Nagoya University · Medicine
Professor Takashi Honda's research lab focuses on the molecular mechanisms underlying chromosome segregation and centromere function during cell division, with a particular emphasis on the roles of histone modifications and regulatory kinases such as Bub1 and Haspin. The lab investigates how phosphorylation of histone H2A-S121 and H3-T3 establishes the inner centromere microenvironment, enabling proper localization of the chromosomal passenger complex and shugoshin proteins essential for genomic stability. Their work bridges fundamental cell biology with implications in chromosomal instability and tumorigenesis, using fission yeast and human cell models. The lab also explores clinical correlates, including neurological complications following neurosurgical interventions and viral hepatitis treatment outcomes in elderly patients.
Figures are computed from collected data and may differ slightly.
Bub1 is a multi-task protein kinase required for proper chromosome segregation in eukaryotes. Impairment of Bub1 in humans may lead to chromosomal instability (CIN) or tumorigenesis. Yet, the primary cellular substrate of Bub1 has remained elusive. Here, we show that Bub1 phosphorylates the conserved serine 121 of histone H2A in fission yeast Schizosaccharomyces pombe. The h2a-SA mutant, in which all cellular H2A-S121 is replaced by alanine, phenocopies the bub1 kinase-dead mutant (bub1-KD) in l
For proper partitioning of chromosomes in mitosis, the chromosomal passenger complex (CPC) including Aurora B and survivin must be localized at the center of paired kinetochores, at the site called the inner centromere. It is largely unknown what defines the inner centromere and how the CPC is targeted to this site. Here, we show that the phosphorylation of histone H3-threonine 3 (H3-pT3) mediated by Haspin cooperates with Bub1-mediated histone 2A-serine 121 (H2A-S121) phosphorylation in targeti
Sinking skin flap syndrome is defined as a series of neurologic symptoms with the skin depression at the site of cranial defect, which develop several weeks to months after large external cerebral decompression.The case of a 28-year-old female with the sinking skin flap syndrome is reported together with the evaluation of cerebral blood flow using xenon computed tomography (CT). Although her general condition stabilized within 7 months after the injury, the skin of the bilateral temporal regions
The SVR rate was lower in elderly patients than in younger patients. However, in elderly patients combination therapy was most beneficial for genotype 1 patients, male patients with HCV RNA concentrations < 2,000,000 IU/ml and patients with genotype 2.
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