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61.
Makoto Takeuchi Eisuke Tsuda Masaaki Yoshikawa Ryuzo Sasaki Hideo Chiba 《Bioscience, biotechnology, and biochemistry》2013,77(11):2789-2797
Bovine κ-casein, a phosphoglycoprotein, has mucin-type carbohydrate chains. Subcellular distribution of enzymes that take part in the post-translational modification of κ-casein was examined. In lactating mammary glands from rats and cows, N-acetyl-galactosaminyl transferase, galactosyl transferase, sialyl transferase, and casein kinase were localized specifically in the Golgi apparatus.The substrate specificities indicate that these enzymes are actually responsible for the processing of κ-casein.The presence of a phosphate group attached to κ-casein did not affect the rate of glycosylation by N-acetyl-galactosaminyl transferase, while the presence of carbohydrate chains attached to κ- casein strongly reduced the rate of phosphorylation by casein kinase. These results suggest that in the Golgi apparatus, phosphorylation of κ-casein precedes glycosylation. 相似文献
62.
Silvia Yuko Eguchi Naomichi Nishio Shiro Nagai 《Bioscience, biotechnology, and biochemistry》2013,77(12):2941-2943
Resting cells of the methanogen strain HU, a formate-utilizing methanogenic bacterium, was able to utilize formate or hydrogen as electron donor for the production of NADPH from NADP+ under suitable conditions. In the presence of 0.2% Triton X-100 and 0.3 m potassium phosphate, pH 9.0 at 30°C, the resting cells could convert ca. 60% of the exogenous NADP+ into NADPH yielding ca. 6 g NADPH/liter. Phosphate ions greatly enhanced the NADPH production. 相似文献
63.
Yusuke Sakai Makiko Koike Hideko Hasegawa Kosho Yamanouchi Akihiko Soyama Mitsuhisa Takatsuki Tamotsu Kuroki Kazuo Ohashi Teruo Okano Susumu Eguchi 《PloS one》2013,8(7)
Cell sheet engineering is attracting attention from investigators in various fields, from basic research scientists to clinicians focused on regenerative medicine. However, hepatocytes have a limited proliferation potential in vitro, and it generally takes a several days to form a sheet morphology and multi-layered sheets. We herein report our rapid and efficient technique for generating multi-layered human hepatic cell (HepaRG® cell) sheets using pre-cultured fibroblast monolayers derived from human skin (TIG-118 cells) as a feeder layer on a temperature-responsive culture dish. Multi-layered TIG-118/HepaRG cell sheets with a thick morphology were harvested on day 4 of culturing HepaRG cells by forceful contraction of the TIG-118 cells, and the resulting sheet could be easily handled. In addition, the human albumin and alpha 1-antitrypsin synthesis activities of TIG-118/HepaRG cells were approximately 1.2 and 1.3 times higher than those of HepaRG cells, respectively. Therefore, this technique is considered to be a promising modality for rapidly fabricating multi-layered human hepatocyte sheets from cells with limited proliferation potential, and the engineered cell sheet could be used for cell transplantation with highly specific functions. 相似文献
64.
Tomohiro Iguchi Sho Nambara Takaaki Masuda Hisateru Komatsu Masami Ueda Shinya Kidogami Yushi Ogawa Qingjiang Hu Kuniaki Sato Tomoko Saito Hidenari Hirata Shotaro Sakimura Ryutaro Uchi Naoki Hayashi Shuhei Ito Hidetoshi Eguchi Keishi Sugimachi Yoshihiko Maehara Koshi Mimori 《PloS one》2016,11(11)
miR-146a plays important roles in cancer as it directly targets NUMB, an inhibitor of Notch signaling. miR-146a is reportedly regulated by a G>C polymorphism (SNP; rs2910164). This polymorphism affects various cancers, including colorectal cancer (CRC). However, the clinical significance of miR-146a polymorphism in CRC remains unclear. A total of 59 patients with CRC were divided into 2 groups: a CC/CG genotype (n = 32) and a GG genotype (n = 27), based on the miR-146a polymorphism. cDNA microarray analysis was performed using 59 clinical samples. Significantly enriched gene sets in each genotype were extracted using GSEA. We also investigated the association between miR-146a polymorphism and miR-146a, NUMB expression or migratory response in CRC cell lines. The CC/CG genotype was associated with significantly more synchronous liver metastasis (p = 0.007). A heat map of the two genotypes showed that the expression profiles were clearly stratified. GSEA indicated that Notch signaling and JAK/STAT3 signaling were significantly associated with the CC/CG genotype (p = 0.004 and p = 0.023, respectively). CRC cell lines with the pre-miR-146a/C revealed significantly higher miR-146a expression (p = 0.034) and higher NUMB expression and chemotactic activity. In CRC, miR-146a polymorphism is involved in liver metastasis. Identification of this polymorphism could be useful to identify patients with a high risk of liver metastasis in CRC. 相似文献
65.
