Nagoya University · 의학
Takashi Honda 교수의 연구실은 세포 분열 과정에서 유전자 안정성과 염색체 분리 메커니즘을 규명하는 데 초점을 맞추고 있습니다. 특히 Bub1 키나제가 히스톤 H2A의 세린 121을 인산화하여 중심점 단백질인 숙소르긴의 고정을 조절하고, 이로 인해 염색체 안정성이 유지되는 메커니즘을 연구하고 있습니다. 또한 Haspin과의 상호작용을 통해 염색체 중심부의 단백질 복합체(CPC)가 정확히 위치하도록 조절되는 분자적 기전을 규명하고 있습니다.
표시된 성과는 수집된 데이터 기준으로 산출되며, 일부 차이가 있을 수 있습니다.
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.