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排序方式: 共有355条查询结果,搜索用时 31 毫秒
51.
Harada N Yamada Y Tsukiyama K Yamada C Nakamura Y Mukai E Hamasaki A Liu X Toyoda K Seino Y Inagaki N 《American journal of physiology. Endocrinology and metabolism》2008,294(1):E61-E68
Gastric inhibitory polypeptide (GIP) is an incretin that potentiates insulin secretion from pancreatic beta-cells by binding to GIP receptor (GIPR) and subsequently increasing the level of intracellular adenosine 3',5'-cyclic monophosphate (cAMP). We have identified a novel GIPR splice variant in mouse beta-cells that retains intron 8, resulting in a COOH-terminal truncated form (truncated GIPR). This isoform was coexpressed with full-length GIPR (wild-type GIPR) in normal GIPR-expressing tissues. In an experiment using cells transfected with both GIPRs, truncated GIPR did not lead to cAMP production induced by GIP but inhibited GIP-induced cAMP production through wild-type GIPR (n = 3-4, P < 0.05). Wild-type GIPR was normally located on the cell surface, but its expression was decreased in the presence of truncated GIPR, suggesting a dominant negative effect of truncated GIPR against wild-type GIPR. The functional relevance of truncated GIPR in vivo was investigated. In high-fat diet-fed obese mice (HFD mice), blood glucose levels were maintained by compensatory increased insulin secretion (n = 8, P < 0.05), and cAMP production (n = 6, P < 0.01) and insulin secretion (n = 10, P < 0.05) induced by GIP were significantly increased in isolated islets, suggesting hypersensitivity of the GIPR. Total GIPR mRNA expression was not increased in the islets of HFD mice, but the expression ratio of truncated GIPR to total GIPR was reduced by 32% compared with that of control mice (n = 6, P < 0.05). These results indicate that a relative reduction of truncated GIPR expression may be involved in hypersensitivity of GIPR and hyperinsulinemia in diet-induced obese mice. 相似文献
52.
Kameshita I Sekiguchi M Hamasaki D Sugiyama Y Hatano N Suetake I Tajima S Sueyoshi N 《Biochemical and biophysical research communications》2008,377(4):1162-1167
DNA methyltransferase 1 (Dnmt1) is an enzyme that recognizes and methylates hemimethylated CpG after DNA replication to maintain methylation patterns. Although the N-terminal region of Dnmt1 is known to interact with various proteins, such as methyl-CpG-binding protein 2 (MeCP2), the associations of protein kinases with this region have not been reported. In the present study, we found that a 110-kDa protein kinase in mouse brain could bind to the N-terminal domain of Dnmt1. This 110-kDa kinase was identified as cyclin-dependent kinase-like 5 (CDKL5) by LC-MS/MS analysis. CDKL5 and Dnmt1 were found to colocalize in nuclei and appeared to interact with each other. Catalytically active CDKL5, CDKL5(1-352), phosphorylated the N-terminal region of Dnmt1 in the presence of DNA. Considering that defects in the MeCP2 or CDKL5 genes cause Rett syndrome, we propose that the interaction between Dnmt1 and CDKL5 may contribute to the pathogenic processes of Rett syndrome. 相似文献
53.
Behavior of Psychrotrophic Lactic Acid Bacteria Isolated from Spoiling Cooked Meat Products
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Yoshikatsu Hamasaki Mitsuko Ayaki Hidetaka Fuchu Masaaki Sugiyama Hidetoshi Morita 《Applied microbiology》2003,69(6):3668-3671
Three kinds of lactic acid bacteria were isolated from spoiling cooked meat products stored below 10°C. They were identified as Leuconostoc mesenteroides subsp. mesenteroides, Lactococcus lactis subsp. lactis, and Leuconostoc citreum. All three strains grew well in MRS broth at 10°C. In particular, L. mesenteroides subsp. mesenteroides and L. citreum grew even at 4°C, and their doubling times were 23.6 and 51.5 h, respectively. On the other hand, although the bacteria were initially below the detection limit (<10 CFU/g) in model cooked meat products, the bacterial counts increased to 108 CFU/g at 10°C after 7 to 12 days. 相似文献
54.
Yuping Li Tomohiro Nishimura Kiichiro Teruya Tei Maki Takaaki Komatsu Takeki Hamasaki Taichi Kashiwagi Shigeru Kabayama Sun-Yup Shim Yoshinori Katakura Kazuhiro Osada Takeshi Kawahara Kazumichi Otsubo Shinkatsu Morisawa Yoshitoki Ishii Zbigniew Gadek Sanetaka Shirahata 《Cytotechnology》2002,40(1-3):139-149
Reactive oxygen species (ROS) cause irreversible damage to biological macromolecules, resulting in many diseases. Reduced
water (RW) such as hydrogen-rich electrolyzed reduced water and natural reduced waters like Hita Tenryosui water in Japan
and Nordenau water in Germany that are known to improve various diseases, could protect a hamster pancreatic β cell line,
HIT-T15 from alloxan-induced cell damage. Alloxan, a diabetogenic compound, is used to induce type 1 diabetes mellitus in
animals. Its diabetogenic effect is exerted via the production of ROS. Alloxan-treated HIT-T15 cells exhibited lowered viability,
increased intracellular ROS levels, elevated cytosolic free Ca2+ concentration, DNA fragmentation, decreased intracellular ATP levels and lowering of glucose-stimulated release of insulin.
