東京大学 · 生化学・遺伝学・分子生物学
Yutaka Suzuki教授の研究室は、がんのゲノム・エピゲノム・トランスクリプトームの統合的解析を柱として、がんにおける遺伝子変異やエピジェネティックな異常と転写調節の関係を解明しています。特に、全ゲノムシーケンシングやRNA-Seq、バイスルファイトシーケンシング、ChIP-Seqを統合した多様体ゲノム解析により、がん細胞の異常な遺伝子発現のメカニズムを解明しています。また、mRNAの転写開始部位を精確に特定することで、プロモーター領域の機能的要因の頻度や構造を解明し、がんの発症機構の理解を深めています。
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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