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J De Rycke - One of the best experts on this subject based on the ideXlab platform.
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Escherichia coli Cytolethal Distending Toxin Blocks the Hela Cell Cycle at the G2/M Transition by Preventing cdc2 Protein
2015Co-Authors: Kinase Dephosphorylation, Eric Oswald, J De RyckeAbstract:Cytolethal distending toxins (CDT) constitute an emerging heterogeneous family of bacterial toxins whose common biological property is to inhibit the proliferation of Cells in culture by blocking their cycle at G2/M phase. In this study, we investigated the molecular mechanisms underlying the block caused by CDT from Escherichia coli on synchronized Hela Cell cultures. To this end, we studied specifically the behavior of the two subunits of the complex that determines entry into mitosis, i.e., cyclin B1, the regulatory unit, and cdc2 protein kinase, the catalytic unit. We thus demonstrate that CDT causes Cell accumulation in G2 and not in M, that it does not slow the progression of Cells through S phase, and that it does not affect the normal increase of cyclin B1 from late S to G2. On the other hand, we show that CDT inhibits the kinase activity of cdc2 by preventing its dephosphorylation, an event which, in normal Cells, triggers mitosis. This inhibitory activity was demonstrated for the three partially related CDTs so far described for E. coli. Moreover, we provide evidence that Cells exposed to CDT during G2 and M phases are blocked only at the subsequent G2 phase. This observation means that the toxin triggers a mechanism of Cell arrest that is initiated in S phase and therefore possibly related to the DNA damage checkpoint system. Cytolethal distending toxins (CDT) constitute an emerging toxin family whose members have been found in several unre-lated bacterial species of medical interest, including Esche-richia coli (12, 23, 24, 30), Shigella dysenteriae (19), Campy-lobacter sp. (18, 25), and Haemophilus ducreyi (3). In all cases, the genetic structure encoding CDT activity included three adjacent or slightly overlapping chromosomal genes (called cdtA, cdtB, and cdtC) encoding proteins with similar molecula
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escherichia coli cytolethal distending toxin blocks the Hela Cell cycle at the g2 m transition by preventing cdc2 protein kinase dephosphorylation and activation
Infection and Immunity, 1997Co-Authors: C Comayras, S Y Peres, Christian Tasca, Eric Oswald, Bernard Ducommun, J De RyckeAbstract:Cytolethal distending toxins (CDT) constitute an emerging heterogeneous family of bacterial toxins whose common biological property is to inhibit the proliferation of Cells in culture by blocking their cycle at G2/M phase. In this study, we investigated the molecular mechanisms underlying the block caused by CDT from Escherichia coli on synchronized Hela Cell cultures. To this end, we studied specifically the behavior of the two subunits of the complex that determines entry into mitosis, i.e., cyclin B1, the regulatory unit, and cdc2 protein kinase, the catalytic unit. We thus demonstrate that CDT causes Cell accumulation in G2 and not in M, that it does not slow the progression of Cells through S phase, and that it does not affect the normal increase of cyclin B1 from late S to G2. On the other hand, we show that CDT inhibits the kinase activity of cdc2 by preventing its dephosphorylation, an event which, in normal Cells, triggers mitosis. This inhibitory activity was demonstrated for the three partially related CDTs so far described for E. coli. Moreover, we provide evidence that Cells exposed to CDT during G2 and M phases are blocked only at the subsequent G2 phase. This observation means that the toxin triggers a mechanism of Cell arrest that is initiated in S phase and therefore possibly related to the DNA damage checkpoint system.
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a new cytolethal distending toxin cdt from escherichia coli producing cnf2 blocks Hela Cell division in g2 m phase
Molecular Microbiology, 1997Co-Authors: S Y Peres, Olivier Marches, F Daigle, Jeanphilippe Nougayrede, Frederic Herault, Christian Tasca, J De Rycke, Eric OswaldAbstract:Escherichia coli strain 1404, isolated from a septicaemic calf, carries a transferable plasmid called pVir which codes for the cytotoxic necrotizing factor type 2 (CNF2). A 4h interaction between strain 1404 and Hela Cells induced the formation of giant mononucleated Cells blocked in G2/M phase. Mating experiments between strain 1404 and a non-pathogenic recipient strain demonstrated that the factor(s) encoded by pVir mediated the Cell-cycle arrest. A 3.3 kb DNA fragment isolated from a DNA bank of pVir was shown to code for the factor(s) causing the Cell-cycle arrest. Nucleotide sequence analysis revealed the presence of three genes encoding proteins sharing significant amino acid homology with the cytolethal distending toxins (CDTs) previously isolated from E. coli, Campylobacter jejuni and Shigella dysenteriae. Southern hybridization experiments demonstrated that the pVir of other CNF2-producing E. coli strains contained sequences related to cdt. Although the amino acid sequences amongst CDT diverged significantly, the two other CDTs previously isolated from E. coli were also able to block the Hela Cell cycle. In conclusion, this study demonstrates the mode of action of CDT and will help us to elucidate the role of this emerging toxin family in microbial pathogenesis.
