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1.
Biochemical and genetic characterization of three hamster cell mutants resistant to diphtheria toxin 总被引:2,自引:0,他引:2
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RK Draper D Chin D Eurey-Owens IE Scheffler MI Simon 《The Journal of cell biology》1979,83(1):116-125
We describe here three different hamster cell mutants which are resistant to diphtheria toxin and which provide models for investigating some of the functions required by the toxin inactivates elongation factor 2 (EF-2). Cell-free extracts from mutants Dtx(r)-3 was codominant. The evidence suggests that the codominant phenotype is the result of a mutation in a gene coding for EF-2. The recessive phenotype might arise by alteration of an enzyme which modifies the structure of EF-2 so that it becomes a substrate for reaction with the toxin. Another mutant, Dtx(r)-2, contained EF-2 that was sensitive to the toxin and this phenotype was recessive. Pseudomonas aeruginosa exotoxin is known to inactivate EF-2 as does diphtheria toxin and we tested the mutants for cross-resistance to pseudomonas exotoxin. Dtx(r)-1 and Dtx(r)-3 were cross-resistant while Dtx(r)-2 was not. It is known that diphtheria toxin does not penetrate to the cytoplasm of mouse cells and that these cell have a naturally occurring phenotype of diphtheria toxin resistance. We fused each of the mutants with mouse 3T3 cells and measured the resistance. We fused each of the mutants with mouse 3T3 cells and measured the resistance of the hybrid cells to diphtheria toxin. Intraspecies hybrids containing the genome of mutants Dtx(r)-1 and Dtx(r)-3 had some resistance while those formed with Dtx(r)-2 were as sensitive as hybrids derived from fusions between wild-type hamster cells and mouse 3T3 cells. 相似文献
2.
本文用脑室灌注和Fura2测定细胞内游离钙技术观察了地塞米松(dexamethasone,DEX)对家兔乙二醇双(2氨基乙醚)四乙酸性发热效应和下丘脑细胞内游离钙浓度([Ca2+]i)的影响,借此深入探讨地塞米松解热作用的中枢机制。结果发现:脑室灌注乙二醇双(2氨基乙醚)四乙酸(06nmol)引起家兔结肠温度明显升高,静脉注射地塞米松(5mg/kg)显著抑制家兔乙二醇双(2氨基乙醚)四乙酸性发热,地塞米松(60~120μmol/L)并不影响下丘脑细胞内[Ca2+]i,而事先脑室灌注抑制基因转录的放线菌素D(3nmol)则完全取消了地塞米松对乙二醇双(2氨基乙醚)四乙酸性发热的解热作用。这些结果提示:地塞米松显著抑制家兔乙二醇双(2氨基乙醚)四乙酸性发热,其机制与地塞米松激活脑内某些基因的表达有关,而与下丘脑神经细胞跨膜钙离子流无关。 相似文献
3.
IE Hughes 《BioEssays : news and reviews in molecular, cellular and developmental biology》1999,21(11):980-981
Instant Pharmacology (1999). Saeb-Parsy K, Assomull RG, Kahn FZ, Saeb-Parsy K, and Kelly E. John Wiley and Sons 349 pp. £19.99 pbk; ISBN 0471976393 © 1999 John Wiley & Sons, Inc. 相似文献
4.
本文利用激光散斑屈光测试系统详细探讨了夜近视(night myopia)的产生机制。夜近视在环境亮度降低到产生暗视觉时出现,并随亮度继续降低而增大,平均值为1.35D。实验证明眼睛球差和色差不是造成夜近视的主要因素。夜近视数值在暗适应过程中呈增大的趋势。在暗视觉时,由于视野中缺少适宜的刺激,眼睛处于暗焦(dark focus)休止状态,这是造成夜近视的主要原因。 相似文献
5.
Pefani DE Dimaki M Spella M Karantzelis N Mitsiki E Kyrousi C Symeonidou IE Perrakis A Taraviras S Lygerou Z 《The Journal of biological chemistry》2011,286(26):23234-23246
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7.
The distribution of the Golgi enzyme beta1, 6-N-
acetylglucosaminyltransferase (core 2 GlcNAc-T for short) has been
investigated in several tissue and cell systems by combining the potentials
of a polyclonal antibody and a novel, sensitive fluorescent enzyme assay.
