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- W3207063312 endingPage "1598" @default.
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- W3207063312 abstract "Down syndrome (DS), also known as trisomy 21, is the most frequent genetic cause of intellectual disability. Although the mechanism remains unknown, delayed brain development is assumed to be involved in DS intellectual disability. Analyses with human with DS and mouse models have shown that defects in embryonic cortical neurogenesis may lead to delayed brain development. Cre-loxP-mediated chromosomal engineering has allowed the generation of a variety of mouse models carrying various partial Mmu16 segments. These mouse models are useful for determining genotype-phenotype correlations and identifying dosage-sensitive genes involved in the impaired neurogenesis. In this review, we summarize several candidate genes and pathways that have been linked to defective cortical neurogenesis in DS." @default.
- W3207063312 created "2021-10-25" @default.
- W3207063312 creator A5050114315 @default.
- W3207063312 date "2021-10-11" @default.
- W3207063312 modified "2023-10-03" @default.
- W3207063312 title "Genes Associated with Disturbed Cerebral Neurogenesis in the Embryonic Brain of Mouse Models of Down Syndrome" @default.
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- W3207063312 doi "https://doi.org/10.3390/genes12101598" @default.
- W3207063312 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/8535956" @default.
- W3207063312 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/34680993" @default.
- W3207063312 hasPublicationYear "2021" @default.
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