Eric Oswald - One of the best experts on this subject based on the ideXlab platform.
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Escherichia coli Cytolethal Distending Toxin Blocks the Hela Cell Cycle at the G2/M Transition by Preventing cdc2 Protein
2015Co-Authors: Kinase Dephosphorylation, Eric Oswald, J De RyckeAbstract:Cytolethal distending toxins (CDT) constitute an emerging heterogeneous family of bacterial toxins whose common biological property is to inhibit the proliferation of Cells in culture by blocking their cycle at G2/M phase. In this study, we investigated the molecular mechanisms underlying the block caused by CDT from Escherichia coli on synchronized Hela Cell cultures. To this end, we studied specifically the behavior of the two subunits of the complex that determines entry into mitosis, i.e., cyclin B1, the regulatory unit, and cdc2 protein kinase, the catalytic unit. We thus demonstrate that CDT causes Cell accumulation in G2 and not in M, that it does not slow the progression of Cells through S phase, and that it does not affect the normal increase of cyclin B1 from late S to G2. On the other hand, we show that CDT inhibits the kinase activity of cdc2 by preventing its dephosphorylation, an event which, in normal Cells, triggers mitosis. This inhibitory activity was demonstrated for the three partially related CDTs so far described for E. coli. Moreover, we provide evidence that Cells exposed to CDT during G2 and M phases are blocked only at the subsequent G2 phase. This observation means that the toxin triggers a mechanism of Cell arrest that is initiated in S phase and therefore possibly related to the DNA damage checkpoint system. Cytolethal distending toxins (CDT) constitute an emerging toxin family whose members have been found in several unre-lated bacterial species of medical interest, including Esche-richia coli (12, 23, 24, 30), Shigella dysenteriae (19), Campy-lobacter sp. (18, 25), and Haemophilus ducreyi (3). In all cases, the genetic structure encoding CDT activity included three adjacent or slightly overlapping chromosomal genes (called cdtA, cdtB, and cdtC) encoding proteins with similar molecula
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escherichia coli cytolethal distending toxin blocks the Hela Cell cycle at the g2 m transition by preventing cdc2 protein kinase dephosphorylation and activation
Infection and Immunity, 1997Co-Authors: C Comayras, S Y Peres, Christian Tasca, Eric Oswald, Bernard Ducommun, J De RyckeAbstract:Cytolethal distending toxins (CDT) constitute an emerging heterogeneous family of bacterial toxins whose common biological property is to inhibit the proliferation of Cells in culture by blocking their cycle at G2/M phase. In this study, we investigated the molecular mechanisms underlying the block caused by CDT from Escherichia coli on synchronized Hela Cell cultures. To this end, we studied specifically the behavior of the two subunits of the complex that determines entry into mitosis, i.e., cyclin B1, the regulatory unit, and cdc2 protein kinase, the catalytic unit. We thus demonstrate that CDT causes Cell accumulation in G2 and not in M, that it does not slow the progression of Cells through S phase, and that it does not affect the normal increase of cyclin B1 from late S to G2. On the other hand, we show that CDT inhibits the kinase activity of cdc2 by preventing its dephosphorylation, an event which, in normal Cells, triggers mitosis. This inhibitory activity was demonstrated for the three partially related CDTs so far described for E. coli. Moreover, we provide evidence that Cells exposed to CDT during G2 and M phases are blocked only at the subsequent G2 phase. This observation means that the toxin triggers a mechanism of Cell arrest that is initiated in S phase and therefore possibly related to the DNA damage checkpoint system.
