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Oncostatin M receptor - Revision history
2024-03-29T07:08:44Z
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<td colspan="2" style="background-color: #fff; color: #202122; text-align: center;">← Older revision</td>
<td colspan="2" style="background-color: #fff; color: #202122; text-align: center;">Revision as of 18:31, 27 November 2018</td>
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<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>{{Infobox_gene}}</div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>{{Infobox_gene}}</div></td></tr>
<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><br/></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><br/></td></tr>
<tr><td class="diff-marker" data-marker="−"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #ffe49c; vertical-align: top; white-space: pre-wrap;"><div>'''Oncostatin-M specific receptor subunit beta''' also known as the '''<del style="font-weight: bold; text-decoration: none;">oncostatin </del>M receptor''', is one of the receptor proteins for [[oncostatin M]], that in humans is encoded by the ''OSMR'' [[gene]].<ref name="entrez"/><ref name="pmid8999038">{{cite journal |vauthors=Mosley B, De Imus C, Friend D, Boiani N, Thoma B, Park LS, Cosman D | title = Dual oncostatin M (OSM) receptors. Cloning and characterization of an alternative signaling subunit conferring OSM-specific receptor activation | journal = <del style="font-weight: bold; text-decoration: none;">J. Biol. Chem. </del>| volume = 271 | issue = 51 | pages = 32635–43 |date=December 1996 | pmid = 8999038 | doi = 10.1074/jbc.271.51.32635<del style="font-weight: bold; text-decoration: none;">| url = </del>}}</ref></div></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div>'''Oncostatin-M specific receptor subunit beta''' also known as the '''<ins style="font-weight: bold; text-decoration: none;">Oncostatin </ins>M receptor <ins style="font-weight: bold; text-decoration: none;">(OSMR)</ins>''' , is one of the receptor proteins for [[oncostatin M]], that in humans is encoded by the ''OSMR'' [[gene]].<ref name="entrez"/><ref name="pmid8999038">{{cite journal | vauthors = Mosley B, De Imus C, Friend D, Boiani N, Thoma B, Park LS, Cosman D | title = Dual oncostatin M (OSM) receptors. Cloning and characterization of an alternative signaling subunit conferring OSM-specific receptor activation | journal = <ins style="font-weight: bold; text-decoration: none;">The Journal of Biological Chemistry </ins>| volume = 271 | issue = 51 | pages = 32635–43 | date = December 1996 | pmid = 8999038 | doi = 10.1074/jbc.271.51.32635 }}</ref></div></td></tr>
<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><br/></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><br/></td></tr>
<tr><td class="diff-marker" data-marker="−"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #ffe49c; vertical-align: top; white-space: pre-wrap;"><div>OSMR is a member of the [[type I cytokine receptor]] family. This protein heterodimerizes with [[glycoprotein 130|interleukin 6 signal transducer]] to form the type II oncostatin M receptor and with interleukin 31 receptor A to form the [[IL31RA|interleukin 31 receptor]], and thus transduces [[oncostatin M]] and [[interleukin 31]] induced signaling events.<ref name="entrez">{{cite web | title = Entrez Gene: oncostatin M receptor| url = https://www.ncbi.nlm.nih.gov/sites/entrez?Db=gene&Cmd=ShowDetailView&TermToSearch=9180| <del style="font-weight: bold; text-decoration: none;">accessdate </del>= }}</ref></div></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div>OSMR is a member of the [[type I cytokine receptor]] family. This protein heterodimerizes with [[glycoprotein 130|interleukin 6 signal transducer]] to form the type II oncostatin M receptor and with interleukin 31 receptor A to form the [[IL31RA|interleukin 31 receptor]], and thus transduces [[oncostatin M]] and [[interleukin 31]] induced signaling events.<ref name="entrez">{{cite web | title = Entrez Gene: oncostatin M receptor| url = https://www.ncbi.nlm.nih.gov/sites/entrez?Db=gene&Cmd=ShowDetailView&TermToSearch=9180| <ins style="font-weight: bold; text-decoration: none;">access-date </ins>= <ins style="font-weight: bold; text-decoration: none;">}}</ref></ins></div></td></tr>
