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{{Infobox_gene}}
{{Infobox_gene}}


'''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>
'''Oncostatin-M specific receptor subunit beta''' also known as the '''Oncostatin M receptor (OSMR)''' , 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 = The Journal of Biological Chemistry | volume = 271 | issue = 51 | pages = 32635–43 | date = December 1996 | pmid = 8999038 | doi = 10.1074/jbc.271.51.32635 }}</ref>


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>
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| access-date = }}</ref>
 
=== Expression ===
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>=
 
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>
 
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>
 
=== Signaling ===
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>
 
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 }}</ref>


== Clinical significance ==
== Clinical significance ==


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>
The oncostatin M receptor is associated with [[primary cutaneous amyloidosis]].<ref name="pmid18179886">{{cite journal | vauthors = Arita K, South AP, Hans-Filho G, 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 | title = Oncostatin M receptor-beta mutations underlie familial primary localized cutaneous amyloidosis | journal = American Journal of Human Genetics | volume = 82 | issue = 1 | pages = 73–80 | date = January 2008 | pmid = 18179886 | pmc = 2253984 | doi = 10.1016/j.ajhg.2007.09.002 }}</ref>
 
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 | pages = 21861–75 | date = July 2013 | pmid = 23760275 | pmc = 3724642 | doi = 10.1074/jbc.M113.461905 }}</ref>
 
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>
 
==== Heart Disease ====
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>
 
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"/>
 
==== Cancer ====
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>
 
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>
 
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>
 
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>
 
''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 }}</ref>


==References==
== References ==
{{reflist}}
{{reflist}}


==External links==
== External links ==
* {{MeshName|Oncostatin+M+Receptor}}
* {{MeshName|Oncostatin+M+Receptor}}


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[[Category:Type I cytokine receptors]]
[[Category:Type I cytokine receptors]]
{{gene-5-stub}}

Latest revision as of 18:31, 27 November 2018

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Orthologs
SpeciesHumanMouse
Entrez

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Ensembl

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UniProt

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RefSeq (mRNA)

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RefSeq (protein)

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Oncostatin-M specific receptor subunit beta also known as the Oncostatin M receptor (OSMR) , is one of the receptor proteins for oncostatin M, that in humans is encoded by the OSMR gene.[1][2]

OSMR is a member of the type I cytokine receptor family. This protein heterodimerizes with interleukin 6 signal transducer to form the type II oncostatin M receptor and with interleukin 31 receptor A to form the interleukin 31 receptor, and thus transduces oncostatin M and interleukin 31 induced signaling events.[1]

Expression

OSMR is widely expressed across non-haematopoietic, hepatocytes, mesothelial cells, glial cells and epithelial cell types across various organs and mammary glands.[3] OSM receptor is abundantly expressed on endothelial and stromal/fibroblast cells in the lung of mice.[4]=

In vitro expression of OSMR  in fetal hepatocytes is upregulated by OSM stimulation.[5]

OSMR expression has been shown to be induced by parathyroid hormone in osteoblasts and OSM.[6][7]

Signaling

Intracellular cell signalling occurs as a consequence of extracellular binding of the ligand OSM to OSMR complexes, formed from dimerization with receptor subunits such as gp130. Activation of the OSMR-gp130 complex by OSM triggers Janus Kinase 1 (JAK1) and 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, PI3K cascade and STAT3 activation.[8][9]

OSM induced recruitment of SHC to the OSMRβ sub-unit has been shown to enhance Ras/Raf/MAPK signaling and lead p38 and JNK activation.[10]

Clinical significance

The oncostatin M receptor is associated with primary cutaneous amyloidosis.[11]

OSM signaling via the OSMR is believed to play an important role in bone turnover as Mice lacking the OSMR receptor have osteopetrotic phenotypes.[12] Lack of OSMRβ activity has also been linked to adipose tissue inflammation and insulin resistance preceding obesity.[13]

