共查询到20条相似文献,搜索用时 31 毫秒
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DUCHON L 《Annales de l'Institut Pasteur》1952,83(1):145-147
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Mitchell 《Journal of applied microbiology》1998,84(S1):119S-124S
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The epidermolytic toxins are serine proteases 总被引:9,自引:0,他引:9
Certain strains of Staphylococcus aureus usually belonging to phage group II produce epidermolytic toxins (ETA and ETB) which cause intraepidermal splitting in mice, neonates and occasionally adults. Amino acid sequences of ETA and ETB have been reported but the mechanism of epidermolysis remains unknown. A search of the NBRF-PIR computer database showed the toxins to have significant sequence similarity with staphylococcal V8 protease and that the catalytic triad of V8 protease is present in ETA and ETB. Comparison of ETA, ETB and V8 protease with other members of the trypsin-like serine protease family revealed little homology save for the immediate vicinity of the residues constituting the catalytic triad. The toxins, therefore, exhibit a distant relationship to mammalian serine proteases. A potential Ca2(+)-binding loop was identified in ETA (but not ETB) on the basis of sequence similarity with the second calcium-binding loop of rat intestinal calcium-binding protein. Epidermolysis produced by ETA in the mouse bioassay was shown to be inhibited by the presence of EDTA consistent with a Ca2(+)-dependent mechanism. 相似文献
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The properties of phospholipase enzymes in staphylococcal toxins 总被引:24,自引:0,他引:24
H M Doery B J Magnusson J Gulasekharam J E Pearson 《Journal of general microbiology》1965,40(2):283-296
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Rosado CJ Kondos S Bull TE Kuiper MJ Law RH Buckle AM Voskoboinik I Bird PI Trapani JA Whisstock JC Dunstone MA 《Cellular microbiology》2008,10(9):1765-1774
Pore-forming toxins (PFTs) are commonly associated with bacterial pathogenesis. In eukaryotes, however, PFTs operate in the immune system or are deployed for attacking prey (e.g. venoms). This review focuses upon two families of globular protein PFTs: the cholesterol-dependent cytolysins (CDCs) and the membrane attack complex/perforin superfamily (MACPF). CDCs are produced by Gram-positive bacteria and lyse or permeabilize host cells or intracellular organelles during infection. In eukaryotes, MACPF proteins have both lytic and non-lytic roles and function in immunity, invasion and development. The structure and molecular mechanism of several CDCs are relatively well characterized. Pore formation involves oligomerization and assembly of soluble monomers into a ring-shaped pre-pore which undergoes conformational change to insert into membranes, forming a large amphipathic transmembrane β-barrel. In contrast, the structure and mechanism of MACPF proteins has remained obscure. Recent crystallographic studies now reveal that although MACPF and CDCs are extremely divergent at the sequence level, they share a common fold. Together with biochemical studies, these structural data suggest that lytic MACPF proteins use a CDC-like mechanism of membrane disruption, and will help understand the roles these proteins play in immunity and development. 相似文献
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Bacterial infections may constitute an important risk factor of developing cancer disease. Molecular mechanisms by which bacteria contribute to cancer are extremely complex and still remain not fully understood. So far, it is generally accepted that Helicobacter pylori infections are associated with induction of gastric adenocarcinoma and MALT lymphoma. Two H. pylori toxins which modulate many cellular functions are VacA and CagA. So far, CagA is the only one known bacterial oncoprotein. However, many other bacteria produce toxins or effector proteins perturbing host cell homeostasis or/and evoking chronic inflammation. Both processes may be associated with tumour formation. Bacterial toxins which interfere, with various host signal transduction pathways, deregulate processes of cell division, proliferation and differentiation and modulate apoptosis. Some toxins cause even direct DNA damage. This review discuss the potential links between action of bacterial toxins and cancer. 相似文献
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A remarkable group of proteins challenge the notions that protein sequence determines a unique three-dimensional structure, and that membrane and soluble proteins are very distinct. The pore-forming toxins typically transform from soluble, monomeric proteins to oligomers that form transmembrane channels. Recent structural studies provide ideas about how these changes take place. The recently solved structures of the beta-pore-forming toxins LukS, varepsilon-toxin and intermedilysin confirm that the pore-forming regions are initially folded up on the surfaces of the soluble precursors. To create the transmembrane pores, these regions must extend and refold into membrane-inserted beta-barrels. 相似文献
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Snake venom toxins. The amino acid sequences of toxins b and d from Naja melanoleuca venom 总被引:1,自引:0,他引:1
D P Botes 《The Journal of biological chemistry》1972,247(9):2866-2871
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Anthrax toxins 总被引:2,自引:0,他引:2
M. Mourez 《Reviews of Physiology, Biochemistry and Pharmacology》2004,152(1):135-164
Bacillus anthracis, the etiological agent of anthrax, secretes three polypeptides that assemble into toxic complexes on the cell surfaces of the host it infects. One of these polypeptides, protective antigen (PA), binds to the integrin-like domains of ubiquitously expressed membrane proteins of mammalian cells. PA is then cleaved by membrane endoproteases of the furin family. Cleaved PA molecules assemble into heptamers, which can then associate with the two other secreted polypeptides: edema factor (EF) and/or lethal factor (LF). The heptamers of PA are relocalized to lipid rafts where they are quickly endocytosed and routed to an acidic compartment. The low pH triggers a conformational change in the heptamers, resulting in the formation of cation-specific channels and the translocation of EF/LF. EF is a calcium- and calmodulin-dependent adenylate cyclase that dramatically raises the intracellular concentration of cyclic adenosine monophosphate (cAMP). LF is a zinc-dependent endoprotease that cleaves the amino terminus of mitogen-activated protein kinase kinases (Meks). Cleaved Meks cannot bind to their substrates and have reduced kinase activity, resulting in alterations of the signaling pathways they govern. The structures of PA, PA heptamer, EF, and LF have been solved and much is now known about the molecular details of the intoxication mechanism. The in vivo action of the toxins, on the other hand, is still poorly understood and hotly debated. A better understanding of the toxins will help in the design of much-needed anti-toxin drugs and the development of new toxin-based medical applications.Abbreviations CMG2 Capillary morphogenesis protein 2 - DTA Diphtheria toxin A chain - EF Edema factor - EFn N-terminal fragment of EF - ETx Edema toxin - GR Glucocorticoid receptors - GSK3 Glycogen synthase kinase 3 - I domain Integrin-like domain - iNOS Inducible nitric oxide synthase - LF Lethal factor - LFn N-terminal fragment of LF - LTx Lethal toxin - MAPK Mitogen-activated protein kinase - Mek MAPK kinases - PA Protective antigen - PA20 20-kDa N-terminal fragment of PA - PA63 63-kDa C-terminal fragment of PA - TEM8 Tumor endothelial marker 8 相似文献
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Miller TA Bulman AL Thompson CD Macdonald TL 《Bioorganic & medicinal chemistry letters》1999,9(3):407-412
The synthesis of several potent inhibitors of tubulin polymerization that exert their activities through interaction at the colchicine binding site is described. These agents were evaluated for their abilities to inhibit the polymerization of tubulin and the growth of neoplastic cell cultures. Additionally, the inhibition of tubulin polymerization activity of these agents was assessed over a temperature range of 30-45 degrees C to ascertain the effect of temperature on this activity. Several of the compounds possess significant inhibition of tubulin polymerization activity, and select compounds exhibit this activity in a temperature dependent manner. 相似文献