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  • 1
    Publication Date: 2001-06-02
    Description: Listeria monocytogenes is responsible for severe food-borne infections, but the mechanisms by which bacteria cross the intestinal barrier are unknown. Listeria monocytogenes expresses a surface protein, internalin, that interacts with a host receptor, E-cadherin, to promote entry into human epithelial cells. Murine E-cadherin, in contrast to guinea pig E-cadherin, does not interact with internalin, excluding the mouse as a model for addressing internalin function in vivo. In guinea pigs and transgenic mice expressing human E-cadherin, internalin was found to mediate invasion of enterocytes and crossing of the intestinal barrier. These results illustrate how relevant animal models for human infections can be generated.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lecuit, M -- Vandormael-Pournin, S -- Lefort, J -- Huerre, M -- Gounon, P -- Dupuy, C -- Babinet, C -- Cossart, P -- New York, N.Y. -- Science. 2001 Jun 1;292(5522):1722-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Unite des Interactions Bacteries-Cellules, Station Centrale de Microscopie Electronique, Institut Pasteur, 75724 Paris cedex 15, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11387478" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bacterial Proteins/*metabolism ; Bacterial Translocation ; Cadherins/genetics/*metabolism ; Carrier Proteins/genetics ; Colony Count, Microbial ; *Disease Models, Animal ; Enterocytes/metabolism/*microbiology ; Fatty Acid-Binding Proteins ; Guinea Pigs ; Humans ; Intestinal Mucosa/microbiology/pathology ; Intestine, Small/microbiology/pathology ; Listeria monocytogenes/growth & development/metabolism/*pathogenicity ; Listeriosis/*microbiology/pathology ; Liver/microbiology/pathology ; Lymph Nodes/microbiology/pathology ; Male ; Mice ; Mice, Transgenic ; *Neoplasm Proteins ; *Nerve Tissue Proteins ; Promoter Regions, Genetic ; Spleen/microbiology/pathology ; Transgenes ; *Tumor Suppressor Proteins ; Virulence
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 2
    Publication Date: 2001-09-15
    Description: Rickettsia conorii is an obligate intracellular bacterium that causes Mediterranean spotted fever in humans. We determined the 1,268,755-nucleotide complete genome sequence of R. conorii, containing 1374 open reading frames. This genome exhibits 804 of the 834 genes of the previously determined R. prowazekii genome plus 552 supplementary open reading frames and a 10-fold increase in the number of repetitive elements. Despite these differences, the two genomes exhibit a nearly perfect colinearity that allowed the clear identification of different stages of gene alterations with gene remnants and 37 genes split in 105 fragments, of which 59 are transcribed. A 38-kilobase sequence inversion was dated shortly after the divergence of the genus.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ogata, H -- Audic, S -- Renesto-Audiffren, P -- Fournier, P E -- Barbe, V -- Samson, D -- Roux, V -- Cossart, P -- Weissenbach, J -- Claverie, J M -- Raoult, D -- New York, N.Y. -- Science. 2001 Sep 14;293(5537):2093-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Information Genetique & Structurale, CNRS-AVENTIS UMR 1889, 31 chemin Joseph Aiguier, 13402 Marseille Cedex 20, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11557893" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptation, Physiological ; Chlamydia/genetics ; Computational Biology ; DNA, Bacterial/genetics ; DNA, Intergenic ; *Evolution, Molecular ; Gene Dosage ; Gene Silencing ; Gene Transfer, Horizontal ; Genes, Bacterial ; *Genome, Bacterial ; Open Reading Frames ; Phylogeny ; Polymerase Chain Reaction ; Repetitive Sequences, Nucleic Acid ; Rickettsia/genetics ; Rickettsia conorii/*genetics/physiology ; Rickettsia prowazekii/*genetics/physiology ; Sequence Analysis, DNA ; Transcription, Genetic
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 3
    Publication Date: 2001-10-27
