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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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Identification of the carotenoid modifying gene PALE YELLOW PETAL 1 as an essential factor in xanthophyll esterification and yellow flower pigmentation in tomato (Solanum lycopersicum)

TL;DR: This study characterized two allelic tomato mutants, pale yellow petal (pyp) 1-1 and pyp1-2, that have reduced yellow color intensity in the petals and anthers due to loss-of-function mutations and provided insight into the molecular mechanism underlying the production of xanthophyll esters in higher plants, thereby shedding light on a longstanding mystery.
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Genome-wide analysis reveals strong correlation between CpG islands with nearby transcription start sites of genes and their tissue specificity.

TL;DR: It is found that there is a clear peak in the distribution of CpG islands around TSS in the genes of these two species and the tendency that a gene lacking Cpg islands around its TSS is expressed with a higher degree of tissue specificity turned out to be evolutionarily conserved.
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Direct binding of Ataxin-2 to distinct elements in 3' UTRs promotes mRNA stability and protein expression.

TL;DR: The findings suggest that Ataxin-2 is an RNA-binding protein that targets cis-regulatory elements in 3' UTRs to stabilize a subset of mRNAs and increase protein expression.
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Aberrant transcriptional regulations in cancers: genome, transcriptome and epigenome analysis of lung adenocarcinoma cell lines

TL;DR: An integrative multi-omics analysis to understand how cancers harbor various types of aberrations at the genomic, epigenomic and transcriptional levels found that the irregular histone marks were characteristic to EGFR and CDKN1A, while a large genomic deletion and hyper-DNA methylation were most frequent for CDKN2A.