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Yoshitaka Hayashi

Researcher at Nagoya University

Publications -  121
Citations -  7242

Yoshitaka Hayashi is an academic researcher from Nagoya University. The author has contributed to research in topics: Thyroid hormone receptor & Thyroid hormone receptor beta. The author has an hindex of 35, co-authored 114 publications receiving 6770 citations. Previous affiliations of Yoshitaka Hayashi include Aichi Medical University & University of Illinois at Chicago.

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Journal ArticleDOI

The Transcriptional Landscape of the Mammalian Genome

Piero Carninci, +197 more
- 02 Sep 2005 - 
TL;DR: Detailed polling of transcription start and termination sites and analysis of previously unidentified full-length complementary DNAs derived from the mouse genome provide a comprehensive platform for the comparative analysis of mammalian transcriptional regulation in differentiation and development.
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Brief report: resistance to thyrotropin caused by mutations in the thyrotropin-receptor gene.

TL;DR: Hormone-resistance syndromes can be broadly defined as conditions resulting from reduced or absent end-organ responsiveness to biologically active hormones, caused by defects in hormone receptors or post-receptor defects.
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Thyroid hormone action on liver, heart, and energy expenditure in thyroid hormone receptor beta-deficient mice.

TL;DR: It can be concluded that regulation of HR and EE are independent of TR beta, and as previously shown for serum TSH, TR beta is not absolutely necessary for some changes typical of hypothyroidism to occur.
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Increased sensitivity to thyroid hormone in mice with complete deficiency of thyroid hormone receptor α

TL;DR: Mice completely deficient in TRalpha (TRalpha(o/o)) are produced that maintain normal serum thyroid-stimulating hormone (TSH) concentration despite low serum thyroxine (T(4), suggesting increased sensitivity to TH.
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Molecular cloning of an orphan G-protein-coupled receptor that constitutively activates adenylate cyclase.

TL;DR: The mouse ACCA (mACCA) was therefore recloned by PCR, and expression of mACCA in Cos-7 cells demonstrated that the mouse receptor behaved similarly as a constitutive activator of adenylate cyclase.