The University of Tokyo · 생화학·유전·분자생물학
Yutaka Suzuki 교수의 연구실은 전사 조절 메커니즘을 해독하기 위해 대량 유전자 발현 데이터와 고차원 유전체 분석을 융합한 연구를 수행합니다. 특히 mRNA 시작 부위를 정밀하게 특정하고, 프로모터 영역의 전사 조절 요소(예: TATA 박스, 이니시에이터)의 분포를 체계적으로 분석함으로써 유전자 발현 조절의 분자 기반을 규명하고자 합니다. 또한, 암에서의 유전자 변이, 에피유전적 변화 및 전사 조절 이상 간의 상호관계를 다각도로 분석하는 다오미크스 통합 분석도 핵심 연구 분야입니다.
표시된 성과는 수집된 데이터 기준으로 산출되며, 일부 차이가 있을 수 있습니다.
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
