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101.
Interactions between sulfate reduction (SR) and phototrophic nitrogenase activities were investigated in rice soil slurries mixed with rice straw. Activation of SR by adding exogenous sulfate suppressed acetylene-reducing activity (ARA) of the slurries, which was associated with phototrophic purple bacteria (PB) enumerated to 108-109 MPN g-1 dry weight (dw) soil. Adding 5 mm sodium molybdate, an inhibitor of SR, markedly increased ARA. However, in the slurries receiving both molybdate and exogenous sulfate, the effects declined simultaneously with partial recovery of SR. These results indicate outcompetition of sulfate-reducing bacteria (SRB) with PB in rice soil, when sulfate concentrations are high enough to support SR. The increasing effects of molybdate on ARA continued during the incubation in the sulfate-depleted condition, probably because of absence of SR and toxicity of molybdate to methanogenesis. Accordingly, stopping activities of the competitive microorganisms may be efficient to increase N2 fixation in rice soil. 相似文献
102.
Usui I Haruta T Iwata M Takano A Uno T Kawahara J Ueno E Sasaoka T Kobayashi M 《Biochemical and biophysical research communications》2000,275(1):115-120
In the early phase of adipocyte differentiation, transient increase of DNA synthesis, called clonal expansion, and transient hyperphosphorylation of retinoblastoma protein (Rb) are observed. We investigated the role of these phenomena in insulin-induced adipocyte differentiation of 3T3-L1 cells. Insulin-induced clonal expansion, Rb phosphorylation and adipocyte differentiation were all inhibited by the PI 3-kinase inhibitors and rapamycin, but not the MEK inhibitor, whereas the MEK inhibitor, but not PI 3-kinase inhibitors or rapamycin, decreased c-fos induction. We conclude that insulin induces hyperphosphorylation of Rb via PI 3-kinase and mTOR dependent pathway, which promotes clonal expansion and adipocyte differentiation of 3T3-L1 cells. 相似文献
103.
Hirofumi Usui Rintaro Inoue Osamu Tanabe Yasumasa Nishito Masahiro Shimizu Hideyuki Hayashi Hiroyuki Kagamiyama Masao Takeda 《FEBS letters》1998,430(3)
Human erythrocyte protein phosphatase 2A, which comprises a 34-kDa catalytic C subunit, a 63-kDa regulatory A subunit and a 74-kDa regulatory B″ (δ) subunit, was phosphorylated at serine residues of B″ in vitro by cAMP-dependent protein kinase (A-kinase). In the presence and absence of 0.5 μM okadaic acid (OA), A-kinase gave maximal incorporation of 1.7 and 1.0 mol of phosphate per mol of B″, respectively. The Km value of A-kinase for CAB″ was 0.17±0.01 μM in the presence of OA. The major in vitro phosphorylation sites of B″ were identified as Ser-60, -75 and -573 in the presence of OA, and Ser-75 and -573 in the absence of OA. Phosphorylation of B″ did not dissociate B″ from CA, and stimulated the molecular activity of CAB″ toward phosphorylated H1 and H2B histones, 3.8- and 1.4-fold, respectively, but not toward phosphorylase a. 相似文献
104.