    Description: Listeria monocytogenes is a food-borne pathogen with a high mortality rate that has also emerged as a paradigm for intracellular parasitism. We present and compare the genome sequences of L. monocytogenes (2,944,528 base pairs) and a nonpathogenic species, L. innocua (3,011,209 base pairs). We found a large number of predicted genes encoding surface and secreted proteins, transporters, and transcriptional regulators, consistent with the ability of both species to adapt to diverse environments. The presence of 270 L. monocytogenes and 149 L. innocua strain-specific genes (clustered in 100 and 63 islets, respectively) suggests that virulence in Listeria results from multiple gene acquisition and deletion events.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Glaser, P -- Frangeul, L -- Buchrieser, C -- Rusniok, C -- Amend, A -- Baquero, F -- Berche, P -- Bloecker, H -- Brandt, P -- Chakraborty, T -- Charbit, A -- Chetouani, F -- Couve, E -- de Daruvar, A -- Dehoux, P -- Domann, E -- Dominguez-Bernal, G -- Duchaud, E -- Durant, L -- Dussurget, O -- Entian, K D -- Fsihi, H -- Garcia-del Portillo, F -- Garrido, P -- Gautier, L -- Goebel, W -- Gomez-Lopez, N -- Hain, T -- Hauf, J -- Jackson, D -- Jones, L M -- Kaerst, U -- Kreft, J -- Kuhn, M -- Kunst, F -- Kurapkat, G -- Madueno, E -- Maitournam, A -- Vicente, J M -- Ng, E -- Nedjari, H -- Nordsiek, G -- Novella, S -- de Pablos, B -- Perez-Diaz, J C -- Purcell, R -- Remmel, B -- Rose, M -- Schlueter, T -- Simoes, N -- Tierrez, A -- Vazquez-Boland, J A -- Voss, H -- Wehland, J -- Cossart, P -- New York, N.Y. -- Science. 2001 Oct 26;294(5543):849-52.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Genomique des Microorganismes Pathogenes, Unite des Interactions Bacteries-Cellules, Service d'Informatique Scientifique, Institut Pasteur, 25-28 rue du Dr. Roux, 75724 Paris, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11679669" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptation, Physiological ; Amino Acid Motifs ; Bacillus subtilis/genetics ; Bacterial Proteins/chemistry/*genetics/physiology ; Base Composition ; Carrier Proteins/chemistry/genetics ; Chromosomes, Bacterial/genetics ; DNA, Bacterial/chemistry/genetics ; Gene Transfer, Horizontal ; Genes, Bacterial ; *Genome, Bacterial ; Genomics ; Listeria/chemistry/*genetics/physiology ; Listeria monocytogenes/chemistry/*genetics/pathogenicity/physiology ; Membrane Proteins/chemistry/genetics ; Sequence Analysis, DNA ; Staphylococcus aureus/genetics ; Transcription Factors/chemistry/genetics ; Virulence/genetics
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 4
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1997-05-02
    Description: Interest in bacterial pathogenesis has recently increased because of antibiotic resistance, the emergence of new pathogens and the resurgence of old ones, and the lack of effective therapeutics. The molecular and cellular mechanisms of microbial pathogenesis are currently being defined, with precise knowledge of both the common strategies used by multiple pathogenic bacteria and the unique tactics evolved by individual species to help establish infection. What is emerging is a new appreciation of how bacterial pathogens interact with host cells. Many host cell functions, including signal transduction pathways, cytoskeletal rearrangements, and vacuolar trafficking, are exploited, and these are the focus of this review. A bonus of this work is that bacterial virulence factors are providing new tools to study various aspects of mammalian cell functions, in addition to mechanisms of bacterial disease. Together these developments may lead to new therapeutic strategies.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Finlay, B B -- Cossart, P -- New York, N.Y. -- Science. 1997 May 2;276(5313):718-25.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Biotechnology Laboratory, University of British Columbia, Vancouver, B.C., Canada, V6T-1Z3. bfinlay@unixg.ubc.ca〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9115192" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apoptosis ; Bacteria/genetics/*pathogenicity ; *Bacterial Adhesion ; Bacterial Infections/*microbiology ; Bacterial Physiological Phenomena ; Bacterial Toxins/toxicity ; Cells, Cultured ; Cytoskeleton/physiology ; Epithelial Cells ; Epithelium/microbiology ; Humans ; Phagocytosis ; Signal Transduction ; Vacuoles/microbiology ; Virulence/genetics
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 5
    Publication Date: 2008-09-23
