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141.
Duc Manh Hoang Tran Minh Ngoc Nguyen Tien Dat Do Thi Ha Young Ho Kim Hoang Van Luong Jong Seog Ahn KiHwan Bae 《Bioorganic & medicinal chemistry letters》2009,19(23):6759-6761
Bioassay-guided fractionation of the chloroform-soluble fraction of Morus bombycis, using an in vitro PTP1B inhibitory assay led to the identification of three 2-arylbenzofurans, albafuran A (1), mulberrofuran W (2) and mulberrofuran D (6), along with three chalcone-derived Diels–Alder products, kuwanon J (3), kuwanon R (4), and kuwanon V (5). Compounds 1–6 showed remarkable inhibitory activity against PTP1B with IC50 values ranging from 2.7 to 13.8 μM. Inhibition kinetics were analyzed by Lineweaver–Burk plots, which suggested that compounds 1–6 inhibited PTP1B in a mixed-type manner. The present results indicate that the respective lipophilic and hydroxyl groups of 2-arylbenzofurans and chalcone-derived Diels–Alder products play an important role in inhibition of PTP1B. 相似文献
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145.
High Performance Flexible Supercapacitor Electrodes Composed of Ultralarge Graphene Sheets and Vanadium Dioxide 下载免费PDF全文
Little is known regarding the effect of the graphene lateral size on the electrochemical performance of hybrid graphene electrode. This work examines the electrochemical performance of a flexible hybrid supercapacitor electrode composed of ultralarge graphene oxide (UGO; mean lateral size of 47 ± 22 μm) and vanadium dioxide (VO2) nanobelts, referring to a reference electrode composed of small scale graphene oxide (SGO; mean lateral size of 0.8 ± 0.5 μm) and VO2.Thermal treatment converts UGO/VO2 and SGO/VO2 to URGO/VO2 (denoted VURGO) and SRGO/VO2 (denoted VSRGO) electrodes, respectively. The sheet resistance of the VURGO film (0.57 ± 0.03 kΩ sq.–1) was two orders of magnitude lower than that of the VSRGO (55.74 ± 9.35 kΩ sq.–1). The VURGO hybrid electrode showed a specific capacitance of 769 F g?1, which was significantly better than the corresponding values for the VSRGO electrode (385 F/g). These results support the notion that the use of ultralarge graphene sheets (≈22 500 μm2) lowers the intersheet resistance due to the presence of fewer intersheet tunneling barriers. This article highlights the potential utility of URGO (as a conductive support) in hybrid electrode containing VO2 nanobelts for high performance flexible hybrid supercapacitor. 相似文献
146.
Auweter SD Yu HB Arena ET Guttman JA Finlay BB 《Microbes and infection / Institut Pasteur》2012,14(2):148-154
Effectors translocated into the host cell by Salmonella enterica serovar Typhimurium are critical for bacterial virulence. For many effectors, the mechanisms of their interactions with host pathways are not yet understood. We have recently found an interaction between the SPI-2 effector SseL and oxysterol-binding protein (OSBP). We show here that SseL binds the N-terminus of OSBP and that S. Typhimurium infection results in redistribution of OSBP. We furthermore demonstrate that OSBP is required for efficient replication of intracellular S. Typhimurium. This suggests that S. Typhimurium hijacks OSBP-dependent pathways to benefit its intracellular life-style, possibly by SseL- and OSBP-mediated manipulation of host lipid metabolism. 相似文献
147.
转基因在玉米中的遗传分离与整合特性的研究 总被引:23,自引:0,他引:23
用PCR和DNA分子杂交方法研究了转基因Bt在3种不同方法获得的8个转化体后代中的遗传分离、整合性质及其稳定性,结果表明:(1)转基因在大多数转化体后中呈简单的孟德尔遗传;在R1至R2代,部分家系中转化体比例偏低,有的发生转基因丢失,但到R3代以后均趋于正常的孟德尔遗传方式,在群体中固定下来;(2)转基因在不同转化体中的整合类型有一定差异,但整合的位点和拷贝数都较少,且多呈串联或紧密连锁的整合;( 相似文献
148.
