名古屋大学 · 医学
本田隆史教授の研究室は、細胞分裂における染色体分配の精密な制御機構を解明することを目的としています。特に、Bub1キナーゼがヒストンH2Aの特定部位をリン酸化することで、染色体の正確な分離を保証する仕組みを、ショウジョウブエやヒト細胞を用いて解明しています。また、CPC(染色体ペアの中心複合体)の内側染色体領域への局在化に寄与するリン酸化修飾の協働メカニズムについても、ヒストン修飾とセントロメア関連タンパク質の相互作用を解明しています。
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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