<tr><td colspan="2" class="diff-side-deleted"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div> </div></td></tr>
<tr><td colspan="2" class="diff-side-deleted"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;">=== Expression ===</ins></div></td></tr>
<tr><td colspan="2" class="diff-side-deleted"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;">OSMR is widely expressed across non-haematopoietic, hepatocytes, mesothelial cells, glial cells and epithelial cell types across various organs and mammary glands.<ref>{{cite journal | vauthors = West NR, Owens BM, Hegazy AN | title = The oncostatin M-stromal cell axis in health and disease | journal = Scandinavian Journal of Immunology | volume = 88 | issue = 3 | pages = e12694 | date = September 2018 | pmid = 29926972 | doi = 10.1111/sji.12694 }}</ref> OSM receptor is abundantly expressed on endothelial and stromal/fibroblast cells in the lung of mice.<ref>{{cite journal | vauthors = Machiyama T, So T, Okuyama Y, Kobayashi S, Phung HT, Asao A, Harigae H, Ishii N | title = TNF receptor associated factor 5 controls oncostatin M-mediated lung inflammation | journal = Biochemical and Biophysical Research Communications | volume = 499 | issue = 3 | pages = 544–550 | date = May 2018 | pmid = 29596835 | doi = 10.1016/j.bbrc.2018.03.186 }}</ref>=</ins></div></td></tr>
<tr><td colspan="2" class="diff-side-deleted"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div> </div></td></tr>
<tr><td colspan="2" class="diff-side-deleted"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;">In vitro expression of OSMR in fetal hepatocytes is upregulated by OSM stimulation.<ref>{{cite journal | vauthors = Kamiya A, Kinoshita T, Ito Y, Matsui T, Morikawa Y, Senba E, Nakashima K, Taga T, Yoshida K, Kishimoto T, Miyajima A | title = Fetal liver development requires a paracrine action of oncostatin M through the gp130 signal transducer | journal = The EMBO Journal | volume = 18 | issue = 8 | pages = 2127–36 | date = April 1999 | pmid = 10205167 | pmc = 1171297 | doi = 10.1093/emboj/18.8.2127 }}</ref></ins></div></td></tr>
<tr><td colspan="2" class="diff-side-deleted"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div> </div></td></tr>
<tr><td colspan="2" class="diff-side-deleted"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;">OSMR expression has been shown to be induced by parathyroid hormone in osteoblasts and OSM.<ref>{{cite journal | vauthors = Walker EC, Poulton IJ, McGregor NE, Ho PW, Allan EH, Quach JM, Martin TJ, Sims NA | title = Sustained RANKL response to parathyroid hormone in oncostatin M receptor-deficient osteoblasts converts anabolic treatment to a catabolic effect in vivo | journal = Journal of Bone and Mineral Research | volume = 27 | issue = 4 | pages = 902–12 | date = April 2012 | pmid = 22190112 | doi = 10.1002/jbmr.1506 }}</ref><ref>{{cite journal | vauthors = Blanchard F, Wang Y, Kinzie E, Duplomb L, Godard A, Baumann H | title = Oncostatin M regulates the synthesis and turnover of gp130, leukemia inhibitory factor receptor alpha, and oncostatin M receptor beta by distinct mechanisms | journal = The Journal of Biological Chemistry | volume = 276 | issue = 50 | pages = 47038–45 | date = December 2001 | pmid = 11602599 | doi = 10.1074/jbc.M107971200 }}</ref></ins></div></td></tr>
<tr><td colspan="2" class="diff-side-deleted"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div> </div></td></tr>
<tr><td colspan="2" class="diff-side-deleted"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;">=== Signaling ===</ins></div></td></tr>
