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anti-Human Oncostatin M Antibodies:
anti-Mouse (Murine) Oncostatin M Antibodies:
anti-Rat (Rattus) Oncostatin M Antibodies:
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Human Polyclonal Oncostatin M Primary Antibody for FACS, Neut - 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 references for ABIN4899954
Human Polyclonal Oncostatin M Primary Antibody for 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
Human Monoclonal Oncostatin M Primary Antibody for 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 for 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
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 Antibodies) (TF) increased and tissue factor (show F3 Antibodies) pathway inhibitors (TFPI (show TFPI Antibodies))decreased, leading to an imbalance between TF and TFPI (show TFPI Antibodies) eventually. OSM might be related to thrombosis in patients with AF mediated by TF and TFPI (show TFPI Antibodies)
a novel STAT3 (show STAT3 Antibodies)/SMAD3 (show SMAD3 Antibodies)-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 (show NCL Antibodies) stabilizes oncostatin-M mRNA by binding to a GC-rich (show RELB Antibodies) element in its 3'UTR (show UTS2R Antibodies).
Oncostatin M and interleukin-31 (show IL31 Antibodies): Cytokines, receptors, signal transduction and physiology.
Oncostatin M can regulate airway smooth muscle responses alone or in synergy with IL-17A (show IL17A Antibodies).
we demonstrated that recombinant human OSM (rhOSM) promoted tumor angiogenesis in EC cell lines by activating STAT3 (signal transducer and activator of transcription 3 (show STAT3 Antibodies)) and enhanced both cell migration and cell inva
OSM expression in osteoblasts increases in response to Osteopontin (show SPP1 Antibodies)-induced inflammation in vitro.
Data suggest that OSM promotes osteoblastic differentiation of vascular smooth muscle cells through JAK3 (show JAK3 Antibodies)/STAT3 (show STAT3 Antibodies) pathway and may contribute to the development of atherosclerotic calcification.
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 (show OSMR Antibodies))-gp130 (show LRPPRC Antibodies) heterodimer and binds with only very low affinity to mLIFR.
Loss of Oncostatin M Signaling in Adipocytes Induces Insulin (show INS Antibodies) Resistance and Adipose Tissue Inflammation in Vivo.
mechanism of OSM-induced cardiomyocyte dedifferentiation is associated with B-Raf (show SNRPE Antibodies)/Mek (show MDK Antibodies)/Erk (show EPHB2 Antibodies) 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 Antibodies) and bFGF (show FGF2 Antibodies) 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 Antibodies)/Akt (show AKT1 Antibodies) pathway.
OSM-induced osteogenesis and upregulation of osteogenic gene products require activity of PKCdelta (show PKCd Antibodies).
The Notch (show NOTCH1 Antibodies) signaling pathway was found to be one of the signaling pathways that inhibit OSM-induced MC3T3-E1 cell proliferation and differentiation.
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.