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Shioko Kimura

Researcher at National Institutes of Health

Publications -  190
Citations -  14977

Shioko Kimura is an academic researcher from National Institutes of Health. The author has contributed to research in topics: Gene & Thyroid. The author has an hindex of 66, co-authored 185 publications receiving 14052 citations. Previous affiliations of Shioko Kimura include Nagasaki University.

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The T/ebp null mouse: thyroid-specific enhancer-binding protein is essential for the organogenesis of the thyroid, lung, ventral forebrain, and pituitary.

TL;DR: In situ hybridization showed that the T/ebp gene is expressed in the normal thyroid, lung bronchial epithelium, and specific areas of the forebrain during early embryogenesis, establishing that the expression of T/EBP, a transcription factor known to control thyroid-specific gene transcription, is also essential for organogenesis of the thyroid, lungs, ventral forebrain, and pituitary.
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Immune system impairment and hepatic fibrosis in mice lacking the dioxin-binding Ah receptor

TL;DR: The aryl hydrocarbon (Ah) receptor (AHR) mediates many carcinogenic and teratogenic effects of environmentally toxic chemicals such as dioxin and plays an important role in the development of the liver and the immune system.
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Characterization of the common genetic defect in humans deficient in debrisoquine metabolism.

TL;DR: It is shown that poor meta-bolizers have negligible amounts of the cytochrome P450 enzyme P450dbl, providing a molecular explanation for one of man's most commonly defective genes.
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Defects in tracheoesophageal and lung morphogenesis in Nkx2.1(-/-) mouse embryos.

TL;DR: A critical role is demonstrated for Nkx2.1 in morphogenesis of the anterior foregut and the lung as well as in differentiation of pulmonary epithelial cells.
Journal Article

The human debrisoquine 4-hydroxylase (CYP2D) locus: sequence and identification of the polymorphic CYP2D6 gene, a related gene, and a pseudogene.

TL;DR: A hypothesis is presented that the presence of a pseudogene within the CYP2D subfamily transfers detrimental mutations via gene conversions into the CYD2D6 gene, thus accounting for the high frequency of mutations observed in the CYp2D 6 gene in humans.