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Article: Phenotypic and biochemical consequences of collagen X mutations in mice and humans

TitlePhenotypic and biochemical consequences of collagen X mutations in mice and humans
Authors
Issue Date1998
PublisherElsevier BV. The Journal's web site is located at http://www.elsevier.com/locate/matbio
Citation
Matrix Biology, 1998, v. 17 n. 3, p. 169-184 How to Cite?
AbstractSkeletal biology has entered an exciting period with the technological advances in murine transgenesis and human genetics. This review focuses on how these two approaches are being used to address the role of collagen X, the major extracellular matrix component of the focal zone of endochondral ossification, the hypertrophic cartilage zone. The hypothesized role of this unique collagen in skeletal morphogenesis and the phenotypic and biochemical consequences resulting from the disruption of its function are discussed. Specifically, data from three murine models, including transgenic mice with a dominant interference phenotype for collagen X, and two sets of mice with an inactivated collagen X gene through gene targeting and homologous recombination, as well as the human disorder of Schmid metaphyseal chondrodysplasia resulting from mutations in collagen X, are summarized and compared. Several inconsistencies and unresolved issues regarding the murine and human phenotypes and the function of collagen X are discussed.
Persistent Identifierhttp://hdl.handle.net/10722/68010
ISSN
2015 Impact Factor: 4.47
2015 SCImago Journal Rankings: 1.902
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorChan, Den_HK
dc.contributor.authorJacenko, Oen_HK
dc.date.accessioned2010-09-06T06:00:28Z-
dc.date.available2010-09-06T06:00:28Z-
dc.date.issued1998en_HK
dc.identifier.citationMatrix Biology, 1998, v. 17 n. 3, p. 169-184en_HK
dc.identifier.issn0945-053Xen_HK
dc.identifier.urihttp://hdl.handle.net/10722/68010-
dc.description.abstractSkeletal biology has entered an exciting period with the technological advances in murine transgenesis and human genetics. This review focuses on how these two approaches are being used to address the role of collagen X, the major extracellular matrix component of the focal zone of endochondral ossification, the hypertrophic cartilage zone. The hypothesized role of this unique collagen in skeletal morphogenesis and the phenotypic and biochemical consequences resulting from the disruption of its function are discussed. Specifically, data from three murine models, including transgenic mice with a dominant interference phenotype for collagen X, and two sets of mice with an inactivated collagen X gene through gene targeting and homologous recombination, as well as the human disorder of Schmid metaphyseal chondrodysplasia resulting from mutations in collagen X, are summarized and compared. Several inconsistencies and unresolved issues regarding the murine and human phenotypes and the function of collagen X are discussed.en_HK
dc.languageengen_HK
dc.publisherElsevier BV. The Journal's web site is located at http://www.elsevier.com/locate/matbioen_HK
dc.relation.ispartofMatrix Biologyen_HK
dc.rightsMatrix Biology. Copyright © Elsevier BV.en_HK
dc.subject.meshAnimalsen_HK
dc.subject.meshBone and Bones - embryology - pathologyen_HK
dc.subject.meshCartilage - embryology - pathologyen_HK
dc.subject.meshCollagen - physiologyen_HK
dc.subject.meshHumansen_HK
dc.subject.meshMiceen_HK
dc.subject.meshMice, Transgenicen_HK
dc.subject.meshMorphogenesis - physiologyen_HK
dc.subject.meshMutationen_HK
dc.subject.meshOsteochondrodysplasias - embryologyen_HK
dc.titlePhenotypic and biochemical consequences of collagen X mutations in mice and humansen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0945-053X&volume=17&spage=169&epage=184&date=1998&atitle=Phenotypic+and+biochemical+consequences+of+collagen+X+mutations+in+mice+and+humansen_HK
dc.identifier.emailChan, D:chand@hkucc.hku.hken_HK
dc.identifier.authorityChan, D=rp00540en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/S0945-053X(98)90056-7en_HK
dc.identifier.pmid9707340-
dc.identifier.scopuseid_2-s2.0-0031879246en_HK
dc.identifier.hkuros43070en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0031879246&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume17en_HK
dc.identifier.issue3en_HK
dc.identifier.spage169en_HK
dc.identifier.epage184en_HK
dc.identifier.isiWOS:000074926000001-
dc.publisher.placeNetherlandsen_HK
dc.identifier.scopusauthoridChan, D=7402216545en_HK
dc.identifier.scopusauthoridJacenko, O=7003397201en_HK

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