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dc.contributor.authorRanger, Ann M.
dc.contributor.authorGerstenfeld, Louis C.
dc.contributor.authorWang, Jinxi
dc.contributor.authorKon, Tamiyo
dc.contributor.authorBae, Hyunsu
dc.contributor.authorGravallese, Ellen M.
dc.contributor.authorGlimcher, Melvin J.
dc.contributor.authorGlimcher, Laurie H.
dc.date2022-08-11T08:10:51.000
dc.date.accessioned2022-08-23T17:22:24Z
dc.date.available2022-08-23T17:22:24Z
dc.date.issued2000-01-03
dc.date.submitted2015-02-25
dc.identifier.citationJ Exp Med. 2000 Jan 3;191(1):9-22. doi: 10.1084/jem.191.1.9. <a href="http://dx.doi.org/10.1084/jem.191.1.9">Link to article on publisher's website</a>
dc.identifier.issn0022-1007 (Linking)
dc.identifier.doi10.1084/jem.191.1.9
dc.identifier.pmid10620601
dc.identifier.urihttp://hdl.handle.net/20.500.14038/48739
dc.description<p>At the time of publication, Ellen Gravallese was not yet affiliated with the University of Massachusetts Medical School.</p>
dc.description.abstractNuclear factor of activated T cells (NFAT) transcription factors regulate gene expression in lymphocytes and control cardiac valve formation. Here, we report that NFATp regulates chondrogenesis in the adult animal. In mice lacking NFATp, resident cells in the extraarticular connective tissues spontaneously differentiate to cartilage. These cartilage cells progressively differentiate and the tissue undergoes endochondral ossification, recapitulating the development of endochondral bone. Proliferation of already existing articular cartilage cells also occurs in some older animals. At both sites, neoplastic changes in the cartilage cells occur. Consistent with these data, NFATp expression is regulated in mesenchymal stem cells induced to differentiate along a chondrogenic pathway. Lack of NFATp in articular cartilage cells results in increased expression of cartilage markers, whereas overexpression of NFATp in cartilage cell lines extinguishes the cartilage phenotype. Thus, NFATp is a repressor of cartilage cell growth and differentiation and also has the properties of a tumor suppressor.
dc.language.isoen_US
dc.relation<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=10620601&dopt=Abstract">Link to Article in PubMed</a>
dc.rights<p>Publisher PDF posted as allowed by the publisher's author rights policy at http://www.rupress.org/site/subscriptions/terms.xhtml.</p> <p>Beginning six months after publication, RUP grants the public the non-exclusive right to copy, distribute, or display the Work under a Creative Commons Attribution-Noncommercial-Share Alike 3.0 Unported license</p>
dc.rights.urihttp://creativecommons.org/licenses/by-nc/3.0/
dc.subjectAnimals
dc.subjectBone Development
dc.subjectBone and Bones
dc.subjectCartilage
dc.subjectCell Differentiation
dc.subjectCell Division
dc.subject*Chondrogenesis
dc.subjectDNA-Binding Proteins
dc.subjectGenes, Tumor Suppressor
dc.subjectMice
dc.subjectMice, Inbred BALB C
dc.subjectMice, Knockout
dc.subjectNFATC Transcription Factors
dc.subject*Nuclear Proteins
dc.subjectStem Cells
dc.subjectTranscription Factors
dc.subjectcartilage
dc.subjectNFATp
dc.subjectmesenchymal stem cells
dc.subjectchondrosarcoma
dc.subjectdifferentiation
dc.subjectCancer Biology
dc.subjectCell Biology
dc.subjectCellular and Molecular Physiology
dc.titleThe nuclear factor of activated T cells (NFAT) transcription factor NFATp (NFATc2) is a repressor of chondrogenesis
dc.typeJournal Article
dc.source.journaltitleThe Journal of experimental medicine
dc.source.volume191
dc.source.issue1
dc.identifier.legacyfulltexthttps://escholarship.umassmed.edu/cgi/viewcontent.cgi?article=1025&amp;context=rheumatology_pubs&amp;unstamped=1
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/rheumatology_pubs/26
dc.identifier.contextkey6724677
refterms.dateFOA2022-08-23T17:22:24Z
html.description.abstract<p>Nuclear factor of activated T cells (NFAT) transcription factors regulate gene expression in lymphocytes and control cardiac valve formation. Here, we report that NFATp regulates chondrogenesis in the adult animal. In mice lacking NFATp, resident cells in the extraarticular connective tissues spontaneously differentiate to cartilage. These cartilage cells progressively differentiate and the tissue undergoes endochondral ossification, recapitulating the development of endochondral bone. Proliferation of already existing articular cartilage cells also occurs in some older animals. At both sites, neoplastic changes in the cartilage cells occur. Consistent with these data, NFATp expression is regulated in mesenchymal stem cells induced to differentiate along a chondrogenic pathway. Lack of NFATp in articular cartilage cells results in increased expression of cartilage markers, whereas overexpression of NFATp in cartilage cell lines extinguishes the cartilage phenotype. Thus, NFATp is a repressor of cartilage cell growth and differentiation and also has the properties of a tumor suppressor.</p>
dc.identifier.submissionpathrheumatology_pubs/26
dc.contributor.departmentDepartment of Medicine, Division of Rheumatology
dc.source.pages9-22


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<p>Publisher PDF posted as allowed by the publisher's author rights policy at http://www.rupress.org/site/subscriptions/terms.xhtml.</p>
<p>Beginning six months after publication, RUP grants the public the non-exclusive right to copy, distribute, or display the Work under a Creative Commons Attribution-Noncommercial-Share Alike 3.0 Unported license</p>
Except where otherwise noted, this item's license is described as <p>Publisher PDF posted as allowed by the publisher's author rights policy at http://www.rupress.org/site/subscriptions/terms.xhtml.</p> <p>Beginning six months after publication, RUP grants the public the non-exclusive right to copy, distribute, or display the Work under a Creative Commons Attribution-Noncommercial-Share Alike 3.0 Unported license</p>