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352 results on '"Tsukiyama, T."'

3. Distribution, structure, organ-specific expression, and phylogenic analysis of the pathogenesisrelated protein-3 chitinase gene family in rice (Oryza sativa L.)

Author

Nakazaki, T., Tsukiyama, T., Okumoto, Y., Kageyama, D., Naito, K., Inouye, K., and Tanisaka, T.

Subjects
Genetic aspects, Research, Rice -- Research -- Genetic aspects, Genomics -- Research -- Genetic aspects
Abstract

Rice (Oryza sativa L.) pathogenesis-related (PR)-3 chitinases, like other PR proteins, are each coded by one of the genes of a multigene family in the plant genome. We assembled the [...]

Published
2006

22. Status report KfK contribution to the development of DEMO-relevant test blankets for NET/ITER. Part 2: BOT helium cooled solid breeder blanket. Vol. 2: detailed version

Author

Dalle Donne, M., Adelhelm, C., Baschek, H.D., Boccaccini, L.V., Bogusch, E., Bojarsky, E., Deckers, H., Dienst, W., Doerr, L., Fischer, U., Fritsch, W., Giese, H., Guenther, E., Haefner, H.E., Hofmann, P., Kappler, F., Knitter, R., Kuechle, M., Möllendorff, U.Von, Norajitra, P., Penzhorn, R.D., Reimann, G., Reiser, H., Schulz, B., Schumacher, G., Schwenk-Ferrero, A., Sordon, G., Tsukiyama, T., Wedemeyer, H., Weimar, P., Werle, H., Wiegner, E., and Zimmermann, H.

Subjects
ddc:620, Engineering & allied operations
Published
1991

23. Status report KfK contribution to the development of DEMO-relevant test blankets for NET/ITER. Part 2: BOT helium cooled solid breeder blanket. Vol. 1: Summary

Author

Dalle Donne, M., Adelhelm, C., Baschek, H. D., Boccaccini, L. V., Bogusch, E., Bojarsky, E., Deckers, H., Dienst, W., Doerr, L., Fischer, U., Fritsch, W., Giese, H., Guenther, E., Haefner, H. E., Hofmann, P., Kappler, F., Knitter, R., Kuechle, M., Möllendorff, U. von, Norajitra, P., Penzhorn, R. D., Reimann, G., Reiser, H., Schulz, B., Schumacher, G., Schwenk-Ferrero, A., Sordon, G., Tsukiyama, T., Wedemeyer, H., Weimar, P., Werle, H., Wiegner, E., and Zimmermann, H.

Subjects
ddc:620, Engineering & allied operations
Published
1991
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31. ATP-dependent Remodeling of Chromatin

Author

WU, C., primary, TSUKIYAMA, T., additional, GDULA, D., additional, GEORGEL, P., additional, MARTINEZ-BALBAS, M., additional, MIZUGUCHI, G., additional, OSSIPOW, V., additional, SANDALTZOPOULOS, R., additional, and WANG, H.-M., additional

Published
1998
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38. The canonical Wnt signaling pathway is not involved in renal cyst development in the kidneys of inv mutant mice.

Author

Sugiyama N, Tsukiyama T, Yamaguchi TP, Yokoyama T, Sugiyama, Noriyuki, Tsukiyama, Tadasuke, Yamaguchi, Terry P, and Yokoyama, Takahiko

Abstract

Recent studies have identified several genes whose defects cause hereditary renal cystic diseases with most of the gene products located in the primary cilia. It has been suggested that primary cilia are involved in signaling pathways, defects of which result in abnormal cell proliferation and randomization of oriented cell division in the kidney leading to cyst formation. Mice with a mutation in the inv gene are a model for human nephronophthisis type 2 and develop multiple renal cysts. Inv protein (also called inversin) is located in the base of primary cilia and acts as a switch from canonical to non-canonical Wnt signaling. Here, we studied the orientation of cell division and proliferation in the kidneys of inv mutant mice, as its loss is thought to maintain activation of the canonical Wnt signaling. To establish if canonical signaling was involved in this process, we mated inv mutant with BATlacZ mice to measure canonical Wnt activity. Based on these reporter mice, nuclear localization and phosphorylation of β-catenin, and responsiveness to Wnt ligands in inv mutant cells, we found that random oriented cell division is an initial event for renal tubule expansion and precedes cell proliferation. Thus, our results do not support the hypothesis that canonical Wnt signaling causes renal cyst development in these mice. [ABSTRACT FROM AUTHOR]

Published
2011
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46. Aberrant cell cycle checkpoint function and early embryonic death in Chk1(-/-) mice.

