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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Skeletal metamorphosis in fibrodysplasia ossificans progressiva (FOP)</title><author><name sortKey="Kaplan, Frederick S" sort="Kaplan, Frederick S" uniqKey="Kaplan F" first="Frederick S." last="Kaplan">Frederick S. Kaplan</name></author><author><name sortKey="Shen, Qi" sort="Shen, Qi" uniqKey="Shen Q" first="Qi" last="Shen">Qi Shen</name></author><author><name sortKey="Lounev, Vitali" sort="Lounev, Vitali" uniqKey="Lounev V" first="Vitali" last="Lounev">Vitali Lounev</name></author><author><name sortKey="Seemann, Petra" sort="Seemann, Petra" uniqKey="Seemann P" first="Petra" last="Seemann">Petra Seemann</name></author><author><name sortKey="Groppe, Jay" sort="Groppe, Jay" uniqKey="Groppe J" first="Jay" last="Groppe">Jay Groppe</name></author><author><name sortKey="Katagiri, Takenobu" sort="Katagiri, Takenobu" uniqKey="Katagiri T" first="Takenobu" last="Katagiri">Takenobu Katagiri</name></author><author><name sortKey="Pignolo, Robert J" sort="Pignolo, Robert J" uniqKey="Pignolo R" first="Robert J." last="Pignolo">Robert J. Pignolo</name></author><author><name sortKey="Shore, Eileen M" sort="Shore, Eileen M" uniqKey="Shore E" first="Eileen M." last="Shore">Eileen M. Shore</name></author></titleStmt><publicationStmt><idno type="wicri:source">PMC</idno><idno type="pmid">18979151</idno><idno type="pmc">3620015</idno><idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3620015</idno><idno type="RBID">PMC:3620015</idno><idno type="doi">10.1007/s00774-008-0879-8</idno><date when="2008">2008</date><idno type="wicri:Area/Pmc/Corpus">003A11</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">003A11</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Skeletal metamorphosis in fibrodysplasia ossificans progressiva (FOP)</title><author><name sortKey="Kaplan, Frederick S" sort="Kaplan, Frederick S" uniqKey="Kaplan F" first="Frederick S." last="Kaplan">Frederick S. Kaplan</name></author><author><name sortKey="Shen, Qi" sort="Shen, Qi" uniqKey="Shen Q" first="Qi" last="Shen">Qi Shen</name></author><author><name sortKey="Lounev, Vitali" sort="Lounev, Vitali" uniqKey="Lounev V" first="Vitali" last="Lounev">Vitali Lounev</name></author><author><name sortKey="Seemann, Petra" sort="Seemann, Petra" uniqKey="Seemann P" first="Petra" last="Seemann">Petra Seemann</name></author><author><name sortKey="Groppe, Jay" sort="Groppe, Jay" uniqKey="Groppe J" first="Jay" last="Groppe">Jay Groppe</name></author><author><name sortKey="Katagiri, Takenobu" sort="Katagiri, Takenobu" uniqKey="Katagiri T" first="Takenobu" last="Katagiri">Takenobu Katagiri</name></author><author><name sortKey="Pignolo, Robert J" sort="Pignolo, Robert J" uniqKey="Pignolo R" first="Robert J." last="Pignolo">Robert J. Pignolo</name></author><author><name sortKey="Shore, Eileen M" sort="Shore, Eileen M" uniqKey="Shore E" first="Eileen M." last="Shore">Eileen M. Shore</name></author></analytic><series><title level="j">Journal of bone and mineral metabolism</title><idno type="ISSN">0914-8779</idno><idno type="eISSN">1435-5604</idno><imprint><date when="2008">2008</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p id="P1">Metamorphosis, the transformation of one normal tissue or organ system into another, is a biological process rarely studied in higher vertebrates or mammals, but exemplified pathologically by the extremely disabling autosomal dominant disorder fibrodysplasia ossificans progressiva (FOP). The recurrent single nucleotide missense mutation in the gene encoding activin receptor IA/activin-like kinase-2 (ACVR1/ALK2), a bone morphogenetic protein type I receptor that causes skeletal metamorphosis in all classically affected individuals worldwide, is the first identified human metamorphogene. Physiological studies of this metamorphogene are beginning to provide deep insight into a highly conserved signaling pathway that regulates tissue stability following morphogenesis, and that when damaged at a highly specific locus (c.617G > A; R206H), and triggered by an inflammatory stimulus permits the renegade metamorphosis of normal functioning connective tissue into a highly ramified skeleton of heterotopic bone. A comprehensive understanding of the process of skeletal metamorphosis, as revealed by the rare condition FOP, will lead to the development of more effective treatments for FOP and, possibly, for more common disorders of skeletal metamorphosis.</p></div></front></TEI><pmc article-type="research-article"><pmc-comment>The publisher of this article does not allow downloading of the full text in XML form.</pmc-comment>
<pmc-dir>properties manuscript</pmc-dir>