66.
Qu Wei-Min Huang Zhi-Li Mochizuki Takatoshi Eguchi Naomi Chen Jiang-Fan Schwarzschild Michael A. Fink Stephen J. Urade Yoshihiro Hayaishi Osamu 《Sleep and biological rhythms》2016,2(1):S55-S55
Sleep and Biological Rhythms - 相似文献
67.
68.
Takeda N Maemura K Horie S Oishi K Imai Y Harada T Saito T Shiga T Amiya E Manabe I Ishida N Nagai R 《The Journal of biological chemistry》2007,282(45):32561-32567
Cardiovascular diseases are closely related to circadian rhythm, which is under the control of an internal biological clock mechanism. Although a biological clock exists not only in the hypothalamus but also in each peripheral tissue, the biological relevance of the peripheral clock remains to be elucidated. In this study we searched for clock-controlled genes in vascular endothelial cells using microarray technology. The expression of a total of 229 genes was up-regulated by CLOCK/BMAL2. Among the genes that we identified, we examined the thrombomodulin (TM) gene further, because TM is an integral membrane glycoprotein that is expressed primarily in vascular endothelial cells and plays a major role in the regulation of intravascular coagulation. TM mRNA and protein expression showed a clear circadian oscillation in the mouse lung and heart. Reporter analyses, gel shift assays, and chromatin immunoprecipitation analyses using the TM promoter revealed that a heterodimer of CLOCK and BMAL2 binds directly to the E-box of the TM promoter, resulting in TM promoter transactivation. Indeed, the oscillation of TM gene expression was abolished in clock mutant mice, suggesting that TM expression is regulated by the clock gene in vivo. Finally, the phase of circadian oscillation of TM mRNA expression was altered by temporal feeding restriction, suggesting TM gene expression is regulated by the peripheral clock system. In conclusion, these data suggest that the peripheral clock in vascular endothelial cells regulates TM gene expression and that the oscillation of TM expression may contribute to the circadian variation of cardiovascular events. 相似文献
69.
70.
Eguchi S Dempsey PJ Frank GD Motley ED Inagami T 《The Journal of biological chemistry》2001,276(11):7957-7962
In cultured vascular smooth muscle cells (VSMC), the vasculotrophic factor, angiotensin II (AngII) activates three major MAPKs via the G(q)-coupled AT1 receptor. Extracellular signal-regulated kinase (ERK) activation by AngII requires Ca(2+)-dependent "transactivation" of the EGF receptor that may involve a metalloprotease to stimulate processing of an EGF receptor ligand from its precursor. Whether EGF receptor transactivation also contributes to activation of other members of MAPKs such as p38MAPK and c-Jun N-terminal kinase (JNK) by AngII remains unclear. In the present study, we have examined the effects of a synthetic metalloprotease inhibitor BB2116, and the EGF receptor kinase inhibitor AG1478 on AngII-induced activation of MAPKs in cultured VSMC. BB2116 markedly inhibited ERK activation induced by AngII or the Ca(2+) ionophore without affecting the activation by EGF or PDGF. BB2116 as well as HB-EGF neutralizing antibody inhibited the EGF receptor transactivation by AngII, suggesting a critical role of HB-EGF in the metalloprotease-dependent EGF receptor transactivation. In addition to the ERK activation, activation of p38MAPK and JNK by AngII was inhibited by an AT1 receptor antagonist, RNH6270. and EGF markedly activate p38MAPK, whereas but not EGF markedly activates JNK, indicating the possible contribution of the EGF receptor transactivation to the p38MAPK activation. The findings that both BB2116 and AG1478 specifically inhibited activation of p38MAPK but not JNK by AngII support this hypothesis. From these data, we conclude that ERK and p38MAPK activation by AngII requires the metalloprotease-dependent EGF receptor transactivation, whereas the JNK activation is regulated without involvement of EGF receptor transactivation. 相似文献