Takayuki Yamanaka

Subcellular localization of HCV core protein regulates its ability for p53 activation and p21 suppression.

Hepatitis C Virus (HCV) is a single stranded RNA virus causing non-A and non-B hepatitis. Core protein is a viral capsid protein that plays an important role in the pathogenesis of HCV. The companion report revealed that an innate form (amino acids [a.a.] 1-191) regulated subcellular localization of a mature form (a.a. 1-173). It was also shown that the innate form in the cytoplasm enhanced the p21 expression and the mature form in the nucleus suppressed the p21 expression. Here we report that the core protein in the cytoplasm increases the amount of p21 via activating p53, and the core protein in the nucleus decreases the amount of p21 by the p53-independent pathway. These observations suggest that the regulation of p21 expression by the core protein via subcellular localization might decide the fate of infected cells either to the proliferation or to the apoptosis.

Innate form of HCV core protein plays an important role in the localization and the function of HCV core protein

Hepatitis C Virus (HCV) has been identified as the major causative agent of non-A, non-B hepatitis. Core protein is not only a capsid protein of HCV but also a regulator of cellular functions, and plays an important role in the pathogenesis of HCV. Core protein is produced as an innate form (amino acids [a.a.] 1-191), and following processing produces a mature form (a.a. 1-173). This study demonstrates that the innate form regulates subcellular localization of the mature form, and that the innate form in the cytoplasm enhances p21 expression; on the other hand, the mature form in the nucleus suppresses p21 expression. These observations suggest that the innate form is not only a precursor of the mature form but also a regulator of the localization and functions of core protein.

A novel function of cytochrome c (555, Chlorobium thiosulfatophilum) in oxidation of thiosulfate

Abstract Thiosulfate-cytochrome c-551 reductase derived from Chlorobium thiosulfatophilum has been highly purified. The enzyme reduces cytochrome c -551 of C . thiosulfatophilum in the presence of thiosulfate while cytochrome c -555 of the organism is not reduced by the enzyme. Cytochrome c -555 reacts with the enzyme at an appreciable rate only in the presence of cytochrome c -551. However, the reduction rate of cytochrome c -551 by the enzyme is greatly enhanced on addition of a catalytic amount of cytochrome c -555. Therefore, cytochrome c -555 seems to function as an effector on thiosulfate-cytochrome c -551 reductase as well as it acts as the electron donor to the light-excited chlorobium chlorophylls.

Hepatitis C virus core protein binds to a C-terminal region of NS5B RNA polymerase

Hepatitis C virus (HCV) NS5B has been shown to exhibit RNA-dependent RNA polymerase activity for its viral RNA replication. In this study, we demonstrated the formation of a complex between NS5B and the core protein (NS5B-core protein complex) in mammalian cells, as determined by indirect immunofluorescence and immunoprecipitation analyses. The localization of the core protein was observed to change to the same locus in ER as NS5B locates by its coexpression with NS5B, indicating that the localization of the core protein is determined by NS5B. The truncated NS5B molecule lacking the C-terminal region did not form a complex with the core protein, suggesting that the C-terminal region of NS5B is essential for its interaction with the core protein. Moreover, the change in NS5B localization because of C-terminal deletion indicates that this region includes a certain signal for NS5B retention in ER.

Gamow-Teller strengths of the inverse beta transition Yb-176 -> Lu-176 for spectroscopy of proton-proton and other sub-MeV solar neutrinos

Discrete Gamow-Teller (GT) transitions 176Yb-->176Lu at low excitation energies have been measured via the ( 3He,t) reaction at 450 MeV and at 0 degrees. For 176Yb, two low-lying states are observed, setting low thresholds Q(nu) = 301 and 445 keV for neutrino ( nu) capture. Capture rates estimated from the measured GT strengths, the simple two-state excitation structure, and the low Q(nu) in Yb-Lu indicate that Yb-based nu detectors are well suited for a direct measurement of the sub-MeV solar electron-neutrino ( nu(e)) spectrum including pp neutrinos.

KL → π0νν ̄experiment at KEK 12-GeV PS - E391a -

Abstract The K L → π 0 η η decay is one of the most attractive phenomena for the study of the CP violation. The branching ratio can be calculated with a small theoretical ambiguity, which will provide a clean determination of a basic parameter of the present particle physics. It will also play an important role for the search of the new physics as well as for the fundamental unerstanding of the CP-violation. We will start a kind of pilot experiment using a present 12-GeV proton synchrotron (PS) at KEK from early 2004, which is the first dedicated experiment searching for the K L → π 0 η η decay.

KL → π0ηη experiment at KEK12-GeV PS — E391a

Abstract The K L → π 0 η η decay is one of the most attractive phenomena for the study of the CP violation. The branching ratio can be calculated with a small theoretical ambiguity, which will provide a clean determination of a basic parameter of the present particle physics. It will also play an important role for the search of the new physics as well as for the fundamental unerstanding of the CP-violation. We will start a kind of pilot experiment using a present 12-GeV proton synchrotron (PS) at KEK from early 2004, which is the first dedicated experiment searching for the K L → π 0 η η decay.