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Journal articles on the topic 'Cag Type IV Secretion System'

Author: Grafiati

Published: 7 July 2024

Last updated: 31 July 2025

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1

Busler, Valerie J., Victor J. Torres, Mark S. McClain, Oscar Tirado, David B. Friedman, and Timothy L. Cover. "Protein-Protein Interactions among Helicobacter pylori Cag Proteins." Journal of Bacteriology 188, no. 13 (2006): 4787–800. http://dx.doi.org/10.1128/jb.00066-06.

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ABSTRACT Many Helicobacter pylori isolates contain a 40-kb region of chromosomal DNA known as the cag pathogenicity island (PAI). The risk for development of gastric cancer or peptic ulcer disease is higher among humans infected with cag PAI-positive H. pylori strains than among those infected with cag PAI-negative strains. The cag PAI encodes a type IV secretion system that translocates CagA into gastric epithelial cells. To identify Cag proteins that are expressed by H. pylori during growth in vitro, we compared the proteomes of a wild-type H. pylori strain and an isogenic cag PAI deletion m

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2

Pinto-Santini, Delia M., and Nina R. Salama. "Cag3 Is a Novel Essential Component of the Helicobacter pylori Cag Type IV Secretion System Outer Membrane Subcomplex." Journal of Bacteriology 191, no. 23 (2009): 7343–52. http://dx.doi.org/10.1128/jb.00946-09.

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ABSTRACT Helicobacter pylori strains harboring the cag pathogenicity island (PAI) have been associated with more severe gastric disease in infected humans. The cag PAI encodes a type IV secretion (T4S) system required for CagA translocation into host cells as well as induction of proinflammatory cytokines, such as interleukin-8 (IL-8). cag PAI genes sharing sequence similarity with T4S components from other bacteria are essential for Cag T4S function. Other cag PAI-encoded genes are also essential for Cag T4S, but lack of sequence-based or structural similarity with genes in existing databases

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3

Couturier, Marc Roger, Elizabetta Tasca, Cesare Montecucco, and Markus Stein. "Interaction with CagF Is Required for Translocation of CagA into the Host via the Helicobacter pylori Type IV Secretion System." Infection and Immunity 74, no. 1 (2006): 273–81. http://dx.doi.org/10.1128/iai.74.1.273-281.2006.

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ABSTRACT Development of severe gastric diseases is strongly associated with those strains of Helicobacter pylori that contain the cag pathogenicity island (PAI) inserted into the chromosome. The cag PAI encodes a type IV secretion system that translocates the major disease-associated virulence protein, CagA, into the host epithelial cell. CagA then affects host signaling pathways, leading to cell elongations and inflammation. Since the precise mechanism by which the CagA toxin is translocated by the type IV secretion system remained elusive, we used fusion proteins and immunoprecipitation stud

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4

Kumar, Navin, Mohd Shariq, Rajesh Kumari, Rakesh K. Tyagi, and Gauranga Mukhopadhyay. "Cag Type IV Secretion System: CagI Independent Bacterial Surface Localization of CagA." PLoS ONE 8, no. 9 (2013): e74620. http://dx.doi.org/10.1371/journal.pone.0074620.

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5

Cover, Timothy L., D. Borden Lacy, and Melanie D. Ohi. "The Helicobacter pylori Cag Type IV Secretion System." Trends in Microbiology 28, no. 8 (2020): 682–95. http://dx.doi.org/10.1016/j.tim.2020.02.004.

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6

Kutter, Stefan, Renate Buhrdorf, Jürgen Haas, Wulf Schneider-Brachert, Rainer Haas, and Wolfgang Fischer. "Protein Subassemblies of the Helicobacter pylori Cag Type IV Secretion System Revealed by Localization and Interaction Studies." Journal of Bacteriology 190, no. 6 (2008): 2161–71. http://dx.doi.org/10.1128/jb.01341-07.

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ABSTRACT Type IV secretion systems are possibly the most versatile protein transport systems in gram-negative bacteria, with substrates ranging from small proteins to large nucleoprotein complexes. In many cases, such as the cag pathogenicity island of Helicobacter pylori, genes encoding components of a type IV secretion system have been identified due to their sequence similarities to prototypical systems such as the VirB system of Agrobacterium tumefaciens. The Cag type IV secretion system contains at least 14 essential apparatus components and several substrate translocation and auxiliary f

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7

Jurik, Angela, Elisabeth Haußer, Stefan Kutter та ін. "The Coupling Protein Cagβ and Its Interaction Partner CagZ Are Required for Type IV Secretion of the Helicobacter pylori CagA Protein". Infection and Immunity 78, № 12 (2010): 5244–51. http://dx.doi.org/10.1128/iai.00796-10.

