISA Kits) or SMAD3 (show SMAD3 ELISA Kits) resulted in a marked reversion to a non-invasive, epithelial phenotype.
Neutrophils are a major source of OSM-producing cells in patients with chronic rhinosinusitis and severe asthma.
OSM and OSMR are highly expres (show TNF ELISA Kits)sed in inflammatory bowel disease intestinal mucosa compared to control mucosa. OSM promotes inflammatory behavior in human intestinal stroma.
Study showed that in atrial fibrillation (AF) with thrombus, the atrial tissue infiltration of M1 macrophages increased significantly; the OSM expression was also found to increase simultaneously; downstream tissue factor (show F3 ELISA Kits) (TF) increased and tissue factor (show F3 ELISA Kits) pathway inhibitors (TFPI (show TFPI ELISA Kits))decreased, leading to an imbalance between TF and TFPI (show TFPI ELISA Kits) eventually. OSM might be related to thrombosis in patients with AF mediated by TF and TFPI (show TFPI ELISA Kits)
a novel STAT3 (show STAT3 ELISA Kits)/SMAD3 (show SMAD3 ELISA Kits)-signaling axis is required for OSM-mediated senescence.
This result demonstrates that HPV16 oncoproteins upregulate oncostatin M and play an important role to promote oral squamous cell carcinoma development
The identification of the OSM inflammatory pathway as an important mediator of epithelial mesenchymal transition in triple-negative breast cancer (TNBC) may provide a novel potential opportunity to improve therapeutic strategies.
Nucleolin (show NCL ELISA Kits) stabilizes oncostatin-M mRNA by binding to a GC-rich (show RELB ELISA Kits) element in its 3'UTR (show UTS2R ELISA Kits).
OSM mitigated the proliferation of Th17 cells and decreased the expression of IL-17 (show IL17A ELISA Kits) and IL-21 (show IL21 ELISA Kits); it promoted the activation of suppressor of cytokine signaling 3 (SOCS3 (show SOCS3 ELISA Kits)), STAT3 (show STAT3 ELISA Kits), and STAT5 (show STAT5A ELISA Kits); observations suggest that OSM can inhibit Th17 differentiation by reciprocally controlling SOCS3 (show SOCS3 ELISA Kits), STAT3 (show STAT3 ELISA Kits), and STAT5 (show STAT5A ELISA Kits)
In an animal model of anti-TNF (show TNF ELISA Kits)-resistant intestinal inflammation, genetic deletion or pharmacological blockade of OSM significantly attenuates colitis.
these results support the proinflammatory role of OSM when it is overexpressed in the skin. However, OSM expression was not required in the murine model of psoriasis induced by topical application of imiquimod, as demonstrated by the inflammatory phenotype of OSM-deficient mice or wild-type mice treated with anti-OSM antibodies.
OSM (mOSM) signals mainly via an OSM receptor (OSMR)-gp130 heterodimer and binds with only very low affinity to mLIFR.
Loss of Oncostatin M Signaling in Adipocytes Induces Insulin (show INS ELISA Kits) Resistance and Adipose Tissue Inflammation in Vivo.
mechanism of OSM-induced cardiomyocyte dedifferentiation is associated with B-Raf (show SNRPE ELISA Kits)/Mek (show MDK ELISA Kits)/Erk (show EPHB2 ELISA Kits) signaling pathway through the OSM receptor Obeta
Oncostatin M and interleukin-31 (show IL31 ELISA Kits): Cytokines, receptors, signal transduction and physiology.
OSM plays multiple critical roles in the maintenance and development of the hematopoietic microenvironment in the bone marrow at a steady state as well as after injury.
OSM treatment preserved cardiac function, inhibited apoptosis and fibrosis, and stimulated angiogenesis via upregulating VEGF (show VEGFA ELISA Kits) and bFGF (show FGF2 ELISA Kits) in infarct border zone of ischemic myocardium, indicating that OSM could be a novel therapeutic target for MI.
The mechanism of Oncostatin M on cardiac ischemia/reperfusion injury is partly mediated by the Notch3 (show NOTCH3 ELISA Kits)/Akt (show AKT1 ELISA Kits) pathway.
Protein kinase R plays a pivotal role in oncostatin M and interleukin-1 signalling in bovine articular cartilage chondrocytes.
Oncostatin M is a member of a cytokine family that includes leukemia-inhibitory factor, granulocyte colony-stimulating factor, and interleukin 6. This gene encodes a growth regulator which inhibits the proliferation of a number of tumor cell lines. It regulates cytokine production, including IL-6, G-CSF and GM-CSF from endothelial cells.