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a new cytolethal distending toxin cdt from escherichia coli producing cnf2 blocks Hela Cell division in g2 m phase
Molecular Microbiology, 1997Co-Authors: S Y Peres, Olivier Marches, F Daigle, Jeanphilippe Nougayrede, Frederic Herault, Christian Tasca, J De Rycke, Eric OswaldAbstract:Escherichia coli strain 1404, isolated from a septicaemic calf, carries a transferable plasmid called pVir which codes for the cytotoxic necrotizing factor type 2 (CNF2). A 4h interaction between strain 1404 and Hela Cells induced the formation of giant mononucleated Cells blocked in G2/M phase. Mating experiments between strain 1404 and a non-pathogenic recipient strain demonstrated that the factor(s) encoded by pVir mediated the Cell-cycle arrest. A 3.3 kb DNA fragment isolated from a DNA bank of pVir was shown to code for the factor(s) causing the Cell-cycle arrest. Nucleotide sequence analysis revealed the presence of three genes encoding proteins sharing significant amino acid homology with the cytolethal distending toxins (CDTs) previously isolated from E. coli, Campylobacter jejuni and Shigella dysenteriae. Southern hybridization experiments demonstrated that the pVir of other CNF2-producing E. coli strains contained sequences related to cdt. Although the amino acid sequences amongst CDT diverged significantly, the two other CDTs previously isolated from E. coli were also able to block the Hela Cell cycle. In conclusion, this study demonstrates the mode of action of CDT and will help us to elucidate the role of this emerging toxin family in microbial pathogenesis.
S Y Peres - One of the best experts on this subject based on the ideXlab platform.
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escherichia coli cytolethal distending toxin blocks the Hela Cell cycle at the g2 m transition by preventing cdc2 protein kinase dephosphorylation and activation
Infection and Immunity, 1997Co-Authors: C Comayras, S Y Peres, Christian Tasca, Eric Oswald, Bernard Ducommun, J De RyckeAbstract:Cytolethal distending toxins (CDT) constitute an emerging heterogeneous family of bacterial toxins whose common biological property is to inhibit the proliferation of Cells in culture by blocking their cycle at G2/M phase. In this study, we investigated the molecular mechanisms underlying the block caused by CDT from Escherichia coli on synchronized Hela Cell cultures. To this end, we studied specifically the behavior of the two subunits of the complex that determines entry into mitosis, i.e., cyclin B1, the regulatory unit, and cdc2 protein kinase, the catalytic unit. We thus demonstrate that CDT causes Cell accumulation in G2 and not in M, that it does not slow the progression of Cells through S phase, and that it does not affect the normal increase of cyclin B1 from late S to G2. On the other hand, we show that CDT inhibits the kinase activity of cdc2 by preventing its dephosphorylation, an event which, in normal Cells, triggers mitosis. This inhibitory activity was demonstrated for the three partially related CDTs so far described for E. coli. Moreover, we provide evidence that Cells exposed to CDT during G2 and M phases are blocked only at the subsequent G2 phase. This observation means that the toxin triggers a mechanism of Cell arrest that is initiated in S phase and therefore possibly related to the DNA damage checkpoint system.
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a new cytolethal distending toxin cdt from escherichia coli producing cnf2 blocks Hela Cell division in g2 m phase
Molecular Microbiology, 1997Co-Authors: S Y Peres, Olivier Marches, F Daigle, Jeanphilippe Nougayrede, Frederic Herault, Christian Tasca, J De Rycke, Eric OswaldAbstract:Escherichia coli strain 1404, isolated from a septicaemic calf, carries a transferable plasmid called pVir which codes for the cytotoxic necrotizing factor type 2 (CNF2). A 4h interaction between strain 1404 and Hela Cells induced the formation of giant mononucleated Cells blocked in G2/M phase. Mating experiments between strain 1404 and a non-pathogenic recipient strain demonstrated that the factor(s) encoded by pVir mediated the Cell-cycle arrest. A 3.3 kb DNA fragment isolated from a DNA bank of pVir was shown to code for the factor(s) causing the Cell-cycle arrest. Nucleotide sequence analysis revealed the presence of three genes encoding proteins sharing significant amino acid homology with the cytolethal distending toxins (CDTs) previously isolated from E. coli, Campylobacter jejuni and Shigella dysenteriae. Southern hybridization experiments demonstrated that the pVir of other CNF2-producing E. coli strains contained sequences related to cdt. Although the amino acid sequences amongst CDT diverged significantly, the two other CDTs previously isolated from E. coli were also able to block the Hela Cell cycle. In conclusion, this study demonstrates the mode of action of CDT and will help us to elucidate the role of this emerging toxin family in microbial pathogenesis.
Christian Tasca - One of the best experts on this subject based on the ideXlab platform.
