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Novel ITGB6 mutation in autosomal recessive amelogenesis imperfecta

dc.contributor.authorTuna, E. B.
dc.contributor.authorGencay, K.
dc.contributor.authorLEE, K-E
dc.contributor.authorSeymen, Figen
dc.contributor.authorKIM, J-W
dc.contributor.authorKoruyucu, M.
dc.contributor.authorBayram, M.
dc.contributor.authorLEE, Z. H.
dc.date.accessioned2021-03-05T20:40:58Z
dc.date.available2021-03-05T20:40:58Z
dc.date.issued2015
dc.identifier.citationSeymen F., LEE K., Koruyucu M., Gencay K., Bayram M., Tuna E. B. , LEE Z. H. , KIM J., "Novel ITGB6 mutation in autosomal recessive amelogenesis imperfecta", ORAL DISEASES, cilt.21, ss.456-461, 2015
dc.identifier.issn1354-523X
dc.identifier.othervv_1032021
dc.identifier.otherav_d55c104e-1c03-4354-99af-14f10f2a5f84
dc.identifier.urihttp://hdl.handle.net/20.500.12627/140787
dc.identifier.urihttps://doi.org/10.1111/odi.12303
dc.description.abstractObjectiveHereditary defects in tooth enamel formation, amelogenesis imperfecta (AI), can be non-syndromic or syndromic phenotype. Integrins are signaling proteins that mediate cell-cell and cell-extracellular matrix communication, and their involvement in tooth development is well known. The purposes of this study were to identify genetic cause of an AI family and molecular pathogenesis underlying defective enamel formation.
dc.language.isoeng
dc.subjectTıp
dc.subjectDiş Hekimliği
dc.subjectSağlık Bilimleri
dc.subjectKlinik Tıp (MED)
dc.subjectKlinik Tıp
dc.subjectDİŞ HEKİMLİĞİ, ORAL CERRAHİ VE TIP
dc.titleNovel ITGB6 mutation in autosomal recessive amelogenesis imperfecta
dc.typeMakale
dc.relation.journalORAL DISEASES
dc.contributor.departmentSeoul National University (SNU) , ,
dc.identifier.volume21
dc.identifier.issue4
dc.identifier.startpage456
dc.identifier.endpage461
dc.contributor.firstauthorID48240


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