    Description: The ability to cross host barriers is an essential virulence determinant of invasive microbial pathogens. Listeria monocytogenes is a model microorganism that crosses human intestinal and placental barriers, and causes severe maternofetal infections by an unknown mechanism. Several studies have helped to characterize the bacterial invasion proteins InlA and InlB. However, their respective species specificity has complicated investigations on their in vivo role. Here we describe two novel and complementary animal models for human listeriosis: the gerbil, a natural host for L. monocytogenes, and a knock-in mouse line ubiquitously expressing humanized E-cadherin. Using these two models, we uncover the essential and interdependent roles of InlA and InlB in fetoplacental listeriosis, and thereby decipher the molecular mechanism underlying the ability of a microbe to target and cross the placental barrier.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Disson, Olivier -- Grayo, Solene -- Huillet, Eugenie -- Nikitas, Georgios -- Langa-Vives, Francina -- Dussurget, Olivier -- Ragon, Marie -- Le Monnier, Alban -- Babinet, Charles -- Cossart, Pascale -- Lecuit, Marc -- Howard Hughes Medical Institute/ -- England -- Nature. 2008 Oct 23;455(7216):1114-8. doi: 10.1038/nature07303. Epub 2008 Sep 17.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institut Pasteur, Groupe Microorganismes et Barrieres de l'Hote, Unite des Interactions Bacteries-Cellules, F-75015 Paris, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18806773" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bacterial Proteins/genetics/*metabolism ; Cadherins/genetics ; Cells, Cultured ; Disease Models, Animal ; Enterocytes/microbiology ; Epithelial Cells/microbiology ; Female ; Fetal Diseases/*microbiology ; Gerbillinae ; Humans ; Listeria monocytogenes/*physiology ; Listeriosis/microbiology/*transmission ; *Maternal-Fetal Exchange ; Membrane Proteins/genetics/*metabolism ; Mice ; Molecular Sequence Data ; Placenta Diseases/*microbiology ; Pregnancy ; Pregnancy Complications, Infectious/metabolism/microbiology ; Protein Binding ; Receptors, Growth Factor/metabolism ; Species Specificity
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 6
    Publication Date: 2009-05-19
    Description: The bacterium Listeria monocytogenes is ubiquitous in the environment and can lead to severe food-borne infections. It has recently emerged as a multifaceted model in pathogenesis. However, how this bacterium switches from a saprophyte to a pathogen is largely unknown. Here, using tiling arrays and RNAs from wild-type and mutant bacteria grown in vitro, ex vivo and in vivo, we have analysed the transcription of its entire genome. We provide the complete Listeria operon map and have uncovered far more diverse types of RNAs than expected: in addition to 50 small RNAs (〈500 nucleotides), at least two of which are involved in virulence in mice, we have identified antisense RNAs covering several open-reading frames and long overlapping 5' and 3' untranslated regions. We discovered that riboswitches can act as terminators for upstream genes. When Listeria reaches the host intestinal lumen, an extensive transcriptional reshaping occurs with a SigB-mediated activation of virulence genes. In contrast, in the blood, PrfA controls transcription of virulence genes. Remarkably, several non-coding RNAs absent in the non-pathogenic species Listeria innocua exhibit the same expression patterns as the virulence genes. Together, our data unravel successive and coordinated global transcriptional changes during infection and point to previously unknown regulatory mechanisms in bacteria.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Toledo-Arana, Alejandro -- Dussurget, Olivier -- Nikitas, Georgios -- Sesto, Nina -- Guet-Revillet, Helene -- Balestrino, Damien -- Loh, Edmund -- Gripenland, Jonas -- Tiensuu, Teresa -- Vaitkevicius, Karolis -- Barthelemy, Mathieu -- Vergassola, Massimo -- Nahori, Marie-Anne -- Soubigou, Guillaume -- Regnault, Beatrice -- Coppee, Jean-Yves -- Lecuit, Marc -- Johansson, Jorgen -- Cossart, Pascale -- 233348/European Research Council/International -- Howard Hughes Medical Institute/ -- England -- Nature. 2009 Jun 18;459(7249):950-6. doi: 10.1038/nature08080. Epub 2009 May 17.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institut Pasteur, Unite des Interactions Bacteries-Cellules, F-75015 Paris, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19448609" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Gene Expression Regulation, Bacterial ; Genes, Bacterial/genetics ; Genome, Bacterial/genetics ; Intestines/microbiology ; Listeria monocytogenes/*genetics/*pathogenicity ; Mice ; Open Reading Frames/genetics ; Operon/genetics ; RNA, Bacterial/analysis/*genetics ; Regulatory Sequences, Ribonucleic Acid/genetics ; Transcription, Genetic/*genetics ; Untranslated Regions/genetics ; Virulence/genetics
