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Yutaka Suzuki

Researcher at University of Tokyo

Publications -  875
Citations -  42146

Yutaka Suzuki is an academic researcher from University of Tokyo. The author has contributed to research in topics: Gene & Medicine. The author has an hindex of 85, co-authored 767 publications receiving 35471 citations. Previous affiliations of Yutaka Suzuki include Japan Agency for Medical Research and Development & Institute for the Physics and Mathematics of the Universe.

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Remote reprogramming of hepatic circadian transcriptome by breast cancer

TL;DR: A comprehensive characterization of the 4T1-affected hepatic circadian transcriptome is provided that possibly underlies cancer-induced physiological alteration in the liver.
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ADAR1-mediated RNA editing is required for thymic self-tolerance and inhibition of autoimmunity.

TL;DR: It is demonstrated that T cell‐specific deletion of Adar1 in mice causes abnormal thymic T cell maturation including impaired negative selection and autoimmunity such as spontaneous colitis, and prevention of MDA5 sensing of endogenous dsRNA by ADAR1‐mediated RNA editing is required for preventing both innate immune responses and T cell-mediated autoIMmunity.
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Engraftment and tumor formation after allogeneic in utero transplantation of primate embryonic stem cells.

TL;DR: Transplanted cynomolgus ES cells can be engrafted in allogeneic fetuses and will, however, form a tumor if they “leak” into an improper space such as the thoracic cavity.
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A role for transcription from a piRNA cluster in de novo piRNA production

TL;DR: By utilizing a GFP transgene, clonal silkworm BmN4 cell lines producing massively amplified GFP-derived piRNAs capable of silencing GFP in trans are screened and a common transcript from an endogenous piRNA cluster is detected, in which a part of the cluster is uniquely fused with an antisense GFP sequence.
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Hunt for the tipping point during endocrine resistance process in breast cancer by dynamic network biomarkers.

TL;DR: Analysis of time-course mRNA sequence data generated from the tamoxifen-treated estrogen receptor (ER)-positive MCF-7 cell line identified the tipping point of endocrine resistance with its leading molecules and validated the DNB genes associated with the poor survival of breast cancer patients.