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- W2136015585 abstract "AimsHuman congenital heart disease linked to mutations in the homeobox transcription factor, NKX2-5, is characterized by cardiac anomalies, including atrial and ventricular septal defects as well as conduction and occasional defects in contractility. In the mouse, homozygous germline deletion of Nkx2-5 gene results in death around E10.5. It is, however, not established whether Nkx2-5 is necessary for cardiac development beyond this embryonic stage. Because human NKX2-5 mutations are related to septum secundum type atrial septal defects (ASD), we hypothesized that Nkx2-5 deficiency during the processes of septum secundum formation may cause cardiac anomalies; thus, we analysed mice with tamoxifen-inducible Nkx2-5 ablation beginning at E12.5 when the septum secundum starts to develop." @default.
- W2136015585 created "2016-06-24" @default.
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- W2136015585 date "2011-02-01" @default.
- W2136015585 modified "2023-09-26" @default.
- W2136015585 title "Ablation of Nkx2-5 at mid-embryonic stage results in premature lethality and cardiac malformation" @default.
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- W2136015585 doi "https://doi.org/10.1093/cvr/cvr037" @default.
- W2136015585 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3125071" @default.
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