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Human Oncostatin M Protein expressed in HEK-293T Cells - ABIN2039658
Yin, Chain: Suppression of lymphokine production in anti-minor histocompatibility antigen responses. in Cytokine 1991
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Human Oncostatin M Protein expressed in HEK-293T Cells - ABIN2039659
Godoy-Tundidor, Cavarretta, Fuchs, Fiechtl, Steiner, Friedbichler, Bartsch, Hobisch, Culig: Interleukin-6 and oncostatin M stimulation of proliferation of prostate cancer 22Rv1 cells through the signaling pathways of p38 mitogen-activated protein kinase and phosphatidylinositol 3-kinase. in The Prostate 2005
Show all 3 Pubmed References
Human Oncostatin M Protein expressed in Escherichia coli (E. coli) - ABIN413690
Sen, Che, Rajamani, Zerboni, Sung, Ptacek, Arvin: Signal transducer and activator of transcription 3 (STAT3) and survivin induction by varicella-zoster virus promote replication and skin pathogenesis. in Proceedings of the National Academy of Sciences of the United States of America 2012
Show all 2 Pubmed References
Human Oncostatin M Protein expressed in Escherichia coli (E. coli) - ABIN988184
Esmaeli, Allameh, Soleimani, Rahbarizadeh, Frouzandeh-Moghadam: The role of albumin and PPAR-? in differentiation-dependent change of fatty acid profile during differentiation of mesenchymal stem cells to hepatocyte-like cells. in Cell biochemistry and function 2014
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 Proteins))-dependent, and also required a novel intersection with transforming growth factor-beta (TGF-beta)/SMAD (show SMAD1 Proteins) signaling. Removal of OSM or inhibition of STAT3 (show STAT3 Proteins) or SMAD3 (show SMAD3 Proteins) 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 Proteins)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 Proteins) (TF) increased and tissue factor (show F3 Proteins) pathway inhibitors (TFPI (show TFPI Proteins))decreased, leading to an imbalance between TF and TFPI (show TFPI Proteins) eventually. OSM might be related to thrombosis in patients with AF mediated by TF and TFPI (show TFPI Proteins)
a novel STAT3 (show STAT3 Proteins)/SMAD3 (show SMAD3 Proteins)-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 stabilizes oncostatin-M mRNA by binding to a GC-rich element in its 3'UTR.
Oncostatin M and interleukin-31 (show IL31 Proteins): Cytokines, receptors, signal transduction and physiology.
OSM mitigated the proliferation of Th17 cells and decreased the expression of IL-17 (show IL17A Proteins) and IL-21 (show IL21 Proteins); it promoted the activation of suppressor of cytokine signaling 3 (SOCS3 (show SOCS3 Proteins)), STAT3 (show STAT3 Proteins), and STAT5 (show STAT5A Proteins); observations suggest that OSM can inhibit Th17 differentiation by reciprocally controlling SOCS3 (show SOCS3 Proteins), STAT3 (show STAT3 Proteins), and STAT5 (show STAT5A Proteins)
In an animal model of anti-TNF (show TNF Proteins)-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 Proteins) Resistance and Adipose Tissue Inflammation in Vivo.
mechanism of OSM-induced cardiomyocyte dedifferentiation is associated with B-Raf (show SNRPE Proteins)/Mek (show MDK Proteins)/Erk (show EPHB2 Proteins) 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 (show VEGFA Proteins) and bFGF (show FGF2 Proteins) 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 Proteins)/Akt (show AKT1 Proteins) 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.