<tr><td colspan="2" class="diff-side-deleted"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;">Intracellular cell signalling occurs as a consequence of extracellular binding of the ligand [[Oncostatin M|OSM]] to OSMR complexes, formed from dimerization with receptor subunits such as [[Glycoprotein 130|gp130]]. Activation of the OSMR-gp130 complex by OSM triggers Janus Kinase 1 ([[Janus kinase 1|JAK1]]) and [[Janus kinase 2|Jak2]] cross phosphorylation of tyrosine residues on the intracellular receptor domain. Downstream signaling activation of the OSMR-gp130 complex along the JAK1 pathway leads to IL-6 signalling which is linked with activation of the MAPK cascade, [[Phosphoinositide 3-kinase|PI3K]] cascade and [[STAT3]] activation.<ref>{{cite journal | vauthors = Hunter CA, Jones SA | title = IL-6 as a keystone cytokine in health and disease | journal = Nature Immunology | volume = 16 | issue = 5 | pages = 448–57 | date = May 2015 | pmid = 25898198 | doi = 10.1038/ni.3153 }}</ref><ref>{{cite journal | vauthors = Heinrich PC, Behrmann I, Haan S, Hermanns HM, Müller-Newen G, Schaper F | title = Principles of interleukin (IL)-6-type cytokine signalling and its regulation | journal = The Biochemical Journal | volume = 374 | issue = Pt 1 | pages = 1–20 | date = August 2003 | pmid = 12773095 | pmc = 1223585 | doi = 10.1042/bj20030407 }}</ref></ins></div></td></tr>
<tr><td colspan="2" class="diff-side-deleted"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div> </div></td></tr>
<tr><td colspan="2" class="diff-side-deleted"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;">OSM induced recruitment of [[SHC1|SHC]] to the OSMRβ sub-unit has been shown to enhance [[Ras/Raf/MAP kinase|Ras/Raf/MAPK]] signaling and lead [[P38 mitogen-activated protein kinases|p38]] and [[JNK]] activation.<ref>{{cite journal | vauthors = Hermanns HM, Radtke S, Schaper F, Heinrich PC, Behrmann I | title = Non-redundant signal transduction of interleukin-6-type cytokines. The adapter protein Shc is specifically recruited to rhe oncostatin M receptor | journal = The Journal of Biological Chemistry | volume = 275 | issue = 52 | pages = 40742–8 | date = December 2000 | pmid = 11016927 | doi = 10.1074/jbc.M005408200 </ins>}}</ref></div></td></tr>
<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><br/></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><br/></td></tr>
<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>== Clinical significance ==</div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>== Clinical significance ==</div></td></tr>
<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><br/></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><br/></td></tr>
<tr><td class="diff-marker" data-marker="−"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #ffe49c; vertical-align: top; white-space: pre-wrap;"><div>The oncostatin M receptor is associated with [[primary cutaneous amyloidosis]].<ref name="pmid18179886">{{cite journal <del style="font-weight: bold; text-decoration: none;"> </del>|vauthors=Arita K, South AP, Hans-Filho G, <del style="font-weight: bold; text-decoration: none;">etal </del>|title=Oncostatin M <del style="font-weight: bold; text-decoration: none;">Receptor</del>-<del style="font-weight: bold; text-decoration: none;">β Mutations Underlie Familial Primary Localized Cutaneous Amyloidosis </del>|journal=<del style="font-weight: bold; text-decoration: none;">Am. J. Hum. Genet. </del>|volume=82 |issue=1 |pages=73–80 |date=January 2008 |pmid=18179886 |doi=10.1016/j.ajhg.2007.09.002 |<del style="font-weight: bold; text-decoration: none;">url</del>= |pmc=<del style="font-weight: bold; text-decoration: none;">2253984</del>}}</ref></div></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div>The oncostatin M receptor is associated with [[primary cutaneous amyloidosis]].