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Validated All-in-One™ qPCR Primer for OSM(NM_020530.5) Search again
Product ID:
HQP012081
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
-
Gene Description:
oncostatin M
Target Gene Accession:
NM_020530.5(click here to view gene page)
Estimated Delivery:
Approximately 1-3 weeks, but may vary. Please email sales@genecopoeia.com or call 301-762-0888 to confirm ETA.
Important Note:
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Validated result:
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| A | B |
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Each All-in-One™ qPCR Primer is experimentally validated to yield a single dissociation curve peak and to generate a single amplification of the correct size for the targeted gene. A cDNA Pool, containing reverse transcript products of 8 different human tissue total RNA(Liver, Testis,Muscle,Thyroid,Brain,Spleen,Stomach,Small Intestine)),was used as the qPCR validation template. qPCR was performed using 0.2 µM primer with 2XAll-in-One™ qPCR Mix (Catalog#: QP001,QP002,QP004,QP005). Reactions were incubated for 10min. at 95°C, followed by 40 cycles of 95°C for 10 sec.; 60°C, 20 sec. and 72°C, 15sec. using Bio-Rad iQ5™ Instrument. At the end of the last cycle, temperature was increased from 72 to 95°C to produce a melting curve. Panel A: Validated Result for Amplification Curve; Panel B: Validated Result for Melting Curve. |
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Summary
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.
Gene References into function
- We conclude that STAT1 activation is necessary but not sufficient for induction of transcription of IFN gamma-responsive genes; signals provided by IFN gamma other than STAT1 activation cannot be provided in trans to complement the response to OnM.
- Oncostatin M and leukemia inhibitory factor regulate the growth of normal human breast epithelial cells
- Il-6 and oncostatin M act synergistically to promote growth in a new human myeloma cell line.
- role in identifying sterol-indendent regulatory elements in human ATP-binding cassette transporter A1 promoter
- role in inducing alpha1-antitrypsin gene expression
- expression and evidence for STAT3 activation in human ovarian carcinomas
- produced in human dendritic cells in response to bacterial products
- Oncostatin M induces tissue-type plasminogen activator and plasminogen activator inhibitor-1 in lung tumor cells
- Oncostatin M induces procoagulant activity in human vascular smooth muscle cells by modulating the balance between tissue factor and tissue factor pathway inhibitor. OSM might be involved in the thrombotic complications associated with plaque rupture.
- Oncostatin M stimulates (45)Ca release and enhances mRNA expression of receptor activator of NF-kappa B ligand (RANKL) and osteoprotegerin in neonatal mouse calvarial bone cultures, but has no effect on the expression of RANK.
- Raised intraperitoneal levels of OSM during bacterial infections originate from infiltrating neutrophils and regulate mesothelial expression of inflammatory cytokines.
- Kaposi sarcoma-associated viral cyclin K overrides cell growth inhibition mediated by this protein through STAT3 inhibition.
- Increased production of this protein is found in lymphomononuclear cells from HIV-1-infected patients with neuroAIDS.
- oncostatin M, which transmits its signal via the gp130 cell surface receptor, and results in the selective down-modulation of the melanocyte lineage antigens
- Leukemia inhibitory factor (LIF), cardiotrophin-1, and oncostatin M share structural binding determinants in the immunoglobulin-like domain of LIF receptor
- this important cytokine is released from neutrophils as they infiltrate rheumatoid joints and, thus, contribute to the complex cytokine network that characterizes rheumatoid arthritis
- IL-6 stimulates proliferation of prostate cancer 22Rv1 cells, in part through activation of the phosphatidylinositol 3-kinase (PI 3-K) signaling pathway.
- Effects of OSM in 5 glioma cell lines and 7 short-term cultures of human gliomas and in normal cultured human astrocytes.
- The expression of OSM and its receptor in ovarian tissue from fetuses and women suggests a possible role of OSM in growth initiation of human primordial follicles.
- IL-6 and OSM upregulate PAI-1 protein and mRNA in adipose tissue
- OSM may play a role in modulating the inflammatory cascade of chronic periodontitis.
- Oncostatin M is expressed in the human nasal mucosa and is upregulated in the setting of allergic nasal inflammation.
- OSM induces a motile/invasive phenotype in T-47D human breast cancer cells in vitro; OSM may enhance metastasis in vivo.
- Pre-B cell colony-enhancing factor (PBEF) is regulated via IL-6 trans-signaling and the IL-6-related cytokine OSM. PBEF is also actively expressed during arthritis.
- data suggest that OSM promotes angiogenesis and endothelial cell migration and potentiates the effects of IL-1beta in promoting extracellular matrix turnover and human cartilage degradation
- sOSMR is able to bind OSM and interleukin-31 when associated to soluble gp130 or soluble interleukin-31R, respectively, and to neutralize both cytokine properties
- These results suggest that OSM inhibits adiponectin expression by inducing dedifferentiation of adipocytes through signaling pathways involving JAK3 and MEK, but not JAK2.
- OSM and its receptor play an important role in cutaneous inflammatory responses in general and the specific effects of OSM are associated with distinct inflammatory diseases depending on the cytokine environment.
- in addition to growth arrest and induced differentiation, OSM also sensitizes normal and transformed osteoblasts to apoptosis by a mechanism implicating (i) activation and nuclear translocation of STAT5 and p53 and (ii) an increased Bax/Bcl-2 ratio.
- If the effect of oncostatin M on PAI-1 in smooth muscle cells is operative in vivo, it could, via fibrinolysis and proteolysis, be involved in plaque progression, destabilization, thrombus formation, restenosis, and neointima formation.
- Oncostatin M directly lowers the plasma triglycerides in hyperlipidemia by stimulating the transcription of ACSL3/5 in the liver.
- In human proximal tubular cells ERK1/2 signaling represents an important component of oncostatin M inhibitory effect on N-cadherin expression.
- Increased expression of some IL-6 cytokine family members (oncostatin M, gp130, CT-1, LIF) in cutaneous inflammation might contribute to the promotion of hair loss.
- Production of OSM by human mast cells might represent one link between T cell-induced mast cell activation and development of spectrum of structural changes in T cell-mediated inflammatory processes in which mast cells have been found to be involved.
- Our data establish a link between the complement system and the gp130 receptor cytokine family with possible implications for the pathology of inflammatory diseases.
- secretion of OSM and LIF by both epithelial and stromal (paracrine manner) cells seems to promote tumor growth in human breast carcinoma
- Mtb infection of monocytes results in prostaglandin-dependent OSM secretion, which synergizes with TNF-alpha to drive functionally unopposed fibroblast MMP-1/-3 secretion.
- loss of repopulating activity during KIT-ligand stimulation is counteracted by Oncostatin M through the downregulation of ERK pathway signaling
- Oncostatin M is expressed in both chronic obstructive sialadenitis and normal submandibular gland, and is up-regulated in chronic obstructive sialadenitis.
- expressed in epithelialized apical periodontitis lesions
- hXOR is a tumor suppressor-targeted gene and the phosphorylation of SAFB1 is regulated by OSM, which provides a molecular basis for understanding the role of SAFB1-regulated hXOR transcription in cytokine stimulation and tumorigenesis
- human OSM is able to induce CCL1, CCL7, and CCL8 expression to levels comparable to those found for IL-1beta and TNF-alpha