OSM in-vivo regulation of hematopoiesis, through stimulation of stromal cells & hematopoietic progenitors - megakaryocytic and erythrocytic progenitors, is carried out by the OSMRβ receptor.[14]

Heart Disease

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.[15]

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.[16] 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.[16]

Cancer

OSMR activates STAT3 and transforming growth factor β (TGF-β) effector SMAD3 to regulate expression of genes responsible for inducing a mesenchymal/CSC phenotype.[17]

OSM-induced biological effects on breast tumor– derived cell lines were specifically mediated through the gp130/OSMRB complex.[18]

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.[19]

OSM and OSMRβ are co-expressed and lead to STAT 3 activation malignant human ovarian epithelial cells.[20]

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.[21]

References

  1. ↑ 1.0 1.1 "Entrez Gene: oncostatin M receptor".
  2. ↑ Mosley B, De Imus C, Friend D, Boiani N, Thoma B, Park LS, Cosman D (December 1996). "Dual oncostatin M (OSM) receptors. Cloning and characterization of an alternative signaling subunit conferring OSM-specific receptor activation". The Journal of Biological Chemistry. 271 (51): 32635–43. doi:10.1074/jbc.271.51.32635. PMID 8999038.
  3. ↑ West NR, Owens BM, Hegazy AN (September 2018). "The oncostatin M-stromal cell axis in health and disease". Scandinavian Journal of Immunology. 88 (3): e12694. doi:10.1111/sji.12694. PMID 29926972.
  4. ↑ Machiyama T, So T, Okuyama Y, Kobayashi S, Phung HT, Asao A, Harigae H, Ishii N (May 2018). "TNF receptor associated factor 5 controls oncostatin M-mediated lung inflammation". Biochemical and Biophysical Research Communications. 499 (3): 544–550. doi:10.1016/j.bbrc.2018.03.186. PMID 29596835.
  5. ↑ Kamiya A, Kinoshita T, Ito Y, Matsui T, Morikawa Y, Senba E, Nakashima K, Taga T, Yoshida K, Kishimoto T, Miyajima A (April 1999). "Fetal liver development requires a paracrine action of oncostatin M through the gp130 signal transducer". The EMBO Journal. 18 (8): 2127–36. doi:10.1093/emboj/18.8.2127. PMC 1171297. PMID 10205167.
  6. ↑ Walker EC, Poulton IJ, McGregor NE, Ho PW, Allan EH, Quach JM, Martin TJ, Sims NA (April 2012). "Sustained RANKL response to parathyroid hormone in oncostatin M receptor-deficient osteoblasts converts anabolic treatment to a catabolic effect in vivo". Journal of Bone and Mineral Research. 27 (4): 902–12. doi:10.1002/jbmr.1506. PMID 22190112.
  7. ↑ Blanchard F, Wang Y, Kinzie E, Duplomb L, Godard A, Baumann H (December 2001). "Oncostatin M regulates the synthesis and turnover of gp130, leukemia inhibitory factor receptor alpha, and oncostatin M receptor beta by distinct mechanisms". The Journal of Biological Chemistry. 276 (50): 47038–45. doi:10.1074/jbc.M107971200. PMID 11602599.
  8. ↑ Hunter CA, Jones SA (May 2015). "IL-6 as a keystone cytokine in health and disease". Nature Immunology. 16 (5): 448–57. doi:10.1038/ni.3153. PMID 25898198.
  9. ↑ Heinrich PC, Behrmann I, Haan S, Hermanns HM, Müller-Newen G, Schaper F (August 2003). "Principles of interleukin (IL)-6-type cytokine signalling and its regulation". The Biochemical Journal. 374 (Pt 1): 1–20. doi:10.1042/bj20030407. PMC 1223585. PMID 12773095.
  10. ↑ Hermanns HM, Radtke S, Schaper F, Heinrich PC, Behrmann I (December 2000). "Non-redundant signal transduction of interleukin-6-type cytokines. The adapter protein Shc is specifically recruited to rhe oncostatin M receptor". The Journal of Biological Chemistry. 275 (52): 40742–8. doi:10.1074/jbc.M005408200. PMID 11016927.
