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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 08 Dec 2016.

Oncostatin M

oncostatin M, OSM
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. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: Interleukin-6, CAN, STAT3, NMDA receptor, V1a
Papers on oncostatin M
Role of Delta-Notch signaling in cerebral cavernous malformations.
New
Bertalanffy et al., Hannover, Germany. In Neurosurg Rev, Feb 2016
CCM is caused by loss of function mutations in one of the three well-known CCM genes: Krev interaction trapped 1 (KRIT1), OSM, and programmed cell death 10 (PDCD10).
Dehydration effects of a V2 antagonist on endolymphatic hydrops in guinea pigs.
New
Yamasoba et al., Tokyo, Japan. In Hear Res, Jan 2016
In the second series, we investigated the effects of systemic and topical applications of OPC on plasma vasopressin (p-VP) concentrations and plasma osmolality (p-OSM).
Long-term culture and expansion of primary human hepatocytes.
New
Impact
Nahmias et al., Jerusalem, Israel. In Nat Biotechnol, Dec 2015
Here we describe the oncostatin M (OSM)-dependent expansion of primary human hepatocytes by low expression of the human papilloma virus (HPV) genes E6 and E7 coupled with inhibition of epithelial-to-mesenchymal transition.
Metastasis-Free Interval Is Closely Related to Tumor Characteristics and Has Prognostic Value in Breast Cancer Patients with Distant Relapse.
New
Jeong et al., Seoul, South Korea. In J Breast Cancer, Dec 2015
Overall survival after metastasis (OSM) was estimated.
Macrophage Polarization and Bone Formation: A review.
Review
New
Horwood, Oxford, United Kingdom. In Clin Rev Allergy Immunol, Nov 2015
In bone, a number of factors, including oncostatin M, have been shown to promote osteoblast formation both in vitro and in vivo.
Oncostatin M and interleukin-31: Cytokines, receptors, signal transduction and physiology.
Review
New
Hermanns, Würzburg, Germany. In Cytokine Growth Factor Rev, Oct 2015
Oncostatin M (OSM) and interleukin-31 (IL-31) are two cytokines belonging to the IL-6 family which share a common signaling receptor subunit, the OSM receptor beta (OSMRβ).
Leukemia inhibitory factor (LIF).
Review
New
Babon et al., Melbourne, Australia. In Cytokine Growth Factor Rev, Oct 2015
It utilises a receptor that consists of the LIF receptor β and gp130 and this receptor complex is also used by ciliary neurotrophic growth factor (CNTF), oncostatin M, cardiotrophin1 (CT1) and cardiotrophin-like cytokine (CLC).
Analysis of SOST expression using large minigenes reveals the MEF2C binding site in the evolutionarily conserved region (ECR5) enhancer mediates forskolin, but not 1,25-dihydroxyvitamin D3 or TGFβ1 responsiveness.
Review
New
Pike et al., Madison, United States. In J Steroid Biochem Mol Biol, Oct 2015
Diverse stimuli regulate SOST including the vitamin D hormone, forskolin (Fsk), bone morphogenic protein 2 (BMP-2), oncostatin M (OSM), dexamethasone (Dex), and transforming growth factor (TGFβ1).
Immunomodulatory properties of the IL-6 cytokine family in multiple sclerosis.
Review
New
Hellings et al., Diepenbeek, Belgium. In Ann N Y Acad Sci, Sep 2015
This review focuses on the effects of the family members IL-6, leukemia inhibitory factor, oncostatin M, and IL-11 on immune cell subsets and how these effects relate to the pathogenesis of MS.
Myocardial healing requires Reg3β-dependent accumulation of macrophages in the ischemic heart.
New
Impact
Braun et al., Bad Nauheim, Germany. In Nat Med, Apr 2015
Using mass spectrometry-based secretome analysis, we found that dedifferentiating cardiomyocytes release Reg3β in response to the cytokine OSM, which signals through Jak1 and Stat3.
Adiponectin Induces Oncostatin M Expression in Osteoblasts through the PI3K/Akt Signaling Pathway.
Tang et al., Dongyang, China. In Int J Mol Sci, 2014
In this study, we observed the effect of adiponectin on the expression of oncostatin M (OSM), a pro-inflammatory cytokine, in human osteoblastic cells.
Regulation of YKL-40 expression by corticosteroids: effect on pro-inflammatory macrophages in vitro and its modulation in COPD in vivo.
Hiemstra et al., Leiden, Netherlands. In Respir Res, 2014
METHODS: Monocytes of healthy subjects were cultured in vitro for 7 days with either GM-CSF or M-CSF (for MΦ1 and MΦ2, respectively) and stimulated for 24 h with LPS, TNFα, or oncostatin M (OSM).
EndMT contributes to the onset and progression of cerebral cavernous malformations.
Impact
Dejana et al., Milano, Italy. In Nature, 2013
CCM is caused by loss-of-function mutations in one of three genes, namely CCM1 (also known as KRIT1), CCM2 (OSM) and CCM3 (PDCD10), and occurs in both sporadic and familial forms.
STK25 protein mediates TrkA and CCM2 protein-dependent death in pediatric tumor cells of neural origin.
GeneRIF
Fainzilber et al., Israel. In J Biol Chem, 2012
Down-modulation of STK25, but not STK24, rescued medulloblastoma cells from NGF-induced TrkA-dependent cell death, suggesting that STK25 is part of the death-signaling pathway initiated by TrkA and CCM2.
Crystallization and preliminary X-ray analysis of the C-terminal domain of CCM2, part of a novel adaptor protein involved in cerebral cavernous malformations.
GeneRIF
Wang et al., Beijing, China. In Acta Crystallogr Sect F Struct Biol Cryst Commun, 2012
Diffraction data were collected from native and selenomethionine-substituted crystals of CCM2-Ct to resolutions of 2.9 and 2.7 A, respectively
CCM2 gene polymorphisms in Italian sporadic patients with cerebral cavernous malformation: a case-control study.
GeneRIF
Sidoti et al., Messina, Italy. In Int J Mol Med, 2012
The possible association of CCM2 polymorphisms with sporadic cerebral cavernous malformation, was investigated.
Oncostatin M suppresses oestrogen receptor-α expression and is associated with poor outcome in human breast cancer.
GeneRIF
Watson et al., Victoria, Canada. In Endocr Relat Cancer, 2012
Oncostatin M signaling may cause suppression of estrogen receptor-alpha and disease progression i breast cancer.
Protein kinase R plays a pivotal role in oncostatin M and interleukin-1 signalling in bovine articular cartilage chondrocytes.
GeneRIF
Mason et al., Cardiff, United Kingdom. In Eur Cell Mater, 2011
Protein kinase R plays a pivotal role in oncostatin M and interleukin-1 signalling in bovine articular cartilage chondrocytes.
Rewind to recover: dedifferentiation after cardiac injury.
Impact
Morrisey, Philadelphia, United States. In Cell Stem Cell, 2011
In this issue of Cell Stem Cell, Kubin et al. (2011) show that oncostatin M regulates this dedifferentiation which, while beneficial for recovery from acute injury, if persistent results in heart failure in both rodents and humans.
Oncostatin M is a major mediator of cardiomyocyte dedifferentiation and remodeling.
Impact
GeneRIF
Braun et al., Bad Nauheim, Germany. In Cell Stem Cell, 2011
Oncostatin M (OSM) is a major mediator of cardiomyocyte dedifferentiation and remodeling during acute myocardial infarction (MI) and in chronic dilated cardiomyopathy (DCM).
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