Translocation of Helicobacter pylori CagA into gastric epithelial cells by type IV secretion.

By S. Odenbreit, Jürgen Püls, Bettina Sedlmaier, Elke Gerland, W. Fischer, R. Haas. Science, 2000

1,346 citations recorded by the source corpus.

Subfields: Immunology, Small Animals, Surgery

View Paper: https://www.semanticscholar.org/paper/ca02095026e75fe75614d5819a9fd531a2e0dc86

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Immunology

1. R. Peek
2. Keith T. Wilson
3. Lydia E. Wroblewski
4. E. Kuipers
5. A. V. van Vliet
6. J. G. Kusters
7. P. Sansonetti
8. Martin J. Blaser

In Small Animals

1. R. Peek
2. E. Kuipers
3. A. V. van Vliet
4. J. G. Kusters
5. Masanori Hatakeyama

In Surgery

1. R. Peek
2. Martin J. Blaser
3. Keith T. Wilson
4. Lydia E. Wroblewski
5. E. Kuipers
6. A. V. van Vliet
7. J. G. Kusters
8. Masanori Hatakeyama

Citations in the corpus

• Pathogenesis of Helicobacter pylori Infection (2006, background): “The interaction between the type IV structure and the host cell also results in the induction of proinflammatory cytokines in epithelial cells (469, 555).”
• Helicobacter pylori: gastric cancer and beyond (2010, background): “The product of the terminal gene in the island (CagA) is translocated into and phosphorylated within host epithelial cells following bacterial attachmen”
• Protein Injection Machines in Bacteria (2018, positive): “…pylori, the causative agent of stomach ulcers, the T4SS contributes to the most severe forms of the disease by delivering a single effector protein, CagA, which is capable of interfering with major signaling pathways in the host (Covacci et al., 1999; Odenbreit et al., 2000; Segal et al., 1999).”
• Helicobacter pylori and gastrointestinal tract adenocarcinomas (2002, background): “pylori into the epithelial cell, where it undergoes tyrosine phosphorylation — a process that is associated with dephosphorylation of host-cell protein”
• Microbiome and Malignancy (2011, background): “pylori are highly interactive with host cells (Odenbreit et al., 2000), consistent with the Class B model (Figure 3).”
• Helicobacter pylori and Gastric Cancer: Factors That Modulate Disease Risk (2010, background): “tyrosine-alanine (EPIYA) motifs and induces cell morphological changes, initially termed “the hummingbird phenotype,” which are associated with increased cellular migration (20, 226, 279, 292, 293) (see “CagA phosphorylation-dependent host cell signaling”).”
• Oncogenic mechanisms of the Helicobacter pylori CagA protein (2004, background): “The morphological change is also associated with increased cell motility known as cell scattering and is preceded by the phosphorylation of Cag”
• The tight junction: a multifunctional complex. (2004, background): “When Helicobacter pylori adhere to the apical-junctional complex of epithelial cells, the CagA protein is translocated from the bacterium into the epithelial cell (112).”
• Pathogenicity Islands in Bacterial Pathogenesis (2004, background): “Work by several groups has demonstrated that the translocation of CagA into target cells is required for these phenotypes (8, 11, 262, 316, 338).”
• Human Gut Microbiota and Gastrointestinal Cancer (2018, background): “Cag strain infections present a highly increased risk of gastric cancers [36,37].”