<ref name="pmid18179886">{{cite journal | vauthors = Arita K, South AP, Hans-Filho G, <ins style="font-weight: bold; text-decoration: none;">Sakuma TH, Lai-Cheong J, Clements S, Odashiro M, Odashiro DN, Hans-Neto G, Hans NR, Holder MV, Bhogal BS, Hartshorne ST, Akiyama M, Shimizu H, McGrath JA </ins>| title = Oncostatin M <ins style="font-weight: bold; text-decoration: none;">receptor</ins>-<ins style="font-weight: bold; text-decoration: none;">beta mutations underlie familial primary localized cutaneous amyloidosis </ins>| journal = <ins style="font-weight: bold; text-decoration: none;">American Journal of Human Genetics </ins>| volume = 82 | issue = 1 | pages = 73–80 | date = January 2008 | pmid = 18179886 <ins style="font-weight: bold; text-decoration: none;">| pmc = 2253984 </ins>| doi = 10.1016/j.ajhg.2007.09.002 <ins style="font-weight: bold; text-decoration: none;">}}</ref></ins></div></td></tr>
<tr><td colspan="2" class="diff-side-deleted"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div> </div></td></tr>
<tr><td colspan="2" class="diff-side-deleted"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;">OSM signaling via the OSMR is believed to play an important role in bone turnover as Mice lacking the OSMR receptor have osteopetrotic phenotypes.<ref>{{cite journal | vauthors = Walker EC, McGregor NE, Poulton IJ, Solano M, Pompolo S, Fernandes TJ, Constable MJ, Nicholson GC, Zhang JG, Nicola NA, Gillespie MT, Martin TJ, Sims NA | title = Oncostatin M promotes bone formation independently of resorption when signaling through leukemia inhibitory factor receptor in mice | journal = The Journal of Clinical Investigation | volume = 120 | issue = 2 | pages = 582–92 | date = February 2010 | pmid = 20051625 | pmc = 2810087 | doi = 10.1172/jci40568 }}</ref> Lack of OSMRβ activity has also been linked to adipose tissue inflammation and insulin resistance preceding obesity.<ref>{{cite journal | vauthors = Komori T, Tanaka M, Senba E, Miyajima A, Morikawa Y | title = Lack of oncostatin M receptor β leads to adipose tissue inflammation and insulin resistance by switching macrophage phenotype | journal = The Journal of Biological Chemistry | volume = 288 | issue = 30 </ins>| <ins style="font-weight: bold; text-decoration: none;">pages </ins>= <ins style="font-weight: bold; text-decoration: none;">21861–75 | date = July 2013 | pmid = 23760275 </ins>| pmc = <ins style="font-weight: bold; text-decoration: none;">3724642 | doi = 10.1074/jbc.M113.461905 }}</ref></ins></div></td></tr>
<tr><td colspan="2" class="diff-side-deleted"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div> </div></td></tr>
<tr><td colspan="2" class="diff-side-deleted"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;">OSM in-vivo regulation of hematopoiesis, through stimulation of stromal cells & hematopoietic progenitors - megakaryocytic and erythrocytic progenitors, is carried out by the OSMRβ receptor.<ref>{{cite journal | vauthors = Tanaka M, Hirabayashi Y, Sekiguchi T, Inoue T, Katsuki M, Miyajima A | title = Targeted disruption of oncostatin M receptor results in altered hematopoiesis | journal = Blood | volume = 102 | issue = 9 | pages = 3154–62 | date = November 2003 | pmid = 12855584 | doi = 10.1182/blood-2003-02-0367 }}</ref></ins></div></td></tr>
<tr><td colspan="2" class="diff-side-deleted"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div> </div></td></tr>
<tr><td colspan="2" class="diff-side-deleted"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;">==== Heart Disease ====</ins></div></td></tr>
<tr><td colspan="2" class="diff-side-deleted"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;">Inhibition of the OSMRβ extracellular subunit has been shown has been shown to prevent OSM-mediated down-regulation of myoglobin in cardiomyocytes and related apoptosis of cardiomyocytes in inflammatory heart failure.<ref>{{cite journal | vauthors = Pöling J, Gajawada P, Richter M, Lörchner H, Polyakova V, Kostin S, Shin J, Boettger T, Walther T, Rees W, Wietelmann A, Warnecke H, Kubin T, Braun T | title = Therapeutic targeting of the oncostatin M receptor-β prevents inflammatory heart failure | journal = Basic Research in Cardiology | volume = 109 | issue = 1 | pages = 396 | date = January 2014 | pmid = 24292852 | doi = 10.1007/s00395-013-0396-3 }}</ref></ins></div></td></tr>
