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          "alternateName": "Division of Microbiology, Department of Biology, Friedrich Alexander University Erlangen-Nuremberg, Staudtstr. 5, 91058, Erlangen, Germany", 
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          "name": [
            "Division of Microbiology, Department of Biology, Friedrich Alexander University Erlangen-Nuremberg, Staudtstr. 5, 91058, Erlangen, Germany"
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          "name": [
            "Max von Pettenkofer-Institute for Hygiene and Medical Microbiology, Ludwig-Maximilians-University, Munich, Germany", 
            "German Center for Infection Research (DZIF), Munich Site, 80336, Munich, Germany"
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          "name": [
            "Institute for Medical Microbiology, Immunology and Hygiene, Technische Universit\u00e4t M\u00fcnchen, 81675, Munich, Germany", 
            "German Center for Infection Research (DZIF), Munich Site, 80336, Munich, Germany"
          ], 
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            "Institute of Experimental Internal Medicine, Otto von Guericke University, 39120, Magdeburg, Germany"
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    "description": "Various gram-negative pathogens express type IV secretion systems (T4SSs) which translocate bacterial virulence factors into host target cells to hijack cellular processes for their own benefit and causing disease. The pathology of Helicobacter pylori, the causative agent of chronic gastritis, peptic ulcer disease, and gastric cancer in humans, strongly depends on a T4SS encoded by the cag pathogenicity island (cagPAI). This T4SS represents a pilus-like structure and a membrane-spanning complex. T4SS assembly is achieved by various protein\u2013protein interactions and several pilus-associated components (CagL, CagI, CagY, and CagA) that allow docking to the host cell integrin member \u03b15\u03b21 followed by delivery of its major effector protein, CagA, across the host cell membrane. In addition, recent studies have shown that H. pylori exploits human CEACAM receptors via the adhesin HopQ, encoded outside of the cagPAI, for bacterial adherence and translocation of CagA. Here, we review the composition and assembly of the H. pylori T4SS and its fundamental role in the infection process. We discuss major CagA-dependent and CagA-independent signaling events by the T4SS in vitro and in animal models in vivo, which include the induction of cytoskeletal rearrangements, membrane dynamics, disturbance of cell polarity as well as transcriptional responses involved in inflammation, cell proliferation, and anti-apoptosis. The contribution of these signaling cascades to H. pylori colonization, and pathogenesis is reviewed.", 
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        "familyName": "Grohmann", 
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      "secretion system", 
      "cag pathogenicity island", 
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      "Helicobacter pylori type IV secretion system", 
      "H. pylori T4SS", 
      "protein-protein interactions", 
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      "translocation of CagA.", 
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      "contribution", 
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      "benefits"
    ], 
    "name": "The Helicobacter pylori Type IV Secretion System Encoded by the cag Pathogenicity Island: Architecture, Function, and Signaling", 
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