Masato Enomoto

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14-3-3 proteins control various cellular processes, including cell cycle progression and DNA damage checkpoint. At the DNA damage checkpoint, some subtypes of 14-3-3 (beta and zeta isoforms in mammalian cells and Rad24 in fission yeast) bind to Ser345-phosphorylated Chk1 and promote its nuclear retention. Here, we report that 14-3-3gamma forms a complex(More)
The primary cilium is an antenna-like organelle that modulates differentiation, sensory functions, and signal transduction. After cilia are disassembled at the G0/G1 transition, formation of cilia is strictly inhibited in proliferating cells. However, the mechanisms of this inhibition are unknown. In this paper, we show that trichoplein disappeared from the(More)
Chk1, one of the critical transducers in DNA damage/replication checkpoints, prevents entry into mitosis through inhibition of Cdk1 activity. However, it has remained unclear how this inhibition is cancelled at the G(2)/M transition. We reported recently that Chk1 is phosphorylated at Ser(286) and Ser(301) by Cdk1 during mitosis. Here, we show that mitotic(More)
We previously reported Chk1 to be phosphorylated at Ser286 and Ser301 by cyclin-dependent kinase (Cdk) 1 during mitosis [T. Shiromizu et al., Genes Cells 11 (2006) 477-485]. Here, we demonstrated that Chk1-Ser286 and -Ser301 phosphorylation also occurs in hydroxyurea (HU)-treated or ultraviolet (UV)-irradiated cells. Unlike the mitosis case, however, Chk1(More)
The keratin cytoskeleton performs several functions in epithelial cells and provides regulated interaction sites for scaffold proteins, including trichoplein. Previously, we found that trichoplein was localized on keratin intermediate filaments and desmosomes in well-differentiated, non-dividing epithelia. Here, we report that trichoplein is widely(More)
To perform a quantitative simulation using the Phase Field Method (PFM) in a real alloy system, a new strategy of modeling the microstructure evolution of Ni-base superalloy is proposed in the present paper. In this strategy, the Calculation Phase Diagram (CALPHAD) method and Cluster Variation Method (CVM) are combined with the PFM, in which the four(More)
Stimulation of L929 cells with tumor necrosis factor-alpha (TNFalpha) caused cell death accompanied by a release of arachidonic acid (AA). Although the inhibition of caspases has been shown to cause necrosis in TNFalpha-treated L929 cells, its role in the TNFalpha-induced release of AA has not been elucidated. The release of AA is tightly regulated by(More)
Kousuke Kasahara, Hidemasa Goto, Masato Enomoto, Yasuko Tomono, Tohru Kiyono and Masaki Inagaki* Division of Biochemistry, Aichi Cancer Center Research Institute, Nagoya, Aichi, Japan, Department of Cellular Oncology, Nagoya University Graduate School of Medicine, Nagoya, Aichi, Japan, Division of Molecular and Cell Biology, Shigei Medical Research(More)
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