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