排序方式: 共有138条查询结果,搜索用时 490 毫秒
31.
Fernandez-Capetillo O Chen HT Celeste A Ward I Romanienko PJ Morales JC Naka K Xia Z Camerini-Otero RD Motoyama N Carpenter PB Bonner WM Chen J Nussenzweig A 《Nature cell biology》2002,4(12):993-997
Activation of the ataxia telangiectasia mutated (ATM) kinase triggers diverse cellular responses to ionizing radiation (IR), including the initiation of cell cycle checkpoints. Histone H2AX, p53 binding-protein 1 (53BP1) and Chk2 are targets of ATM-mediated phosphorylation, but little is known about their roles in signalling the presence of DNA damage. Here, we show that mice lacking either H2AX or 53BP1, but not Chk2, manifest a G2-M checkpoint defect close to that observed in ATM(-/-) cells after exposure to low, but not high, doses of IR. Moreover, H2AX regulates the ability of 53BP1 to efficiently accumulate into IR-induced foci. We propose that at threshold levels of DNA damage, H2AX-mediated concentration of 53BP1 at double-strand breaks is essential for the amplification of signals that might otherwise be insufficient to prevent entry of damaged cells into mitosis. 相似文献
32.
Arkady A. Schileyko 《ZooKeys》2013,(276):39-54
A new species of the centipede genus Newportia, Newportia stoevi
sp. n., is described from Rio Encantado Cave, Puerto Rico. It differs from all congeners by having sternites distinctly margined laterally and ultimate legs bearing 4 spinous processes on both prefemur and femur, and 2 on tibia. The value of some terms used in the taxonomy of the genus have been analyzed and an amended identification key to the species of Newportia is provided. 相似文献
33.
Teratogen‐induced apoptotic cell death: Does the apoptotic machinery act as a protector of embryos exposed to teratogens? 总被引:1,自引:0,他引:1
Torchinsky A Fein A Toder V 《Birth defects research. Part C, Embryo today : reviews》2005,75(4):353-361
Considerable evidence has been collected demonstrating that many teratogens induce apoptotic cell death in embryonic structures that turn out to be malformed in fetuses and newborns. Apoptosis is a genetically regulated process that is realized by the activation of death and pro-survival signaling cascades, and the interplay between these cascades determines whether the cell exposed to apoptotic stimuli dies or survives. Therefore, there is intense interest in understanding how the apoptotic machinery functions in embryos exposed to teratogens. However, the interpretation of the results obtained remains problematic. The main problem is that excessive embryonic cell death, regardless of its nature, if uncompensated for, ultimately leads to maldevelopment or embryonic death. Therefore, we can easily interpret results when the intensity of teratogen-induced cell death and the severity or incidence of teratogen-induced anomalies directly correlate with each other. However, when teratogen-induced cell death is not followed by the formation of anomalies, a usual explanation is that teratogen-induced apoptotic cell death contributes to the renewal of teratogen-targeted cell populations by promoting the removal of injured cells. It is clear that such an explanation leaves vague the role of the anti-apoptotic signaling mechanism (and, hence, the apoptotic machinery as a whole) with respect to protecting the embryo against teratogenic stress. In this review, we summarize the data from studies addressing the function of the apoptotic machinery in embryos exposed to teratogens, and then we discuss approaches to interpreting the results of these studies. We hypothesize that activation of a proapoptotic signaling in teratogen-targeted cell populations is a necessary condition for an anti-apoptotic signaling that counteracts the process of maldevelopment to be activated. If such a scenario is true, we need to modify our approaches to choosing molecular targets for studies addressing this topic. 相似文献
34.
A new method for determination of RNA polymerase (RNAP) activity is presented. The method uses nucleoside tri- and tetraphosphate derivatives carrying 4-methylumbelliferone residue at the terminal phosphate. Incorporation of such compounds in RNA by RNA polymerase is accompanied by release of di- and triphosphate derivatives of 4-methylumbelliferone. Subsequent treatment by alkaline phosphatase produces free 4-methylumbelliferone that is highly fluorescent and can be easily detected. The sensitivity of the method is higher than that reported in previous studies. The validity of the assay has been demonstrated by retrieving the RNAP inhibitors from a collection of 16,000 compounds. 相似文献
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36.
Yevdokimov YM Skuridin SG Nechipurenko YD Zakharov MA Salyanov VI Kurnosov AA Kuznetsov VD Nikiforov VN 《International journal of biological macromolecules》2005,36(1-2):103-115
We describe the formation and properties of nanoconstruction that consists of the double-stranded DNA molecules located at distance of 35-50 A in the spatial structure of particles of their cholesteric liquid-crystalline dispersions and cross-linked by artificial nanobridges. The resulting nanostructures possess the peculiar spatial and optical properties. 相似文献
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38.
