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Please use this identifier to cite or link to this item: https://biore.bio.bg.ac.rs/handle/123456789/2557
DC FieldValueLanguage
dc.contributor.authorFoster, Jamie W.en_US
dc.contributor.authorDominguez-Steglich, Marina A.en_US
dc.contributor.authorGuioli, Silvanaen_US
dc.contributor.authorKwok, Chenien_US
dc.contributor.authorWeller, Polly A.en_US
dc.contributor.authorStevanović, Milenaen_US
dc.contributor.authorWeissenbach, Jeanen_US
dc.contributor.authorMansour, Saharen_US
dc.contributor.authorYoung, Ian D.en_US
dc.contributor.authorGoodfellow, Peter N.en_US
dc.contributor.authorBrook, J. Daviden_US
dc.contributor.authorSchafer, Alan J.en_US
dc.date.accessioned2019-10-24T19:31:30Z-
dc.date.available2019-10-24T19:31:30Z-
dc.date.issued1994-12-08-
dc.identifier.issn0028-0836-
dc.identifier.urihttps://biore.bio.bg.ac.rs/handle/123456789/2557-
dc.description.abstractInduction of testis development in mammals requires the presence of the Y-chromosome gene SPY. This gene must exert its effect by interacting with other genes in the sex-determination pathway. Cloning of a translocation chromosome breakpoint from a sex-reversed patient with campomelic dysplasia, followed by mutation analysis of an adjacent gene, indicates that SOX9, an SRY-related gene, is involved in both bone formation and control of testis development.en_US
dc.language.isoenen_US
dc.relation.ispartofNatureen_US
dc.titleCampomelic dysplasia and autosomal sex reversal caused by mutations in an SRY-related geneen_US
dc.typeArticleen_US
dc.identifier.doi10.1038/372525a0-
dc.identifier.pmid7990924-
dc.identifier.scopus2-s2.0-0028135336-
dc.identifier.urlhttps://api.elsevier.com/content/abstract/scopus_id/0028135336-
item.cerifentitytypePublications-
item.grantfulltextrestricted-
item.openairetypeArticle-
item.languageiso639-1en-
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.fulltextWith Fulltext-
crisitem.author.deptChair of Biochemistry and Molecular Biology-
crisitem.author.orcid0000-0003-4286-7334-
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