The University of Tokyo · Biochemistry, Genetics and Molecular Biology
Professor Kengo Watanabe's research lab focuses on systems-level molecular mechanisms underlying cellular homeostasis, with a central emphasis on cell volume regulation, osmotic stress responses, and their roles in aging, metabolic disease, and cancer. The lab integrates multi-omics approaches—genomics, proteomics, and metabolomics—with advanced imaging and machine learning to uncover dynamic regulatory networks in human health and disease. Key research directions include the identification of osmosensors like ASK3 in volume recovery, the impact of gut microbiome and polygenic risk on metabolic phenotypes, and the role of ion/water transport in cancer cell migration and therapy resistance. The lab also investigates environmental toxicants and their DNA adducts, linking molecular perturbations to long-term disease outcomes.
Figures are computed from collected data and may differ slightly.
Multiomic profiling can reveal population heterogeneity for both health and disease states. Obesity drives a myriad of metabolic perturbations and is a risk factor for multiple chronic diseases. Here we report an atlas of cross-sectional and longitudinal changes in 1,111 blood analytes associated with variation in body mass index (BMI), as well as multiomic associations with host polygenic risk scores and gut microbiome composition, from a cohort of 1,277 individuals enrolled in a wellness progr
Cells are under threat of osmotic perturbation; cell volume maintenance is critical in cerebral edema, inflammation and aging, in which prominent changes in intracellular or extracellular osmolality emerge. After osmotic stress-enforced cell swelling or shrinkage, the cells regulate intracellular osmolality to recover their volume. However, the mechanisms recognizing osmotic stress remain obscured. We previously clarified that apoptosis signal-regulating kinase 3 (ASK3) bidirectionally responds
Cancer metastasis is the most frequent cause of death for patients with cancer. The main current treatment for cancer metastasis is chemotherapy targeting cancer cells' ability to proliferate. However, some types of cancer cells show resistance to chemotherapy. Recently, cancer cell migration has become the subject of interest as a novel target of cancer therapy. Cell migration requires many factors, such as the cytoskeleton, cell-matrix adhesion and cell volume regulation. Here, we focus on cel
Cell volume regulation is a vital system for cellular activities. When perturbed by hypoosmotic or hyperosmotic stress, cells immediately induce the cell volume recovery system, regulatory volume decrease (RVD) or regulatory volume increase (RVI), respectively. In contrast to the knowledge about effector molecules, the molecular mechanisms linking osmosensing to RVD/RVI induction remain unknown. Additionally, few reciprocal responders in the bidirectional osmotic stress response have been identi
Dihaloalkanes are of toxicological interest because of their high-volume use in industry and their abilities to cause tumors in rodents, particularly dichloromethane and 1,2-dichloroethane. The brominated analogues are not used as extensively but are known to produce more toxicity in some systems. Rats and mice were treated i.p. with (14)C-dichloromethane, -dibromomethane, -1,2-dichloroethane, or -1,2-dibromoethane [5 mg (kg body weight)(-1)], and livers and kidneys were collected to rapidly iso
Aging manifests as progressive deteriorations in homeostasis, requiring systems-level perspectives to investigate the gradual molecular dysregulation of underlying biological processes. Here, we report systemic changes in the molecular regulation of biological processes under multiple lifespan-extending interventions. Differential Rank Conservation (DIRAC) analyses of mouse liver proteomics and transcriptomics data show that mechanistically distinct lifespan-extending interventions (acarbose, 17
Formyl chloride has been indirectly implicated as an intermediate in the oxidation of CH(2)Cl(2) and proposed to be a product of the oxidation of some other compounds. Formyl chloride was synthesized and added to aqueous solutions, with CO formed as a product. The presence of glutathione (GSH) did not reduce the yield of CO at any of the pH values tested. At pH >or= 9, a small amount of S-formyl GSH was detected (<or =3% of CO formed) and identified by comparison with synthetic material using ma
Abstract Cells are under threat of osmotic perturbation; and cell volume maintenance is critical in cerebral edema, inflammation and aging, in which prominent changes in intracellular or extracellular osmolality emerge. After osmotic stress-enforced cell swelling or shrinkage, the cells regulate intracellular osmolality to recover their volume. However, the mechanisms recognizing osmotic stress remain obscured. We previously clarified that apoptosis signal-regulating kinase 3 (ASK3) bidirectiona
本研究では, 酵素添加による洗米排水中固形成分の凝集・沈降現象と固形成分表層の電気化学的性状との関係, 洗米排水中に含まれる陽イオン種 (対イオン種) との関与について検討するとともに, 凝集・沈降性付加による固形成分除去特性についても併せて検討を行った.その結果, 酸性プロテアーゼ・ペプチダーゼを含有するプロテアーゼM添加により得られた洗米排水上清成分中の固形成分は他の酵素剤添加の場合に比べ, 粒子径の平均値などすべてのパラメータにおいて最小値を示し, 本酵素添加は幅広い範囲の粒径の固形成分を沈降分離させることが可能であった.またFT-IRを用い, 洗米排水固形成分表層の負電荷を形成している官能基の特定を行った結果, プロテアーゼM処理により水酸基 (-OH) 由来の吸収増大 (透過率の低下) が確認された.このことから, 洗米排水中の固形成分表層は, プロテアーゼM添加により水酸基 (-OH) 由来の負の表面電位が増大し, 汚泥容積を減少させたものと考えられた.さらに, 種々の金属キレート剤添加による洗米排水の汚泥容積の変化について検討を行った結果, 洗米排水中の固形成分の凝集・沈
The precipitation behavior of carbides in modified 9Cr-1Mo steel (Grade 91) subjected to low-temperature tempering and the influence of those carbides on the mechanical properties at room temperature were investigated. An as-quenched sample (AQ) contained a small amount of metal carbide (MC) in its martensite microstructure. On low-temperature tempering at 300–500°C, intended to suppress the recovery and growth of the dislocation substructure, three types of carbide were formed; these were ident
Abstract Aging manifests as progressive deterioration in cellular and systemic homeostasis, requiring systems-level perspectives to understand the gradual molecular dysregulation of underlying biological processes. Here, we report systems-level changes in the molecular regulation of biological processes under multiple lifespan-extending interventions in mice and across age in humans. In mouse cohorts, Differential Rank Conservation (DIRAC) analyses of liver proteomics and transcriptomics show th
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