Author

Takai, H, Tominaga, K, Motoyama, N, Minamishima, Y A, Nagahama, H, Tsukiyama, T, Ikeda, K, Nakayama, K, Nakanishi, M, and Nakayama, K

Abstract

The recent discovery of checkpoint kinases has suggested the conservation of checkpoint mechanisms between yeast and mammals. In yeast, the protein kinase Chk1 is thought to mediate signaling associated with the DNA damage checkpoint of the cell cycle. However, the function of Chk1 in mammals has remained unknown. Targeted disruption of Chk1 in mice showed that Chk1(-/-) embryos exhibit gross morphologic abnormalities in nuclei as early as the blastocyst stage. In culture, Chk1(-/-) blastocysts showed a severe defect in outgrowth of the inner cell mass and died of apoptosis. DNA replication block and DNA damage failed to arrest the cell cycle before initiation of mitosis in Chk1(-/-) embryos. These results may indicate that Chk1 is indispensable for cell proliferation and survival through maintaining the G(2) checkpoint in mammals.

Published
2000

48. Inorganic pyrophosphatase is a component of the Drosophila nucleosome remodeling factor complex.

Author

Gdula, D A, Sandaltzopoulos, R, Tsukiyama, T, Ossipow, V, and Wu, C

Abstract

The Drosophila nucleosome remodeling factor (NURF) is a protein complex consisting of four polypeptides that facilitates the perturbation of chromatin structure in vitro in an ATP-dependent manner. The 140-kD NURF subunit, imitation switch (ISWI), is related to the SWI2/SNF2 ATPase. Another subunit, NURF-55, is a 55-kD WD repeat protein homologous to the human retinoblastoma-associated protein RbAp48. Here, we report the cloning and characterization of the smallest (38 kD) component of NURF. NURF-38 is strikingly homologous to known inorganic pyrophosphatases. Both recombinant NURF-38 alone and the purified NURF complex are shown to have inorganic pyrophosphatase activity. Inhibition of the pyrophosphatase activity of NURF with sodium fluoride has no significant effect on chromatin remodeling, indicating that these two activities may be biochemically uncoupled. Our results suggest that NURF-38 may serve a structural or regulatory role in the complex. Alternatively, because accumulation of unhydrolyzed pyrophosphate during nucleotide incorporation inhibits polymerization, NURF may also have been adapted to deliver pyrophosphatase to chromatin to assist in replication or transcription by efficient removal of the inhibitory metabolite.

Published
1998

49. Mechanism of suppression of the long terminal repeat of Moloney leukemia virus in mouse embryonal carcinoma cells

Author

Tsukiyama, T, Niwa, O, and Yokoro, K

Abstract

Sequence-specific DNA-binding proteins that bind to the long terminal repeat (LTR) of Moloney leukemia virus in undifferentiated and differentiated mouse embryonal carcinoma (EC) cells were identified by gel retardation assay. The proteins that bind to the CCAAT box were present in both undifferentiated and differentiated EC cells. The amounts and the number of species of the proteins that bind to the enhancer and the GC-rich region were far lower in undifferentiated EC cells than in the differentiated counterparts. These proteins were supposed to be transcriptional activators. Proteins that bind upstream of the enhancer, namely, the -352 to -346 region and the -407 to -404 region, were identified. These proteins were designated the embryonic LTR-binding protein (ELP) and the LTR-binding protein, respectively. The ELP was present only in undifferentiated EC cell lines. The LTR-binding protein was detected in all cell lines tested. The mechanism of suppression of the LTR was investigated by the chloramphenicol acetyltransferase assay. The enhancer and the GC-rich region of the LTR functioned poorly in undifferentiated cells. When eight copies of ELP-binding sequences were inserted upstream of the enhancer region, expression of the chloramphenicol acetyltransferase gene was reduced about threefold in ECA2 cells. From these data, we concluded that two mechanisms, the shortage of activator proteins and the presence of a negative regulatory protein (ELP), are involved in the suppression of the LTR in undifferentiated EC cells.

Published
1989
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