The University of Tokyo · Biochemistry, Genetics and Molecular Biology
Professor Yutaka Suzuki's research lab specializes in integrative genomics and systems biology, focusing on the molecular mechanisms of transcriptional regulation and gene expression control in human diseases, particularly cancer. The lab employs multi-omics approaches—combining whole-genome sequencing, RNA-Seq, epigenomics, and chromatin profiling—to decode the functional impact of genomic, epigenomic, and transcriptional aberrations in cancer genomes. A central theme is the identification and characterization of regulatory elements such as promoters and enhancers, with a strong emphasis on how mutations in these regions disrupt gene regulation. The lab also investigates the role of non-coding regulatory variants in oncogenesis, aiming to uncover novel biomarkers and therapeutic targets.
Figures are computed from collected data and may differ slightly.
To understand the mechanism of transcriptional regulation, it is essential to identify and characterize the promoter, which is located proximal to the mRNA start site. To identify the promoters from the large volumes of genomic sequences, we used mRNA start sites determined by a large-scale sequencing of the cDNA libraries constructed by the "oligo-capping" method. We aligned the mRNA start sites with the genomic sequences and retrieved adjacent sequences as potential promoter regions (PPRs) for
To understand the mechanism of transcriptional regulation, it is essential to identify and characterize the promoter, which is located proximal to the mRNA start site. To identify the promoters from the large volumes of genomic sequences, we used mRNA start sites determined by a large-scale sequencing of the cDNA libraries constructed by the "oligo-capping" method. We aligned the mRNA start sites with the genomic sequences and retrieved adjacent sequences as potential promoter regions (PPRs) for
Here we conducted an integrative multi-omics analysis to understand how cancers harbor various types of aberrations at the genomic, epigenomic and transcriptional levels. In order to elucidate biological relevance of the aberrations and their mutual relations, we performed whole-genome sequencing, RNA-Seq, bisulfite sequencing and ChIP-Seq of 26 lung adenocarcinoma cell lines. The collected multi-omics data allowed us to associate an average of 536 coding mutations and 13,573 mutations in promot
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