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
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  • 7
    Publication Date: 2014-08-26
    Description: Riboswitches are ligand-binding elements contained within the 5' untranslated regions of bacterial transcripts, which generally regulate expression of downstream open reading frames. Here, we show that in Listeria monocytogenes, a riboswitch that binds vitamin B12 controls expression of a noncoding regulatory RNA, Rli55. Rli55, in turn, controls expression of the eut genes, whose products enable ethanolamine utilization and require B12 as a cofactor. Defects in ethanolamine utilization, or in its regulation by Rli55, significantly attenuate Listeria virulence in mice. Rli55 functions by sequestering the two-component response regulator EutV by means of a EutV-binding site contained within the RNA. Thus, Rli55 is a riboswitch-regulated member of the small group of regulatory RNAs that function by sequestering a protein and reveals a distinctive mechanism of signal integration in bacterial gene regulation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mellin, J R -- Koutero, Mikael -- Dar, Daniel -- Nahori, Marie-Anne -- Sorek, Rotem -- Cossart, Pascale -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2014 Aug 22;345(6199):940-3. doi: 10.1126/science.1255083.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Unite des Interactions Bacteries-Cellules, Institut Pasteur, F-75015 Paris, France. INSERM, U604, Paris, F-75015 France. INRA, USC2020, F-75015 Paris, France. ; Department of Molecular Genetics, Weizmann Institute of Science, Rehovot, Israel. ; Unite des Interactions Bacteries-Cellules, Institut Pasteur, F-75015 Paris, France. INSERM, U604, Paris, F-75015 France. INRA, USC2020, F-75015 Paris, France. pcossart@pasteur.fr.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25146292" target="_blank"〉PubMed〈/a〉
    Keywords: 5' Untranslated Regions ; Animals ; Ethanolamine/*metabolism ; *Gene Expression Regulation, Bacterial ; Listeria monocytogenes/*genetics/metabolism/virology ; Mice ; Mice, Inbred BALB C ; Operon ; RNA, Untranslated/*metabolism ; Response Elements ; *Riboswitch ; Vitamin B 12/*metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
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  • 8
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    Unknown
    American Association for the Advancement of Science (AAAS)
    Publication Date: 2004-04-10
    Description: Invasive bacteria actively induce their own uptake by phagocytosis in normally nonphagocytic cells and then either establish a protected niche within which they survive and replicate, or disseminate from cell to cell by means of an actin-based motility process. The mechanisms underlying bacterial entry, phagosome maturation, and dissemination reveal common strategies as well as unique tactics evolved by individual species to establish infection.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cossart, Pascale -- Sansonetti, Philippe J -- New York, N.Y. -- Science. 2004 Apr 9;304(5668):242-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Unite des Interactions Bacteries-Cellules, INSERM Unite 604, Departement de Biologie Cellulaire et Infection, Institut Pasteur, 28 Rue du Docteur Roux, Paris 75015, France. pcossart@pasteur.fr〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15073367" target="_blank"〉PubMed〈/a〉
    Keywords: Actins/physiology ; Animals ; Bacteria/growth & development/*pathogenicity ; Bacterial Adhesion ; *Bacterial Physiological Phenomena ; Bacterial Proteins/metabolism ; Cytosol/microbiology ; Enterobacteriaceae/*pathogenicity/physiology ; Epithelial Cells/*microbiology/physiology ; Humans ; Intestinal Mucosa/*microbiology/physiology ; Listeria monocytogenes/*pathogenicity/physiology ; Mice ; Models, Biological ; Movement ; Phagocytosis ; Phagosomes/microbiology/physiology ; Vacuoles/microbiology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
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  • 9
    Publication Date: 2010-04-24