<tr><td colspan="2" class="diff-side-deleted"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div> </div></td></tr>
<tr><td colspan="2" class="diff-side-deleted"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;">OSMRβ is not only overexpressed in patients with chronic dilated cardiomyopathy but has been shown to control dedifferentiation and loss of sarcomeric structures in myocardial infarction and dilated cardio myopathy.<ref name="Kubin T 2011">{{cite journal | vauthors = Kubin T, Pöling J, Kostin S, Gajawada P, Hein S, Rees W, Wietelmann A, Tanaka M, Lörchner H, Schimanski S, Szibor M, Warnecke H, Braun T | title = Oncostatin M is a major mediator of cardiomyocyte dedifferentiation and remodeling | journal = Cell Stem Cell | volume = 9 | issue = 5 | pages = 420–32 | date = November 2011 | pmid = 22056139 | doi = 10.1016/j.stem.2011.08.013 }}</ref> OSM and OSMRβ mediated dedifferentiation has been shown to increase chances of survival after acute myocardial damage but poor survival rates and compromised pump functions in chronic disease states.<ref name="Kubin T 2011"/></ins></div></td></tr>
<tr><td colspan="2" class="diff-side-deleted"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div> </div></td></tr>
<tr><td colspan="2" class="diff-side-deleted"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;">==== Cancer ====</ins></div></td></tr>
<tr><td colspan="2" class="diff-side-deleted"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;">OSMR activates STAT3 and transforming growth factor β (TGF-β) effector SMAD3 to regulate expression of genes responsible for inducing a mesenchymal/CSC phenotype.<ref>{{cite journal | vauthors = Junk DJ, Bryson BL, Smigiel JM, Parameswaran N, Bartel CA, Jackson MW | title = Oncostatin M promotes cancer cell plasticity through cooperative STAT3-SMAD3 signaling | language = En | journal = Oncogene | volume = 36 | issue = 28 | pages = 4001–4013 | date = July 2017 | pmid = 28288136 | pmc = 5509502 | doi = 10.1038/onc.2017.33 }}</ref></ins></div></td></tr>
<tr><td colspan="2" class="diff-side-deleted"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div> </div></td></tr>
<tr><td colspan="2" class="diff-side-deleted"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;">OSM-induced biological effects on breast tumor– derived cell lines were specifically mediated through the gp130/OSMRB complex.<ref>{{cite journal | vauthors = Underhill-Day N, Heath JK | title = Oncostatin M (OSM) cytostasis of breast tumor cells: characterization of an OSM receptor beta-specific kernel | journal = Cancer Research | volume = 66 | issue = 22 | pages = 10891–901 | date = November 2006 | pmid = 17108126 | doi = 10.1158/0008-5472.CAN-06-1766 }}</ref></ins></div></td></tr>
<tr><td colspan="2" class="diff-side-deleted"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div> </div></td></tr>
<tr><td colspan="2" class="diff-side-deleted"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;">the OSM receptor (OSMR) is overexpressed in cervical squamous cell carcinomas and, independent of tumor stage, is associated with adverse clinical outcomes and higher relative risk of death.<ref>{{cite journal | vauthors = Ng G, Winder D, Muralidhar B, Gooding E, Roberts I, Pett M, Mukherjee G, Huang J, Coleman N | title = Gain and overexpression of the oncostatin M receptor occur frequently in cervical squamous cell carcinoma and are associated with adverse clinical outcome | journal = The Journal of Pathology | volume = 212 | issue = 3 | pages = 325–34 | date = July 2007 | pmid = 17516585 | doi = 10.1002/path.2184 }}</ref></ins></div></td></tr>
<tr><td colspan="2" class="diff-side-deleted"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div> </div></td></tr>