Molecular Dissection of the Rho-associated Protein Kinase (p160ROCK)-regulated Neurite Remodeling in Neuroblastoma N1E-115 Cells 总被引:19,自引:0,他引:19
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Masaya Hirose Toshimasa Ishizaki Naoki Watanabe Masayoshi Uehata Onno Kranenburg Wouter H. Moolenaar Fumio Matsumura Midori Maekawa Haruhiko Bito Shuh Narumiya 《The Journal of cell biology》1998,141(7):1625-1636
A critical role for the small GTPase Rho and one of its targets, p160ROCK (a Rho-associated coiled coil-forming protein kinase), in neurite remodeling was examined in neuroblastoma N1E-115 cells. Using wild-type and a dominant-negative form of p160ROCK and a p160ROCK-specific inhibitor, Y-27632, we show here that p160ROCK activation is necessary and sufficient for the agonist-induced neurite retraction and cell rounding. The neurite retraction was accompanied by elevated phosphorylation of myosin light chain and the disassembly of the intermediate filaments and microtubules. Y-27632 blocked both neurite retraction and the elevation of myosin light chain phosphorylation in a similar concentration-dependent manner. On the other hand, suppression of p160ROCK activity by expression of a dominant-negative form of p160ROCK induced neurites in the presence of serum by inducing the reassembly of the intermediate filaments and microtubules. The neurite outgrowth by the p160ROCK inhibition was blocked by coexpression of dominant-negative forms of Cdc42 and Rac, indicating that p160ROCK constitutively and negatively regulates neurite formation at least in part by inhibiting activation of Cdc42 and Rac. The assembly of microtubules and intermediate filaments to form extended processes by inhibitors of the Rho–ROCK pathway was also observed in Swiss 3T3 cells. These results indicate that Rho/ROCK-dependent tonic inhibition of cell process extension is exerted via activation of the actomysin-based contractility, in conjunction with a suppression of assembly of intermediate filaments and microtubules in many cell types including, but not exclusive to, neuronal cells. 相似文献
105.
Induction of 72-kDa Inducible Heat Shock Protein (HSP72) in Cultured Rat Astrocytes After Energy Depletion 总被引:2,自引:1,他引:1
Naohiko Imuta Satoshi Ogawa ‡Yusuke Maeda †Keisuke Kuwabara †Osamu Hori Hirokazu Ueda Takehiko Yanagihara Masaya Tohyama 《Journal of neurochemistry》1998,70(2):550-557
Abstract: Protein synthesis is important in the readaptive processes for cultured astrocytes after hypoxia and subsequent reoxygenation. We have identified 72-kDa inducible heat shock protein (HSP72) as a major stress protein in reoxygenated astrocytes. To assess the mechanism for reoxygenation-mediated induction of HSP72, a reporter gene that consists of a human HSP promoter fused to the luciferase gene was transfected into cultured astrocytes. Analysis of cellular energy nucleotides showed an increase of the ADP/ATP ratio after reoxygenation, which synchronized with activation of the HSP promoter. Activation of the HSP promoter was also observed after an addition of iodoacetic acid to hypoxic astrocytes, which reached the maximum when the ADP/ATP ratio reached 50%, but further decline in the energy profile caused inactivation of this promoter. Inhibition of protein synthesis after reoxygenation resulted in temporary restoration of the energy profile and suppression of the DNA binding activity of the heat shock factor. Addition of quercetin greatly decreased the [3 H]leucine incorporation in the polysome fraction without any effect on the mature mRNA formation. These data suggest that the energy depletion in reoxygenation triggers induction of HSP72 after reoxygenation, which may act as a pivotal mediator in the stress response of reoxygenated astrocytes by facilitating protein synthesis. 相似文献
106.
107.
Ryunosuke Yoshino Nobuaki Yasuo Daniel Ken Inaoka Yohsuke Hagiwara Kazuki Ohno Masaya Orita Masayuki Inoue Tomoo Shiba Shigeharu Harada Teruki Honma Emmanuel Oluwadare Balogun Josmar Rodrigues da Rocha Carlos Alberto Montanari Kiyoshi Kita Masakazu Sekijima 《PloS one》2015,10(5)
BackgroundChagas disease, caused by the parasite Trypanosoma cruzi, is a neglected tropical disease that causes severe human health problems. To develop a new chemotherapeutic agent for the treatment of Chagas disease, we predicted a pharmacophore model for T. cruzi dihydroorotate dehydrogenase (TcDHODH) by fragment molecular orbital (FMO) calculation for orotate, oxonate, and 43 orotate derivatives.Conclusions/SignificanceFMO-based interaction energy analyses revealed a pharmacophore model for TcDHODH inhibitor. Hydrogen bond acceptor pharmacophores correspond to Lys43 and Lys214, hydrogen bond donor and acceptor pharmacophores correspond to Asn67 and Asn194, and the aromatic ring pharmacophore corresponds to FMN, which shows important characteristics of compounds that inhibit TcDHODH. In addition, the Lys214 residue is not conserved between TcDHODH and human DHODH. Our analysis suggests that these orotate derivatives should preferentially bind to TcDHODH, increasing their selectivity. Our results obtained by pharmacophore modeling provides insight into the structural requirements for the design of TcDHODH inhibitors and their development as new anti-Chagas drugs. 相似文献
108.