    Description: During infection, pathogenic bacteria manipulate the host cell in various ways to allow their own replication, propagation and escape from host immune responses. Post-translational modifications are unique mechanisms that allow cells to rapidly, locally and specifically modify activity or interactions of key proteins. Some of these modifications, including phosphorylation and ubiquitylation, can be induced by pathogens. However, the effects of pathogenic bacteria on SUMOylation, an essential post-translational modification in eukaryotic cells, remain largely unknown. Here we show that infection with Listeria monocytogenes leads to a decrease in the levels of cellular SUMO-conjugated proteins. This event is triggered by the bacterial virulence factor listeriolysin O (LLO), which induces a proteasome-independent degradation of Ubc9, an essential enzyme of the SUMOylation machinery, and a proteasome-dependent degradation of some SUMOylated proteins. The effect of LLO on Ubc9 is dependent on the pore-forming capacity of the toxin and is shared by other bacterial pore-forming toxins like perfringolysin O (PFO) and pneumolysin (PLY). Ubc9 degradation was also observed in vivo in infected mice. Furthermore, we show that SUMO overexpression impairs bacterial infection. Together, our results reveal that Listeria, and probably other pathogens, dampen the host response by decreasing the SUMOylation level of proteins critical for infection.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3627292/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3627292/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ribet, David -- Hamon, Melanie -- Gouin, Edith -- Nahori, Marie-Anne -- Impens, Francis -- Neyret-Kahn, Helene -- Gevaert, Kris -- Vandekerckhove, Joel -- Dejean, Anne -- Cossart, Pascale -- 233348/European Research Council/International -- Howard Hughes Medical Institute/ -- England -- Nature. 2010 Apr 22;464(7292):1192-5. doi: 10.1038/nature08963.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institut Pasteur, Unite des Interactions Bacteries-Cellules, Departement de Biologie Cellulaire et Infection, F-75015 Paris, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20414307" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bacterial Toxins/metabolism ; Cell Line ; HeLa Cells ; Heat-Shock Proteins/metabolism ; Hemolysin Proteins/metabolism ; Humans ; Listeria monocytogenes/genetics/metabolism/*pathogenicity ; Listeriosis/*metabolism/*microbiology ; Mice ; *Protein Processing, Post-Translational ; Small Ubiquitin-Related Modifier Proteins/genetics/*metabolism ; Ubiquitin-Conjugating Enzymes/metabolism ; Virulence Factors/metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 10
    Publication Date: 1996-11-01
    Description: Listeria monocytogenes is a bacterial pathogen that invades cultured nonphagocytic cells. Inhibitors and a dominant negative mutation were used to demonstrate that efficient entry requires the phosphoinositide (PI) 3-kinase p85alpha-p110. Infection with L. monocytogenes caused rapid increases in cellular amounts of PI(3, 4)P2 and PI(3,4,5)P3, indicating that invading bacteria stimulated PI 3-kinase activity. This stimulation required the bacterial protein InlB, host cell tyrosine phosphorylation, and association of p85alpha with one or more tyrosine-phosphorylated proteins. This role for PI 3-kinase in bacterial entry may have parallels in some endocytic events.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ireton, K -- Payrastre, B -- Chap, H -- Ogawa, W -- Sakaue, H -- Kasuga, M -- Cossart, P -- New York, N.Y. -- Science. 1996 Nov 1;274(5288):780-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Unite des Interactions Bacteries-Cellules, Institut Pasteur, Paris, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8864117" target="_blank"〉PubMed〈/a〉
    Keywords: Androstadienes/pharmacology ; Animals ; Bacterial Proteins/physiology ; Cell Line ; Chromones/pharmacology ; Cytochalasin D/pharmacology ; Enzyme Activation ; Enzyme Inhibitors/pharmacology ; Genistein ; Humans ; Isoflavones/pharmacology ; Listeria monocytogenes/*enzymology/*pathogenicity ; Membrane Proteins/physiology ; Morpholines/pharmacology ; Phosphatidylinositol 3-Kinases ; Phosphatidylinositol Phosphates/metabolism ; Phosphoproteins/metabolism ; Phosphorylation ; Phosphotransferases (Alcohol Group Acceptor)/antagonists & inhibitors/*metabolism ; Phosphotyrosine/metabolism ; Tumor Cells, Cultured
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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