  11. ↑ Arita K, South AP, Hans-Filho G, 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 (January 2008). "Oncostatin M receptor-beta mutations underlie familial primary localized cutaneous amyloidosis". American Journal of Human Genetics. 82 (1): 73–80. doi:10.1016/j.ajhg.2007.09.002. PMC 2253984. PMID 18179886.
  12. ↑ 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 (February 2010). "Oncostatin M promotes bone formation independently of resorption when signaling through leukemia inhibitory factor receptor in mice". The Journal of Clinical Investigation. 120 (2): 582–92. doi:10.1172/jci40568. PMC 2810087. PMID 20051625.
  13. ↑ Komori T, Tanaka M, Senba E, Miyajima A, Morikawa Y (July 2013). "Lack of oncostatin M receptor β leads to adipose tissue inflammation and insulin resistance by switching macrophage phenotype". The Journal of Biological Chemistry. 288 (30): 21861–75. doi:10.1074/jbc.M113.461905. PMC 3724642. PMID 23760275.
  14. ↑ Tanaka M, Hirabayashi Y, Sekiguchi T, Inoue T, Katsuki M, Miyajima A (November 2003). "Targeted disruption of oncostatin M receptor results in altered hematopoiesis". Blood. 102 (9): 3154–62. doi:10.1182/blood-2003-02-0367. PMID 12855584.
  15. ↑ 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 (January 2014). "Therapeutic targeting of the oncostatin M receptor-β prevents inflammatory heart failure". Basic Research in Cardiology. 109 (1): 396. doi:10.1007/s00395-013-0396-3. PMID 24292852.
  16. ↑ 16.0 16.1 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 (November 2011). "Oncostatin M is a major mediator of cardiomyocyte dedifferentiation and remodeling". Cell Stem Cell. 9 (5): 420–32. doi:10.1016/j.stem.2011.08.013. PMID 22056139.
  17. ↑ Junk DJ, Bryson BL, Smigiel JM, Parameswaran N, Bartel CA, Jackson MW (July 2017). "Oncostatin M promotes cancer cell plasticity through cooperative STAT3-SMAD3 signaling". Oncogene. 36 (28): 4001–4013. doi:10.1038/onc.2017.33. PMC 5509502. PMID 28288136.
  18. ↑ Underhill-Day N, Heath JK (November 2006). "Oncostatin M (OSM) cytostasis of breast tumor cells: characterization of an OSM receptor beta-specific kernel". Cancer Research. 66 (22): 10891–901. doi:10.1158/0008-5472.CAN-06-1766. PMID 17108126.
  19. ↑ Ng G, Winder D, Muralidhar B, Gooding E, Roberts I, Pett M, Mukherjee G, Huang J, Coleman N (July 2007). "Gain and overexpression of the oncostatin M receptor occur frequently in cervical squamous cell carcinoma and are associated with adverse clinical outcome". The Journal of Pathology. 212 (3): 325–34. doi:10.1002/path.2184. PMID 17516585.
  20. ↑ Savarese TM, Campbell CL, McQuain C, Mitchell K, Guardiani R, Quesenberry PJ, Nelson BE (March 2002). "Coexpression of oncostatin M and its receptors and evidence for STAT3 activation in human ovarian carcinomas". Cytokine. 17 (6): 324–34. doi:10.1006/cyto.2002.1022. PMID 12061840.
  21. ↑ 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 (August 2009). "Promoter DNA methylation of oncostatin m receptor-beta as a novel diagnostic and therapeutic marker in colon cancer". PLOS One. 4 (8): e6555. doi:10.1371/journal.pone.0006555. PMC 2717211. PMID 19662090.

External links

This article incorporates text from the United States National Library of Medicine, which is in the public domain.

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