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escherichia coli cytolethal distending toxin blocks the Hela Cell cycle at the g2 m transition by preventing cdc2 protein kinase dephosphorylation and activation
Infection and Immunity, 1997Co-Authors: C Comayras, S Y Peres, Christian Tasca, Eric Oswald, Bernard Ducommun, J De RyckeAbstract:Cytolethal distending toxins (CDT) constitute an emerging heterogeneous family of bacterial toxins whose common biological property is to inhibit the proliferation of Cells in culture by blocking their cycle at G2/M phase. In this study, we investigated the molecular mechanisms underlying the block caused by CDT from Escherichia coli on synchronized Hela Cell cultures. To this end, we studied specifically the behavior of the two subunits of the complex that determines entry into mitosis, i.e., cyclin B1, the regulatory unit, and cdc2 protein kinase, the catalytic unit. We thus demonstrate that CDT causes Cell accumulation in G2 and not in M, that it does not slow the progression of Cells through S phase, and that it does not affect the normal increase of cyclin B1 from late S to G2. On the other hand, we show that CDT inhibits the kinase activity of cdc2 by preventing its dephosphorylation, an event which, in normal Cells, triggers mitosis. This inhibitory activity was demonstrated for the three partially related CDTs so far described for E. coli. Moreover, we provide evidence that Cells exposed to CDT during G2 and M phases are blocked only at the subsequent G2 phase. This observation means that the toxin triggers a mechanism of Cell arrest that is initiated in S phase and therefore possibly related to the DNA damage checkpoint system.
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a new cytolethal distending toxin cdt from escherichia coli producing cnf2 blocks Hela Cell division in g2 m phase
Molecular Microbiology, 1997Co-Authors: S Y Peres, Olivier Marches, F Daigle, Jeanphilippe Nougayrede, Frederic Herault, Christian Tasca, J De Rycke, Eric OswaldAbstract:Escherichia coli strain 1404, isolated from a septicaemic calf, carries a transferable plasmid called pVir which codes for the cytotoxic necrotizing factor type 2 (CNF2). A 4h interaction between strain 1404 and Hela Cells induced the formation of giant mononucleated Cells blocked in G2/M phase. Mating experiments between strain 1404 and a non-pathogenic recipient strain demonstrated that the factor(s) encoded by pVir mediated the Cell-cycle arrest. A 3.3 kb DNA fragment isolated from a DNA bank of pVir was shown to code for the factor(s) causing the Cell-cycle arrest. Nucleotide sequence analysis revealed the presence of three genes encoding proteins sharing significant amino acid homology with the cytolethal distending toxins (CDTs) previously isolated from E. coli, Campylobacter jejuni and Shigella dysenteriae. Southern hybridization experiments demonstrated that the pVir of other CNF2-producing E. coli strains contained sequences related to cdt. Although the amino acid sequences amongst CDT diverged significantly, the two other CDTs previously isolated from E. coli were also able to block the Hela Cell cycle. In conclusion, this study demonstrates the mode of action of CDT and will help us to elucidate the role of this emerging toxin family in microbial pathogenesis.
Faramarz Rahmatizadeh - One of the best experts on this subject based on the ideXlab platform.
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reduction in the viability of human cervical cancer Hela Cell line via indirect co culture with amniotic fluid derived mesenchymal stem Cells
International Journal of Women's Health, 2019Co-Authors: Faramarz Rahmatizadeh, Fatima Pashaeiasl, Manijeh Mohammadi Dehcheshmeh, Sara Rahbar, Maryam Laleataei, Shiva Gholizadehghaleh Aziz, Jafar Soleimani Rad, Maryam PashaiaslAbstract:ObjectivesThis experiment was carried out to evaluate the impacts of unmodified human amniotic fluid-derived mesenchymal stromal/stem Cells (hAF-MSCs) on the viability of Hela Cells, as well as the impact of these Cells on the expression of common pro-apoptotic and pro-survival genes in tumor Cells by establishing an indirect co-culture system.Materials and MethodsTo this end, an indirect co-culture system was established, and hAF-MSCs were co-cultured with Hela Cells at a ratio of 1:2 for five days. The Cell viability of co-cultured tumor Cells was determined after the incubation period. Then, several parameters were examined, including the gene expression of tumor protein 53 (TP53), BCL2-associated X protein (BAX), B-Cell lymphoma 2 (BCL-2), and cyclin-dependent kinase inhibitor 1A (CDKN1A). Finally, gene regulatory networks were analyzed as well.ResultsThe results of this study confirmed that the co-culture of hAF-MSCs with Hela Cells could decrease the viability of tumor Cells. The reduction of Hela Cell viability was accompanied by an increase in BAX, TP53, and CDKN1A while a decrease in BCL-2 gene expression. Eventually, the analysis of the regulatory network revealed that the co-culture of Hela Cells with hAF-MSCs activated several transcriptional factors and microRNAs which regulated the expression of these genes.ConclusionsIn general, hAF-MSCs exerted the inhibitive effects on the growth of Hela Cells, along with alterations in the expression of common pro-apoptotic and pro-survival genes in a timely and concentration-dependent manner.