<tr><td colspan="2" class="diff-side-deleted"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;">OSM and OSMRβ are co-expressed and lead to STAT 3 activation malignant human ovarian epithelial cells.<ref>{{cite journal | vauthors = Savarese TM, Campbell CL, McQuain C, Mitchell K, Guardiani R, Quesenberry PJ, Nelson BE | title = Coexpression of oncostatin M and its receptors and evidence for STAT3 activation in human ovarian carcinomas | journal = Cytokine | volume = 17 | issue = 6 | pages = 324–34 | date = March 2002 | pmid = 12061840 | doi = 10.1006/cyto.2002.1022 }}</ref></ins></div></td></tr>
<tr><td colspan="2" class="diff-side-deleted"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div> </div></td></tr>
<tr><td colspan="2" class="diff-side-deleted"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;">''The OSMR β'' promoter gene is highly methylated in primary Colorectal Cancer tissues and fecal DNA, it is a highly specific diagnostic biomarker of Colorectal Cancer.<ref>{{cite journal | vauthors = Kim MS, Louwagie J, Carvalho B, Terhaar Sive Droste JS, Park HL, Chae YK, Yamashita K, Liu J, Ostrow KL, Ling S, Guerrero-Preston R, Demokan S, Yalniz Z, Dalay N, Meijer GA, Van Criekinge W, Sidransky D | title = Promoter DNA methylation of oncostatin m receptor-beta as a novel diagnostic and therapeutic marker in colon cancer | journal = PLOS One | volume = 4 | issue = 8 | pages = e6555 | date = August 2009 | pmid = 19662090 | pmc = 2717211 | doi = 10.1371/journal.pone.0006555 </ins>}}</ref></div></td></tr>
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<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>{{reflist}}</div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>{{reflist}}</div></td></tr>
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'''Oncostatin-M specific receptor subunit beta''' also known as the '''oncostatin M receptor''', is one of the receptor proteins for [[oncostatin M]], that in humans is encoded by the ''OSMR'' [[gene]].<ref name="entrez"/><ref name="pmid8999038">{{cite journal |vauthors=Mosley B, De Imus C, Friend D, Boiani N, Thoma B, Park LS, Cosman D | title = Dual oncostatin M (OSM) receptors. Cloning and characterization of an alternative signaling subunit conferring OSM-specific receptor activation | journal = J. Biol. Chem. | volume = 271 | issue = 51 | pages = 32635–43 |date=December 1996 | pmid = 8999038 | doi = 10.1074/jbc.271.51.32635| url = }}</ref><br />
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OSMR is a member of the [[type I cytokine receptor]] family. This protein heterodimerizes with [[glycoprotein 130|interleukin 6 signal transducer]] to form the type II oncostatin M receptor and with interleukin 31 receptor A to form the [[IL31RA|interleukin 31 receptor]], and thus transduces [[oncostatin M]] and [[interleukin 31]] induced signaling events.<ref name="entrez">{{cite web | title = Entrez Gene: oncostatin M receptor| url = https://www.ncbi.nlm.nih.gov/sites/entrez?Db=gene&Cmd=ShowDetailView&TermToSearch=9180| accessdate = }}</ref><br />
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== Clinical significance ==<br />
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The oncostatin M receptor is associated with [[primary cutaneous amyloidosis]].<ref name="pmid18179886">{{cite journal |vauthors=Arita K, South AP, Hans-Filho G, etal |title=Oncostatin M Receptor-β Mutations Underlie Familial Primary Localized Cutaneous Amyloidosis |journal=Am. J. Hum. Genet. |volume=82 |issue=1 |pages=73–80 |date=January 2008 |pmid=18179886 |doi=10.1016/j.ajhg.2007.09.002 |url= |pmc=2253984}}</ref><br />
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==References==<br />
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==External links==<br />
* {{MeshName|Oncostatin+M+Receptor}}<br />
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[[Category:Type I cytokine receptors]]<br />
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