In normal rat tissues, levels of the protein were found to vary and as a
general trend did not correlate with enzyme activities. Additionally, we
observed tissue-specific core 2 GlcNAc-T forms of various size: 75 kDa
(liver), 70 kDa (spleen), 60 kDA (heart), and 50 kDa (heart and lung).
These forms might arise from differential protein modifications;
alternatively, the smaller form may be a product of proteolytic cleavage,
given the presence of a catalytically inactive 50 kDa species in rat serum.
Chinese hamster ovary (CHO), MDAY-D2, PSA- 5E, and PYS-2 cell lines
consistently displayed a 70 kDa enzyme. When induced to retrodifferentiate
in the presence of butyrate + cholera toxin, CHO cells exhibited a 21-fold
increase in enzyme activity, while protein levels remained constant. A
similar trend was observed in the embryonal endoderm cell lines PSA-5E and
PYS-2, where an approximately 100-fold difference in core 2 GlcNAc-T
activity was found notwithstanding unchanged amounts of the protein and
identical mRNA levels, as evidenced by RT-PCR. In contrast, levels of core
2 GlcNAc-T activity in MDAY-D2 cells correlated well with protein
expression. Taken together, these observations demonstrate that core 2
GlcNAc-T expression may be subjected to multiple mechanisms of regulation
and suggest that in at least some instances (i.e., PSA-5E and PYS-2 cells)
expression may be regulated exclusively via posttranslational mechanism(s)
of control.
相似文献
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9.
Ioanna-Eleni Symeonidou Panagiotis Kotsantis Vassilis Roukos Maria-Anna Rapsomaniki Hernán E. Grecco Philippe Bastiaens Stavros Taraviras Zoi Lygerou 《The Journal of biological chemistry》2013,288(50):35852-35867
Once-per-cell cycle replication is regulated through the assembly onto chromatin of multisubunit protein complexes that license DNA for a further round of replication. Licensing consists of the loading of the hexameric MCM2–7 complex onto chromatin during G1 phase and is dependent on the licensing factor Cdt1. In vitro experiments have suggested a two-step binding mode for minichromosome maintenance (MCM) proteins, with transient initial interactions converted to stable chromatin loading. Here, we assess MCM loading in live human cells using an in vivo licensing assay on the basis of fluorescence recovery after photobleaching of GFP-tagged MCM protein subunits through the cell cycle. We show that, in telophase, MCM2 and MCM4 maintain transient interactions with chromatin, exhibiting kinetics similar to Cdt1. These are converted to stable interactions from early G1 phase. The immobile fraction of MCM2 and MCM4 increases during G1 phase, suggestive of reiterative licensing. In late G1 phase, a large fraction of MCM proteins are loaded onto chromatin, with maximal licensing observed just prior to S phase onset. Fluorescence loss in photobleaching experiments show subnuclear concentrations of MCM-chromatin interactions that differ as G1 phase progresses and do not colocalize with sites of DNA synthesis in S phase. 相似文献
10.
Papazahariadou M Athanasiadis GI Papadopoulos E Symeonidou I Hatzistilianou M Castellani ML Bhattacharya K Shanmugham LN Conti P Frydas S 《The International journal of biological markers》2007,22(2):144-153
Host resistance against pathogens depends on a complex interplay of innate and adaptive immune mechanisms. Acting as an early line of defence, the immune system includes activation of neutrophils, tissue macrophages, monocytes, dendritic cells, eosinophils and natural killer (NK) cells. NK cells are lymphoid cells that can be activated without previous stimulation and are therefore like macrophages in the first line of defence against tumor cells and a diverse range of pathogens. NK cells mediate significant activity and produce high levels of proinflammatory cytokines in response to infection. Their cytotoxicity production is induced principally by monocyte-, macrophage- and dendritic cell-derived cytokines, but their activation is also believed to be cytokine-mediated. Recognition of infection by NK cells is accomplished by numerous activating and inhibitory receptors on the NK cells' surface that selectively trigger the cytolytic activity in a major histocompability complex-independent manner. NK cells have trypanocidal activity of fibroblast cells and mediate direct destruction of extracellular epimastigote and trypomastigote forms of T. cruzi and T. lewisi in vitro; moreover, they kill plasmodia-infected erythrocytes directly through cell-cell interaction. This review provides a more detailed analysis of how NK cells recognize and respond to parasites and how they mediate cytotoxicity against tumor cells. Also the unique role of NK cells in innate immunity to infection and the relationship between parasites and carcinogenesis are discussed. 相似文献