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Hitoshi Shimano

Researcher at University of Texas Southwestern Medical Center

Publications -  10
Citations -  4868

Hitoshi Shimano is an academic researcher from University of Texas Southwestern Medical Center. The author has contributed to research in topics: Sterol regulatory element-binding protein & Sterol Regulatory Element Binding Protein 1. The author has an hindex of 9, co-authored 10 publications receiving 4706 citations.

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Journal ArticleDOI

Overproduction of cholesterol and fatty acids causes massive liver enlargement in transgenic mice expressing truncated SREBP-1a.

TL;DR: It is indicated that the NH2-terminal domain of SREBP-1a can produce major effects on lipid synthesis and storage in the liver, owing to the engorgement of hepatocytes with cholesterol and triglycerides.
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Isoform 1c of sterol regulatory element binding protein is less active than isoform 1a in livers of transgenic mice and in cultured cells.

TL;DR: SRE BP-1a is the most active form of SREBP-1 and that SREbp-1c may be produced when cells require a lower rate of transcription of genes regulating cholesterol and fatty acid metabolism.
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Differential expression of exons 1a and 1c in mRNAs for sterol regulatory element binding protein-1 in human and mouse organs and cultured cells.

TL;DR: It is shown that the ratio of SREBP-1c to 1a transcripts varies markedly among organs of the adult mouse and is controlled independently by regulatory regions that respond differentially to organ-specific and metabolic factors.
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Activation of cholesterol synthesis in preference to fatty acid synthesis in liver and adipose tissue of transgenic mice overproducing sterol regulatory element-binding protein-2.

TL;DR: It is concluded that SREBP-2 is a relatively selective activator of cholesterol synthesis, as opposed to fatty acid synthesis, in liver and adipose tissue of mice.
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Regulation of sterol regulatory element binding proteins in livers of fasted and refed mice

TL;DR: It is concluded that SREBPs are regulated by food consumption in the mouse liver and that the decline in nuclear SREBP-1c upon fasting may explain in part the decrease in mRNAs encoding enzymes of the fatty acid biosynthetic pathway.