RW completely prevented the generation of alloxan-induced ROS, increase of cytosolic Ca2+ concentration, decrease of intracellular ATP level, and lowering of glucose-stimulated insulin release, and strongly blocked
DNA fragmentation, partially suppressing the lowering of viability of alloxan-treated cells. Intracellular ATP levels and
glucose-stimulated insulin secretion were increased by RW to 2–3.5 times and 2–4 times, respectively, suggesting that RW enhances
the glucose-sensitivity and glucose response of β-cells. The protective activity of RW was stable at 4 °C for over a month,
but was lost by autoclaving. These results suggest that RW protects pancreatic β-cells from alloxan-induced cell damage by
preventing alloxan-derived ROS generation. RW may be useful in preventing alloxan-induced type 1-diabetes mellitus.
This revised version was published online in August 2006 with corrections to the Cover Date. 相似文献
55.
K. Yamamoto Y. Tsuji Y. Aso T. Hamasaki S. Shirahata Y. Katakura 《Journal of Applied Entomology》2011,135(4):320-325
We investigated the effects of exposure to diazinon, an organophosphate insecticide, on the expression of antioxidant and detoxification factors in the silkmoth. Exposure to diazinon resulted in induction of mRNA encoding manganese containing superoxide dismutase (SOD) and omega‐class glutathione S‐transferases (GST), whereas no changes were observed in catalase, other class of GST and acetylcholinesterase. Liquid chromatography showed that the amount of reactive oxygen species was increased, whereas the amount of glutathione was decreased in the silkmoth fat body after exposure to diazinon. These results suggest that SOD and omega‐class GSTs can contribute to organophosphate resistance in Lepidopterans. 相似文献
56.
57.
58.
Short communication. Biomass and production of cyanobacteria in a coastal water of Sagami Bay, Japan
Hamasaki K; Satoh F; Kikuchi T; Toda T; Taguchi S 《Journal of plankton research》1999,21(8):1583-1591
Cyanobacteria were relatively small contributors to carbon biomass
(097-18%) in the euphotic zone. However, a higher contribution to
production obtained at the surface water (16-45%) implies that they
contribute more to carbon cycling than is expected from their biomass
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59.
Enzymatic Formation of G-Group Aflatoxins and Biosynthetic Relationship between G- and B-Group Aflatoxins 总被引:6,自引:3,他引:3
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We detected biosynthetic activity for aflatoxins G1 and G2 in cell extracts of Aspergillus parasiticus NIAH-26. We found that in the presence of NADPH, aflatoxins G1 and G2 were produced from O-methylsterigmatocystin and dihydro-O-methylsterigmatocystin, respectively. No G-group aflatoxins were produced from aflatoxin B1, aflatoxin B2, 5-methoxysterigmatocystin, dimethoxysterigmatocystin, or sterigmatin, confirming that B-group aflatoxins are not the precursors of G-group aflatoxins and that G- and B-group aflatoxins are independently produced from the same substrates (O-methylsterigmatocystin and dihydro-O-methylsterigmatocystin). In competition experiments in which the cell-free system was used, formation of aflatoxin G2 from dihydro-O-methylsterigmatocystin was suppressed when O-methylsterigmatocystin was added to the reaction mixture, whereas aflatoxin G1 was newly formed. This result indicates that the same enzymes can catalyze the formation of aflatoxins G1 and G2. Inhibition of G-group aflatoxin formation by methyrapone, SKF-525A, or imidazole indicated that a cytochrome P-450 monooxygenase may be involved in the formation of G-group aflatoxins. Both the microsome fraction and a cytosol protein with a native mass of 220 kDa were necessary for the formation of G-group aflatoxins. Due to instability of the microsome fraction, G-group aflatoxin formation was less stable than B-group aflatoxin formation. The ordA gene product, which may catalyze the formation of B-group aflatoxins, also may be required for G-group aflatoxin biosynthesis. We concluded that at least three reactions, catalyzed by the ordA gene product, an unstable microsome enzyme, and a 220-kDa cytosol protein, are involved in the enzymatic formation of G-group aflatoxins from either O-methylsterigmatocystin or dihydro-O-methylsterigmatocystin. 相似文献
60.