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Human Oncostatin M Protein expressed in HEK-293T Cells - ABIN2039659
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 - ABIN2039658
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
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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
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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
downregulation of miR (显示 MLXIP 蛋白)-20a-5p is caused by promoter hypermethylation. MiR (显示 MLXIP 蛋白)-20a-5p could also suppress the production of IL-17 (显示 IL17A 蛋白) by targeting OSM and CCL1 (显示 CCL1 蛋白) production in CD4 (显示 CD4 蛋白)(+) T cells in patients with active VKH.
our findings suggested that OSM suppresses SLUG expression and tumor metastasis of lung adenocarcinoma cells through inducing the inhibitory effect of the STAT1 (显示 STAT1 蛋白)-dependent pathway and suppressing the activating effect of STAT3 (显示 STAT3 蛋白)-dependent signaling
Genistein (a specific Tyr (显示 TYR 蛋白) phosphorylation inhibitor) leads to the interaction of CHOP (C/EBP Homologous Protein (显示 DDIT3 蛋白)) with C/EBP-beta (显示 CEBPB 蛋白), thus negatively regulating it. Knockdown of C/EBP-beta (显示 CEBPB 蛋白) 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 (显示 STAT3 蛋白))-dependent, and also required a novel intersection with transforming growth factor-beta (TGF-beta)/SMAD (显示 SMAD1 蛋白) signaling. Removal of OSM or inhibition of STAT3 (显示 STAT3 蛋白) or SMAD3 (显示 SMAD3 蛋白) 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 (显示 TNF 蛋白)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 (显示 F3 蛋白) (TF) increased and tissue factor (显示 F3 蛋白) pathway inhibitors (TFPI (显示 TFPI 蛋白))decreased, leading to an imbalance between TF and TFPI (显示 TFPI 蛋白) eventually. OSM might be related to thrombosis in patients with AF mediated by TF and TFPI (显示 TFPI 蛋白)
a novel STAT3 (显示 STAT3 蛋白)/SMAD3 (显示 SMAD3 蛋白)-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
OSM mitigated the proliferation of Th17 cells and decreased the expression of IL-17 (显示 IL17A 蛋白) and IL-21 (显示 IL21 蛋白); it promoted the activation of suppressor of cytokine signaling 3 (SOCS3 (显示 SOCS3 蛋白)), STAT3 (显示 STAT3 蛋白), and STAT5 (显示 STAT5A 蛋白); observations suggest that OSM can inhibit Th17 differentiation by reciprocally controlling SOCS3 (显示 SOCS3 蛋白), STAT3 (显示 STAT3 蛋白), and STAT5 (显示 STAT5A 蛋白)
In an animal model of anti-TNF (显示 TNF 蛋白)-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 (显示 INS 蛋白) Resistance and Adipose Tissue Inflammation in Vivo.
mechanism of OSM-induced cardiomyocyte dedifferentiation is associated with B-Raf (显示 SNRPE 蛋白)/Mek (显示 MDK 蛋白)/Erk (显示 EPHB2 蛋白) signaling pathway through the OSM receptor Obeta
Oncostatin M and interleukin-31 (显示 IL31 蛋白): 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 (显示 VEGFA 蛋白) and bFGF (显示 FGF2 蛋白) 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 (显示 NOTCH3 蛋白)/Akt (显示 AKT1 蛋白) 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.