Truong Quoc Phong Do Thi Thu Ha Uwe Volker Elke Hammer 《Indian journal of microbiology》2015,55(2):219-230
Reports in recent years indicate that the increasing emergence of resistance to drugs be using to TB treatment. The resistance to them severely affects to options for effective treatment. The emergence of multidrug-resistant tuberculosis has increased interest in understanding the mechanism of drug resistance in M. tuberculosis and the development of new therapeutics, diagnostics and vaccines. In this study, a label-free quantitative proteomics approach has been used to analyze proteome of multidrug-resistant and susceptible clinical isolates of M. tuberculosis and identify differences in protein abundance between the two groups. With this approach, we were able to identify a total of 1,583 proteins. The majority of identified proteins have predicted roles in lipid metabolism, intermediary metabolism, cell wall and cell processes. Comparative analysis revealed that 68 proteins identified by at least two peptides showed significant differences of at least twofolds in relative abundance between two groups. In all protein differences, the increase of some considering proteins such as NADH dehydrogenase, probable aldehyde dehydrogenase, cyclopropane mycolic acid synthase 3, probable arabinosyltransferase A, putative lipoprotein, uncharacterized oxidoreductase and six membrane proteins in resistant isolates might be involved in the drug resistance and to be potential diagnostic protein targets. The decrease in abundance of proteins related to secretion system and immunogenicity (ESAT-6-like proteins, ESX-1 secretion system associated proteins, O-antigen export system and MPT63) in the multidrug-resistant strains can be a defensive mechanism undertaken by the resistant cell.
Electronic supplementary material
The online version of this article (doi:10.1007/s12088-015-0511-2) contains supplementary material, which is available to authorized users. 相似文献149.
Nguyen H Martinez B Oganesyan N Kim R 《Journal of structural and functional genomics》2004,5(1-2):23-27
One of the first key steps in structural genomics is high-throughput expression and rapid screening to select highly soluble proteins, the preferred candidates for crystal production. Here we describe the methodology used at the Berkeley Structural Genomics Center (BSGC) for automated parallel expression and small-scale purification of fusion proteins using a 96-well format. Our robotic method includes cell lysis, soluble fraction separation and purification with affinity resins. For detection of His-tagged proteins in the soluble fractions and after affinity resin elution, a dot-blot procedure with an anti-His-antibody is used. The expression level and molecular mass of recombinant proteins are checked by SDS-PAGE. With this approach, we are able to obtain beneficial information to be used for large-scale protein expression and purification. 相似文献
150.
Thuy-Ai Nguyen Scott D. Slattery Sung-Hwan Moon Yolanda F. Darlington Xiongbin Lu Lawrence A. Donehower 《DNA Repair》2010,9(7):813-823
Nucleotide excision repair (NER) is the only mechanism in humans to repair UV-induced DNA lesions such as pyrimidine (6-4) pyrimidone photoproducts and cyclobutane pyrimidine dimers (CPDs). In response to UV damage, the ataxia telangiectasia mutated and Rad3-related (ATR) kinase phosphorylates and activates several downstream effector proteins, such as p53 and XPA, to arrest cell cycle progression, stimulate DNA repair, or initiate apoptosis. However, following the completion of DNA repair, there must be active mechanisms that restore the cell to a prestressed homeostatic state. An important part of this recovery must include a process to reduce p53 and NER activity as well as to remove repair protein complexes from the DNA damage sites. Since activation of the damage response occurs in part through phosphorylation, phosphatases are obvious candidates as homeostatic regulators of the DNA damage and repair responses. Therefore, we investigated whether the serine/threonine wild-type p53-induced phosphatase 1 (WIP1/PPM1D) might regulate NER. WIP1 overexpression inhibits the kinetics of NER and CPD repair, whereas WIP1 depletion enhances NER kinetics and CPD repair. This NER suppression is dependent on WIP1 phosphatase activity, as phosphatase-dead WIP1 mutants failed to inhibit NER. Moreover, WIP1 suppresses the kinetics of UV-induced damage repair largely through effects on NER, as XPD-deficient cells are not further suppressed in repairing UV damage by overexpressed WIP1. Wip1 null mice quickly repair their CPD and undergo less UV-induced apoptosis than their wild-type counterparts. In vitro phosphatase assays identify XPA and XPC as two potential WIP1 targets in the NER pathway. Thus WIP1 may suppress NER kinetics by dephosphorylating and inactivating XPA and XPC and other NER proteins and regulators after UV-induced DNA damage is repaired. 相似文献