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anti-Human Oncostatin M Antikörper:
anti-Mouse (Murine) Oncostatin M Antikörper:
anti-Rat (Rattus) Oncostatin M Antikörper:
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Human Polyclonal Oncostatin M Primary Antibody für CyTOF, FACS - ABIN4899954
Ohsaka, Hirota-Komatsu, Shibata, Ezaki, Shinohara, Yoshida: Specific association of increased vascular endothelial growth factor expression and its receptors with macrophage differentiation of HL-60 leukemia cells. in Biochemical and biophysical research communications 2008
Show all 2 Pubmed References
Human Monoclonal Oncostatin M Primary Antibody für IHC, IHC (p) - ABIN4341424
Kang, Kim, Jang, Park, Lee, Kim: 22q11-q13 as a hot spot for prediction of disease-free survival in bile duct cancer: integrative analysis of copy number variations. in Cancer genetics 2014
Human Polyclonal Oncostatin M Primary Antibody für IHC, IHC (p) - ABIN4341425
Guo, Chen, Shi, Wang, Chen, Diao, Hu, Yu, Qian, Guo: Stat3-coordinated Lin-28-let-7-HMGA2 and miR-200-ZEB1 circuits initiate and maintain oncostatin M-driven epithelial-mesenchymal transition. in Oncogene 2013
Human Polyclonal Oncostatin M Primary Antibody für ELISA (Detection), FACS - ABIN4899952
Hurst, McLoughlin, Monslow, Owens, Morgan, Fuller, Topley, Jones: Secretion of oncostatin M by infiltrating neutrophils: regulation of IL-6 and chemokine expression in human mesothelial cells. in Journal of immunology (Baltimore, Md. : 1950) 2002
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 Antikörper))-dependent, and also required a novel intersection with transforming growth factor-beta (TGF-beta)/SMAD (zeige SMAD1 Antikörper) signaling. Removal of OSM or inhibition of STAT3 (zeige STAT3 Antikörper) or SMAD3 (zeige SMAD3 Antikörper) 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 Antikörper)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 Antikörper) (TF) increased and tissue factor (zeige F3 Antikörper) pathway inhibitors (TFPI (zeige TFPI Antikörper))decreased, leading to an imbalance between TF and TFPI (zeige TFPI Antikörper) eventually. OSM might be related to thrombosis in patients with AF mediated by TF and TFPI (zeige TFPI Antikörper)
a novel STAT3 (zeige STAT3 Antikörper)/SMAD3 (zeige SMAD3 Antikörper)-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 Antikörper) stabilizes oncostatin-M mRNA by binding to a GC-rich (zeige RELB Antikörper) element in its 3'UTR (zeige UTS2R Antikörper).
Oncostatin M and interleukin-31 (zeige IL31 Antikörper): Cytokines, receptors, signal transduction and physiology.
OSM mitigated the proliferation of Th17 cells and decreased the expression of IL-17 (zeige IL17A Antikörper) and IL-21 (zeige IL21 Antikörper); it promoted the activation of suppressor of cytokine signaling 3 (SOCS3 (zeige SOCS3 Antikörper)), STAT3 (zeige STAT3 Antikörper), and STAT5 (zeige STAT5A Antikörper); observations suggest that OSM can inhibit Th17 differentiation by reciprocally controlling SOCS3 (zeige SOCS3 Antikörper), STAT3 (zeige STAT3 Antikörper), and STAT5 (zeige STAT5A Antikörper)
In an animal model of anti-TNF (zeige TNF Antikörper)-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 Antikörper) Resistance and Adipose Tissue Inflammation in Vivo.
mechanism of OSM-induced cardiomyocyte dedifferentiation is associated with B-Raf (zeige SNRPE Antikörper)/Mek (zeige MDK Antikörper)/Erk (zeige EPHB2 Antikörper) 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 Antikörper) and bFGF (zeige FGF2 Antikörper) 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 Antikörper)/Akt (zeige AKT1 Antikörper) 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.