Alina P. Ryumina Ekaterina O. Serebrovskaya Marina V. Shirmanova Ludmila B. Snopova Maria M. Kuznetsova Ilya V. Turchin Nadezhda I. Ignatova Natalia V. Klementieva Arkady F. Fradkov Boris E. Shakhov Elena V. Zagaynova Konstantin A. Lukyanov Sergey A. Lukyanov 《Biochimica et Biophysica Acta (BBA)/General Subjects》2013
Background
Genetically encoded photosensitizers are a promising optogenetic instrument for light-induced production of reactive oxygen species in desired locations within cells in vitro or whole body in vivo. Only two such photosensitizers are currently known, GFP-like protein KillerRed and FMN-binding protein miniSOG. In this work we studied phototoxic effects of miniSOG in cancer cells.Methods
HeLa Kyoto cell lines stably expressing miniSOG in different localizations, namely, plasma membrane, mitochondria or chromatin (fused with histone H2B) were created. Phototoxicity of miniSOG was tested on the cells in vitro and tumor xenografts in vivo.Results
Blue light induced pronounced cell death in all three cell lines in a dose-dependent manner. Caspase 3 activation was characteristic of illuminated cells with mitochondria- and chromatin-localized miniSOG, but not with miniSOG in the plasma membrane. In addition, H2B-miniSOG-expressing cells demonstrated light-induced activation of DNA repair machinery, which indicates massive damage of genomic DNA. In contrast to these in vitro data, no detectable phototoxicity was observed on tumor xenografts with HeLa Kyoto cell lines expressing mitochondria- or chromatin-localized miniSOG.Conclusions
miniSOG is an excellent genetically encoded photosensitizer for mammalian cells in vitro, but it is inferior to KillerRed in the HeLa tumor.General significance
This is the first study to assess phototoxicity of miniSOG in cancer cells. The results suggest an effective ontogenetic tool and may be of interest for molecular and cell biology and biomedical applications. 相似文献39.
Researchers have reported on the stiffness of running in holistic terms, i.e. for the structures that are undergoing deformation as a whole rather than in terms of specific locations. This study aimed to estimate both the natural frequency and the viscous damping coefficient of the human foot-surface cushion, during the period between the heel strike and the mid-stance phase of running, using a purposely developed one degree-of-freedom inverted pendulum state space model of the leg. The model, which was validated via a comparison of measured and estimated ground reaction forces, incorporated a novel use of linearized and extended Kalman filter estimators. Investigation of the effect of variation of the natural frequency and/or the damping of the cushioning mechanism during running, using the said model, revealed the natural frequency of running on said foot-surface cushion, during the stance phase, to lie between 5 and 11 Hz. The "extended Kalman filter (EKF)" approach, that was used here for the first time to directly apply measured ground forces, may be widely applicable to the identification process of combined estimation of both unknown physiological state and mechanical characteristics of the environment in an inverse dynamic model. 相似文献
40.
SEPYLRFamide acts as an inhibitory modulator of acetylcholine (ACh) receptors in Helix lucorum neurones. Ouabain, a specific inhibitor of Na,K-pump, (0.1 mM, bath application) decreased the ACh-induced inward current (ACh-current) and increased the leak current. Ouabain decreased the modulatory SEPYLRFamide effect on the ACh-current. There was a correlation between the effects of ouabain on the amplitude of the ACh-current and on the modulatory peptide effect. Ouabain and SEPYLRFamide inhibited the activity of Helix aspersa brain Na,K-ATPase. Activation of Na,K-pump by intracellular injection of 3 M Na acetate or 3 M NaCl reduced the modulatory peptide effect on the ACh-current. An inhibitor of Na/Ca-exchange, benzamil (25 muM, bath application), and an inhibitor of Ca(2+)-pump in the endoplasmic reticulum, thapsigargin (TG, applied intracellularly), both prevented the effect of ouabain on SEPYLRFamide-mediated modulatory effect. Another inhibitor of Ca(2+)-pump in the endoplasmic reticulum, cyclopiazonic acid (applied intracellularly), did not prevent the effect of ouabain on SEPYLRFamide-mediated modulatory effect. These results indicate that Na,K-pump is responsible for the SEPYLRFamide-mediated inhibition of ACh receptors in Helix neurons. Na/Ca-exchange and intracellular Ca(2+) released from internal pools containing TG-sensitive Ca(2+)-pump are involved in the Na,K-pump pathway for the SEPYLRFamide-mediated inhibition of ACh receptors. 相似文献