ZFPM2/FOG2 andHEY2 genes analysis in nonsyndromic tricuspid atresia
ZFPM2/FOG2 andHEY2 genes analysis in nonsyndromic tricuspid atresia
Tricuspid atresia (TriAt), the third most common cyanotic congenital heart defect (CHD), consists of complete lack of tricuspid valve formation, with no connection between the right atrium and the right ventricle. To date, the genetic mechanism responsible of TriAt is still obscure. However, animal models have suggested a role of cardiogenic Zfpm2/Fog2 and Hey2 genes in the pathogenesis of TriAt. Therefore, we screened 40 individuals affected by nonsyndromic TriAt for ZFPM2/FOG2 and HEY2 gene mutations. No pathogenetic mutation has been identified, thus failing to demonstrate a major role of ZFPM2/FOG2 and HEY2 genes in the pathogenesis of human TriAt.
Adult, Male, Adolescent, Tricuspid Atresia, DNA-Binding Proteins, Repressor Proteins, Child, Preschool, Mutation, Basic Helix-Loop-Helix Transcription Factors, Humans, Female, Child, Transcription Factors
Adult, Male, Adolescent, Tricuspid Atresia, DNA-Binding Proteins, Repressor Proteins, Child, Preschool, Mutation, Basic Helix-Loop-Helix Transcription Factors, Humans, Female, Child, Transcription Factors
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