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Shuji Takada

Researcher at University of Cambridge

Publications -  9
Citations -  1420

Shuji Takada is an academic researcher from University of Cambridge. The author has contributed to research in topics: Genomic imprinting & Gene. The author has an hindex of 8, co-authored 9 publications receiving 1349 citations. Previous affiliations of Shuji Takada include University of Queensland.

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Journal ArticleDOI

Asymmetric regulation of imprinting on the maternal and paternal chromosomes at the Dlk1-Gtl2 imprinted cluster on mouse chromosome 12

TL;DR: It is shown that deletion of the IG-DMR from the maternally inherited chromosome causes bidirectional loss of imprinting of all genes in the 1-Mb cluster and indicates that the two parental chromosomes control allele-specific gene expression differently.
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Epigenetic analysis of the Dlk1–Gtl2 imprinted domain on mouse chromosome 12: implications for imprinting control from comparison with Igf2–H19

TL;DR: A detailed methylation analysis is described of the Dlk1-Gtl2 domain, a reciprocally imprinted genes located 80 kb apart on mouse chromosome 12, which has both unique and common features compared to those identified in the Igf2-H19 domain.
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Delta-like and gtl2 are reciprocally expressed, differentially methylated linked imprinted genes on mouse chromosome 12.

TL;DR: Gtl2 is expressed from the maternal allele and methylated at the 5' end of the silent paternal allele and a reciprocally imprinted gene, Delta-like (Dlk), with homology to genes involved in the Notch signalling pathway was identified 80kb upstream of Gtl2.
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Comparative sequence analysis of the imprinted Dlk1-Gtl2 locus in three mammalian species reveals highly conserved genomic elements and refines comparison with the Igf2-H19 region.

TL;DR: Comparative genomic examination of the Dlk1-Gtl2 domain indicates that although there are similarities, other features are very different, including the location of conserved CTCF-binding sites, and the level of conservation at regulatory regions.
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Genomic imprinting contributes to thyroid hormone metabolism in the mouse embryo.

TL;DR: It is demonstrated that disruption of the imprinting status of Dio3 results in abnormal thyroid hormone levels and may contribute to the phenotypic abnormalities in UPD12 mice and UPD14 humans.