Extended Data Fig. 7: Overview of experimental evidence regarding the genetic basis of heart defects in mouse models of Down syndrome. | Nature Genetics

Extended Data Fig. 7: Overview of experimental evidence regarding the genetic basis of heart defects in mouse models of Down syndrome.

From: Triplication of the interferon receptor locus contributes to hallmarks of Down syndrome in a mouse model

Extended Data Fig. 7: Overview of experimental evidence regarding the genetic basis of heart defects in mouse models of Down syndrome.The alternative text for this image may have been generated using AI.

Diagram depicts genetic variants on human chromosome 21 (HSA21) that may contribute to risk of congenital heart defects (CHDs) in humans with trisomy 21 (T21, yellow), genes with functional evidence whose triplication is necessary or sufficient to increase incidence of CHDs in mouse models of Down syndrome (DS, blue), and genes with supporting evidence in both humans and mouse models of DS (green)3,16,23,24,57,58,59. Relative cytogenetic locations and number of bolded protein-coding genes are indicated along ideogram of the q arm of HSA21 colored according to Giemsa banding. Sources supporting this summary overview is provided in Source Data Extended Data Fig. 7.

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