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Human Oncostatin M ELISA Kit für 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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Human Oncostatin M ELISA Kit für 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
Mouse (Murine) Oncostatin M ELISA Kit für 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
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 (zeige STAT3 ELISA Kits))-dependent, and also required a novel intersection with transforming growth factor-beta (TGF-beta)/SMAD (zeige SMAD1 ELISA Kits) signaling. Removal of OSM or inhibition of STAT3 (zeige STAT3 ELISA Kits) or SMAD3 (zeige 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 (zeige 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 (zeige F3 ELISA Kits) (TF) increased and tissue factor (zeige F3 ELISA Kits) pathway inhibitors (TFPI (zeige TFPI ELISA Kits))decreased, leading to an imbalance between TF and TFPI (zeige TFPI ELISA Kits) eventually. OSM might be related to thrombosis in patients with AF mediated by TF and TFPI (zeige TFPI ELISA Kits)
a novel STAT3 (zeige STAT3 ELISA Kits)/SMAD3 (zeige 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 (zeige NCL ELISA Kits) stabilizes oncostatin-M mRNA by binding to a GC-rich (zeige RELB ELISA Kits) element in its 3'UTR (zeige UTS2R ELISA Kits).
Oncostatin M and interleukin-31 (zeige IL31 ELISA Kits): Cytokines, receptors, signal transduction and physiology.
OSM mitigated the proliferation of Th17 cells and decreased the expression of IL-17 (zeige IL17A ELISA Kits) and IL-21 (zeige IL21 ELISA Kits); it promoted the activation of suppressor of cytokine signaling 3 (SOCS3 (zeige SOCS3 ELISA Kits)), STAT3 (zeige STAT3 ELISA Kits), and STAT5 (zeige STAT5A ELISA Kits); observations suggest that OSM can inhibit Th17 differentiation by reciprocally controlling SOCS3 (zeige SOCS3 ELISA Kits), STAT3 (zeige STAT3 ELISA Kits), and STAT5 (zeige STAT5A ELISA Kits)
In an animal model of anti-TNF (zeige 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 (zeige INS ELISA Kits) Resistance and Adipose Tissue Inflammation in Vivo.
mechanism of OSM-induced cardiomyocyte dedifferentiation is associated with B-Raf (zeige SNRPE ELISA Kits)/Mek (zeige MDK ELISA Kits)/Erk (zeige EPHB2 ELISA Kits) signaling pathway through the OSM receptor Obeta
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 (zeige VEGFA ELISA Kits) and bFGF (zeige 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 (zeige NOTCH3 ELISA Kits)/Akt (zeige 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.