A5056171331- DNA Repair Mechanisms
- Cancer-related Molecular Pathways
- Microtubule and mitosis dynamics
- Carcinogens and Genotoxicity Assessment
- Gastric Cancer Management and Outcomes
- Genomics and Chromatin Dynamics
- PARP inhibition in cancer therapy
- Sirtuins and Resveratrol in Medicine
- Pancreatic and Hepatic Oncology Research
- Calcium signaling and nucleotide metabolism
- Acute Myeloid Leukemia Research
- Growth Hormone and Insulin-like Growth Factors
- Pediatric Hepatobiliary Diseases and Treatments
Shimadzu (Japan)
2024
Kyoto University
2013-2014
Tokyo Medical and Dental University
2007-2013
The Fanconi anemia (FA) pathway is critically involved in the maintenance of hematopoietic stem cells and suppression carcinogenesis. A key FA protein, FANCD2, monoubiquitinated accumulates chromatin response to DNA interstrand crosslinks (ICLs), where it coordinates repair through mechanisms that are still poorly understood. Here, we report CtIP protein directly interacts with FANCD2. region spanning amino acids 166 273 monoubiquitination FANCD2 both essential for FANCD2-CtIP interaction...
Abstract Nicotinamide adenine dinucleotide (NAD + ) is an essential metabolite for fundamental biological phenomena, including aging. mononucleotide (NMN) a key NAD intermediate that has been extensively tested as effective -boosting compound in mice and humans. However, the accurate measurement of NMN samples long challenge field. Here, we have established accurate, quantitative methodology measuring by using liquid chromatography-triple quadrupole mass spectrometry (LC-MS/MS) with double...
During tumorigenesis, cells acquire immortality in association with the development of genomic instability. However, it is still elusive how instability spontaneously generates during process tumorigenesis. Here, we show that precancerous DNA lesions induced by oncogene acceleration, which induce situations identical to initial stages cancer development, trigger tetraploidy/aneuploidy generation mitotic aberration. Although acceleration primarily induces replication stress and resulting S...
When DNA replication is stalled at sites of damage, a cascade responses activated in the cell to halt cycle progression and promote repair. A pathway initiated by kinase Ataxia teleangiectasia Rad3 related (ATR) its partner ATR interacting protein (ATRIP) plays an important role this response. The Fanconi anemia (FA) also following genomic stress, defects cause cancer-prone hematologic disorder humans. Little known about how these two pathways are coordinated. We report here that cellular...
Normal cells, both in vivo and vitro, become quiescent after serial cell proliferation. During this process, cells can develop immortality with genomic instability, although the mechanisms by which is regulated are unclear. Here, we show that a growth-arrested cellular status produced down-regulation of histone H2AX normal cells. mouse embryonic fibroblast preserve an diminished through p53 regulation stable-diploidy maintenance. However, such quiescence abrogated under continuous growth...
Stalled replication forks undergo DNA double‐strand breaks ( DSB s) under certain conditions. However, the precise mechanism underlying induction and cellular response to persistent fork stalling are not fully understood. Here we show that, in hydroxyurea exposure, s generated an A rtemis nuclease‐dependent manner following prolonged with subsequent activation of ataxia–telangiectasia mutated ATM ) signaling pathway. The kinase activity catalytic subunit ‐dependent protein kinase, a...