Po-sung Chu Hirotoshi Ebinuma Nobuhiro Nakamoto Kazuo Sugiyama Shingo Usui Yuko Wakayama Nobuhito Taniki Akihiro Yamaguchi Shunsuke Shiba Yoshiyuki Yamagishi Takaji Wakita Toshifumi Hibi Hidetsugu Saito Takanori Kanai 《PloS one》2015,10(5)
Hepatitis C virus (HCV) genotype 1 infections are significantly more difficult to eradicate with PEG-IFN/ribavirin therapy, compared to HCV genotype 2. The aim of this work is to investigate the difference of immunological impairments underlying this phenomenon. Pre-treatment NKG2D expression on peripheral CD56+CD3+ lymphocytes and CD56+CD3− NK cells from cases of chronic hepatitis C were analyzed and assessed by treatment effect. Two strains of HCV were used to co-incubate with immune cells in vitro. NKG2D expression on peripheral CD56+CD3+ lymphocytes, but not NK cells, was significantly impaired in genotype 1 infection, compared to genotype 2. When peripheral blood mononuclear cells from healthy donors were co-incubated with TNS2J1, a genotype 1b/2a chimera strain, or with JFH1, a genotype 2a strain, genotype-specific decrease of NKG2D on CD56+CD3+ lymphocytes, but not NK cells, was observed. Pre-treatment NKG2D expression on peripheral CD56+CD3+ lymphocytes significantly correlated with reduction in serum HCV RNA levels from week 0 to week 4, and predicted treatment response. Ex vivo stimulation of peripheral CD56+CD3+ lymphocytes showed NKG2D expression-correlated IFN-γ production. In conclusion, Decreased NKG2D expression on CD56+CD3+ lymphocytes in chronic HCV genotype 1 infection predicts inferior treatment response to PEG-IFN/ribavirin therapy compared to genotype 2. 相似文献
109.
Ryotaro Yabe Akane Miura Tatsuya Usui Ingrid Mudrak Egon Ogris Takashi Ohama Koichi Sato 《PloS one》2015,10(12)
Protein phosphatase 2A (PP2A) is a conserved essential enzyme that is implicated as a tumor suppressor based on its central role in phosphorylation-dependent signaling pathways. Protein phosphatase methyl esterase (PME-1) catalyzes specifically the demethylation of the C-terminal Leu309 residue of PP2A catalytic subunit (PP2Ac). It has been shown that PME-1 affects the activity of PP2A by demethylating PP2Ac, but also by directly binding to the phosphatase active site, suggesting loss of PME-1 in cells would enhance PP2A activity. However, here we show that PME-1 knockout mouse embryonic fibroblasts (MEFs) exhibit lower PP2A activity than wild type MEFs. Loss of PME-1 enhanced poly-ubiquitination of PP2Ac and shortened the half-life of PP2Ac protein resulting in reduced PP2Ac levels. Chemical inhibition of PME-1 and rescue experiments with wild type and mutated PME-1 revealed methyl-esterase activity was necessary to maintain PP2Ac protein levels. Our data demonstrate that PME-1 methyl-esterase activity protects PP2Ac from ubiquitin/proteasome degradation. 相似文献
110.
Masaya Ito Kate H. Bentley Yuki Oe Shun Nakajima Hiroko Fujisato Noriko Kato Mitsuhiro Miyamae Ayako Kanie Masaru Horikoshi David H. Barlow 《PloS one》2015,10(4)