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Your search keyword '"Hirai, Hidenori"' showing total 27 results
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27 results on '"Hirai, Hidenori"'

9. A potentially versatile nucleotide hydrolysis activity of group II chaperonin monomers from Thermoplasma acidophilum

Author

Noi, Kentaro, Hirai, Hidenori, Hongo, Kunihiro, Mizobata, Tomohiro, and Kawata, Yasushi

Subjects
Adenylic acid -- Chemical properties, Archaeabacteria -- Physiological aspects, Archaeabacteria -- Genetic aspects, Aspartate -- Chemical properties, Gene mutations -- Analysis, High performance liquid chromatography -- Usage, Hydrolysis -- Analysis, Biological sciences, Chemistry
Abstract

The purification of monomeric forms of archaeal group II chaperonin [alpha] and [beta] from Thermoplasma acidophilum which display a strong AMPase activity in the presence of divalent ions, especially [Co.sup.2+] ion, in addition to ATPase and ADPase activities is described. The analyses of the products of hydrolysis via use of HPLC revealed that the monomeric chaperonin successively hydrolyzed the phosphoanhydride and phosphoester bonds of ATP in the order of [gamma] to [alpha] is strongly suppressed by point mutation of specific essential aspartic acid residues.

Published
2009

23. Genetic variations in complement factors in patients with congenital thrombotic thrombocytopenic purpura with renal insufficiency

Author

Fujimura, Yoshihiro, Mansouri Taleghani, Magnus, Miyata, Toshiyuki, Fan, Xinping, Shirotani-Ikejima, Hiroko, Yoshida, Yoko, Hirai, Hidenori, Kremer Hovinga, Johanna Anna, Von Krogh, Anne-Sophie, Kokame, Koichi, Eura, Yuka, Honda, Shigenori, and Lämmle, Bernhard

Subjects
hemic and lymphatic diseases, urologic and male genital diseases, 610 Medicine & health, 3. Good health
Abstract

The congenital form of thrombotic thrombocytopenic purpura (TTP) is caused by genetic mutations in ADAMTS13. Some, but not all, congenital TTP patients manifest renal insufficiency in addition to microangiopathic hemolysis and thrombocytopenia. We included 32 congenital TTP patients in the present study, which was designed to assess whether congenital TTP patients with renal insufficiency have predisposing mutations in complement regulatory genes, as found in many patients with atypical hemolytic uremic syndrome (aHUS). In 13 patients with severe renal insufficiency, six candidate complement or complement regulatory genes were sequenced and 11 missense mutations were identified. One of these missense mutations, C3:p.K155Q mutation, is a rare mutation located in the macroglobulin-like 2 domain of C3, where other mutations predisposing for aHUS cluster. Several of the common missense mutations identified in our study have been reported to increase disease-risk for aHUS, but were not more common in patients with as compared to those without renal insufficiency. Taken together, our results show that the majority of the congenital TTP patients with renal insufficiency studied do not carry rare genetic mutations in complement or complement regulatory genes.

25. Hexacarbonylmolybdenum(0)-Catalyzed Reaction of Allylic Carbonates with Arylsulfonyl-Stabilized Carbanions

Author

Masuyama, Yoshiro, Hirai, Hidenori, Kurusu, Yasuhiko, and Segawa, Koh-ichi

Abstract

p-Tolylsulfonylacetonitrile reacted with allylic carbonates in the presence of a catalytic amount of hexacarbonylmolybdenum(0) to give monoallylated derivatives. Using sodium hydride as a base, methyl p-tolylsulfonylacetate reacted with those to give mixtures of mono- and di-allylated derivatives. No nucleophilic attack of bulky bis-(phenylsulfonyl)methane occurred, whether sodium hydride was present or absent.

Published
1987
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