<front><journal-meta><journal-id journal-id-type="nlm-journal-id">9436705</journal-id><journal-id journal-id-type="pubmed-jr-id">21202</journal-id><journal-id journal-id-type="nlm-ta">J Bone Miner Metab</journal-id><journal-id journal-id-type="iso-abbrev">J. Bone Miner. Metab.</journal-id><journal-title-group><journal-title>Journal of bone and mineral metabolism</journal-title></journal-title-group><issn pub-type="ppub">0914-8779</issn><issn pub-type="epub">1435-5604</issn></journal-meta><article-meta><article-id pub-id-type="pmid">18979151</article-id><article-id pub-id-type="pmc">3620015</article-id><article-id pub-id-type="doi">10.1007/s00774-008-0879-8</article-id><article-id pub-id-type="manuscript">NIHMS436635</article-id><article-categories><subj-group subj-group-type="heading"><subject>Article</subject></subj-group></article-categories><title-group><article-title>Skeletal metamorphosis in fibrodysplasia ossificans progressiva (FOP)</article-title></title-group><contrib-group><contrib contrib-type="author" corresp="yes"><name><surname>Kaplan</surname><given-names>Frederick S.</given-names></name><email>frederick.kaplan@uphs.upenn.edu</email><aff id="A1">Departments of Orthopaedic Surgery and Medicine, c/o Department of Orthopaedic Surgery, Hospital of the University of Pennsylvania, Silverstein 2, 3400 Spruce Street, Philadelphia, PA 19104, USA Tel. +1-215-349-8726; Fax +1-215-349-5928</aff></contrib><contrib contrib-type="author"><name><surname>Shen</surname><given-names>Qi</given-names></name><aff id="A2">Department of Orthopaedic Surgery, University of Pennsylvania School of Medicine, Philadelphia, PA, USA</aff></contrib><contrib contrib-type="author"><name><surname>Lounev</surname><given-names>Vitali</given-names></name><aff id="A3">Department of Orthopaedic Surgery, University of Pennsylvania School of Medicine, Philadelphia, PA, USA</aff></contrib><contrib contrib-type="author"><name><surname>Seemann</surname><given-names>Petra</given-names></name><aff id="A4">Max Planck Institute for Molecular Genetics, Development and Disease, Berlin, Germany</aff></contrib><contrib contrib-type="author"><name><surname>Groppe</surname><given-names>Jay</given-names></name><aff id="A5">Department of Biomedical Sciences, Baylor College of Dentistry, Texas A & M University Health Science Center, Dallas, TX, USA</aff></contrib><contrib contrib-type="author"><name><surname>Katagiri</surname><given-names>Takenobu</given-names></name><aff id="A6">Division of Pathophysiology, Research Center for Genomic Medicine, Saitama Medical University, Saitama, Japan</aff></contrib><contrib contrib-type="author"><name><surname>Pignolo</surname><given-names>Robert J.</given-names></name><aff id="A7">Department of Medicine, University of Pennsylvania School of Medicine, Philadelphia, PA, USA</aff></contrib><contrib contrib-type="author"><name><surname>Shore</surname><given-names>Eileen M.</given-names></name><aff id="A8">Departments of Orthopaedic Surgery & Genetics, University of Pennsylvania School of Medicine, Philadelphia, PA, USA</aff></contrib></contrib-group><pub-date pub-type="nihms-submitted"><day>18</day><month>3</month><year>2013</year></pub-date><pub-date pub-type="epub"><day>01</day><month>11</month><year>2008</year></pub-date><pub-date pub-type="ppub"><year>2008</year></pub-date><pub-date pub-type="pmc-release"><day>08</day><month>4</month><year>2013</year></pub-date><volume>26</volume><issue>6</issue><fpage>521</fpage><lpage>530</lpage><permissions><copyright-statement>© The Japanese Society for Bone and Mineral Research and Springer 2008</copyright-statement><copyright-year>2008</copyright-year></permissions><abstract><p id="P1">Metamorphosis, the transformation of one normal tissue or organ system into another, is a biological process rarely studied in higher vertebrates or mammals, but exemplified pathologically by the extremely disabling autosomal dominant disorder fibrodysplasia ossificans progressiva (FOP). The recurrent single nucleotide missense mutation in the gene encoding activin receptor IA/activin-like kinase-2 (ACVR1/ALK2), a bone morphogenetic protein type I receptor that causes skeletal metamorphosis in all classically affected individuals worldwide, is the first identified human metamorphogene. Physiological studies of this metamorphogene are beginning to provide deep insight into a highly conserved signaling pathway that regulates tissue stability following morphogenesis, and that when damaged at a highly specific locus (c.617G > A; R206H), and triggered by an inflammatory stimulus permits the renegade metamorphosis of normal functioning connective tissue into a highly ramified skeleton of heterotopic bone. A comprehensive understanding of the process of skeletal metamorphosis, as revealed by the rare condition FOP, will lead to the development of more effective treatments for FOP and, possibly, for more common disorders of skeletal metamorphosis.</p></abstract><kwd-group><kwd>morphogen</kwd><kwd>metamorphogene</kwd><kwd>ACVR1</kwd><kwd>fibrodysplasia ossificans progressiva (FOP)</kwd><kwd>bone morphogenetic protein (BMP)</kwd><kwd>BMP receptor</kwd><kwd>heterotopic ossification</kwd></kwd-group><funding-group><award-group><funding-source country="United States">National Institute of Arthritis and Musculoskeletal and Skin Diseases : NIAMS</funding-source><award-id>R01 AR041916 || AR</award-id></award-group></funding-group></article-meta></front></pmc></record>Pour manipuler ce document sous Unix (Dilib)
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