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International Journal of Peptide Research and Therapeutics - Membrane proteins play important functions, such as cellular communication and transferring materials in the cell. Many membrane...  相似文献   
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Background and Aims: Helicobacter pylori is a highly diverse pathogen, which encounters epithelial cells as the initial defense barrier during its lifelong infection. The structure of epithelial cells can be disrupted through cleavage of microfilaments. Cytokeratin 18 (CK18) is an intermediate filament, the cleavage of which is considered an early event during apoptosis following activation of effector caspases. Methods: Helicobacter pylori strains were isolated from 76 dyspeptic patients. cagA 3’ variable region and CagA protein status were analyzed by PCR and western blotting, respectively. Eight hours post‐co‐culture of AGS cells with different H. pylori strains, flow cytometric analysis was performed using M30 monoclonal antibody specific to CK18 cleavage‐induced neo‐epitope. Results: Higher rates of CK18 cleavage were detected during co‐culture of AGS cells with H. pylori strains bearing greater numbers of cagA EPIYA‐C and multimerization (CM) motifs. On the other hand, H. pylori strains with greater numbers of EPIYA‐B relative to EPIYA‐C demonstrated a decrease in CK18 cleavage rate. Thus, H. pylori‐mediated cleavage of CK18 appeared proportional to the number of CagA EPIYA‐C and CM motifs, which seemed to be downplayed in the presence of EPIYA‐B motifs. Conclusions: Our observation associating the heterogeneity of cagA variants with the potential of H. pylori strains in the induction of CK18 cleavage as an early indication of apoptosis in gastric epithelial cells supports the fact that apoptosis may be a type‐specific trait. However, additional cagA‐targeted experiments are required to clearly identify the role of EPIYA and CM motifs in apoptosis and/or the responsible effector molecules.  相似文献   
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Europium‐doped yttrium oxide nanoparticles (Y2O3:Eu NPs) modified by captopril were prepared in aqueous solution. In this study, we report the effect of pyridoxine hydrochloride on the photoluminescence intensity of Y2O3:Eu NPs in pH 7.2 buffer solution. By increasing the pyridoxine concentration, the luminescence intensity of Y2O3:Eu NPs is quenched. The results show that this method demonstrates high sensitivity for pyridoxine determination. A linear relationship is observed between 0.0 and 62.0 μM with a correlation coefficient of 0.995 and a detection limit of 0.023 μM. Copyright © 2014 John Wiley & Sons, Ltd.  相似文献   
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This study evaluated the effects of Zataria multiflora essential oil (EO) and nisin on fresh rainbow trout fillets during storage at 4?°C. Treatments included the following: A (control samples without EO and nisin), E1 (treated samples with 0.2% EO), E2 (treated samples with 0.4% EO), N (treated samples with 150?IU nisin/g), E1N (treated samples with 0.2% EO and nisin) and E2N (treated samples with 0.4% EO and nisin). Chemical and oxidation changes were investigated in this study as the functions of treatment and storage time. E1N and E2N had better effects on oxidation changes and maintaining values of peroxide value and thiobarbituric acid than A, E1, E2 and N treatments. Lower total volatile base nitrogen was found in E2N than in other treatments during storage time.  相似文献   
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Polycomb Group (PcG) proteins are epigenetic repressors essential for control of development and cell differentiation. They form multiple complexes of which PRC1 and PRC2 are evolutionary conserved and obligatory for repression. The targeting of PRC1 and PRC2 is poorly understood and was proposed to be hierarchical and involve tri-methylation of histone H3 (H3K27me3) and/or monoubiquitylation of histone H2A (H2AK118ub). Here, we present a strict test of this hypothesis using the Drosophila model. We discover that neither H3K27me3 nor H2AK118ub is required for targeting PRC complexes to Polycomb Response Elements (PREs). We find that PRC1 can bind PREs in the absence of PRC2 but at many PREs PRC2 requires PRC1 to be targeted. We show that one role of H3K27me3 is to allow PcG complexes anchored at PREs to interact with surrounding chromatin. In contrast, the bulk of H2AK118ub is unrelated to PcG repression. These findings radically change our view of how PcG repression is targeted and suggest that PRC1 and PRC2 can communicate independently of histone modifications.  相似文献   
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