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- W2106827802 abstract "Birth defects occur in nearly 5% of all live births and are the major cause of infant mortality and morbidity. Despite the recent progress in molecular and developmental biology, the underlying genetic etiology of most congenital anomalies remains unknown. Heterozygous deletion of the 22q11.2 locus results in the most common human genetic deletion syndrome, known as DiGeorge syndrome, and has served as an entry to understanding the basis for numerous congenital heart and craniofacial anomalies, among many other defects. Extensive human genetic analyses, mouse modeling and studies of developmental molecular cascades involved in 22q11 deletion syndrome are revealing complex networks of signaling and transcriptional events that are essential for normal embryonic development. Armed with this knowledge, we can now begin to consider the multiple genetic hits that might contribute to developmental anomalies, some of which could provide targets for in utero prevention of birth defects." @default.
- W2106827802 created "2016-06-24" @default.
- W2106827802 creator A5061410044 @default.
- W2106827802 creator A5081460416 @default.
- W2106827802 date "2003-09-01" @default.
- W2106827802 modified "2023-09-27" @default.
- W2106827802 title "Unraveling the genetic and developmental mysteries of 22q11 deletion syndrome" @default.
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- W2106827802 doi "https://doi.org/10.1016/s1471-4914(03)00141-2" @default.
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