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ABSTRACT Bacterial type IV secretion systems are macromolecule transporters with essential functions for horizontal gene transfer and for symbiotic and pathogenic interactions with eukaryotic host cells. Helicobacter pylori, the causative agent of type B gastritis, peptic ulcers, gastric adenocarcinoma, and mucosa-associated lymphoid tissue (MALT) lymphoma, uses the Cag type IV secretion system to inject its effector protein CagA into gastric cells. This protein translocation results in altered host cell gene expression profiles and cytoskeletal rearrangements, and it has been linked to cancer

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8

Terradot, Laurent, and Gabriel Waksman. "Architecture of the Helicobacter pylori Cag-type IV secretion system." FEBS Journal 278, no. 8 (2011): 1213–22. http://dx.doi.org/10.1111/j.1742-4658.2011.08037.x.

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9

Chung, Jeong Min, Michael J. Sheedlo, Anne M. Campbell, et al. "Structure of the Helicobacter pylori Cag Type IV Secretion System." Biophysical Journal 118, no. 3 (2020): 295a. http://dx.doi.org/10.1016/j.bpj.2019.11.1671.

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10

Lettl, Clara, and Wolfgang Fischer. "Export von Gefahrgut: Helicobacter pylori und sein CagA-Protein." BIOspektrum 26, no. 6 (2020): 597–99. http://dx.doi.org/10.1007/s12268-020-1454-7.

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Abstract Pathogenic bacteria often utilize type IV secretion systems to interact with host cells and to modify their microenvironment in a favourable way. The human pathogen Helicobacter pylori produces such a system to inject only a single protein, CagA, into gastric cells, but this injection represents a major risk factor for gastric cancer development. Here, we discuss the unusual structure of the Cag secretion nanomachine and other features that make it unique among bacterial protein transporters.

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11

Chang, Yi-Wei, Carrie L. Shaffer, Lee A. Rettberg, Debnath Ghosal, and Grant J. Jensen. "In Vivo Structures of the Helicobacter pylori cag Type IV Secretion System." Cell Reports 23, no. 3 (2018): 673–81. http://dx.doi.org/10.1016/j.celrep.2018.03.085.

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12

Skoog, Emma C., Miriam E. Martin, Roberto M. Barrozo, et al. "Maintenance of Type IV Secretion Function During Helicobacter pylori Infection in Mice." mBio 11, no. 6 (2020): e03147-20. http://dx.doi.org/10.1128/mbio.03147-20.

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ABSTRACTThe Helicobacter pylori type IV secretion system (T4SS) encoded on the cag pathogenicity island (cagPAI) secretes the CagA oncoprotein and other effectors into the gastric epithelium. During murine infection, T4SS function is lost in an immune-dependent manner, typically as a result of in-frame recombination in the middle repeat region of cagY, though single nucleotide polymorphisms (SNPs) in cagY or in other essential genes may also occur. Loss of T4SS function also occurs in gerbils, nonhuman primates, and humans, suggesting that it is biologically relevant and not simply an artifact

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13

Sheedlo, Michael J., Melanie D. Ohi, D. Borden Lacy, and Timothy L. Cover. "Molecular architecture of bacterial type IV secretion systems." PLOS Pathogens 18, no. 8 (2022): e1010720. http://dx.doi.org/10.1371/journal.ppat.1010720.

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Bacterial type IV secretion systems (T4SSs) are a versatile group of nanomachines that can horizontally transfer DNA through conjugation and deliver effector proteins into a wide range of target cells. The components of T4SSs in gram-negative bacteria are organized into several large subassemblies: an inner membrane complex, an outer membrane core complex, and, in some species, an extracellular pilus. Cryo-electron tomography has been used to define the structures of T4SSs in intact bacteria, and high-resolution structural models are now available for isolated core complexes from conjugation s

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14

Wroblewski, Lydia E., Eunyoung Choi, Christine Petersen, et al. "Targeted mobilization of Lrig1+ gastric epithelial stem cell populations by a carcinogenic Helicobacter pylori type IV secretion system." Proceedings of the National Academy of Sciences 116, no. 39 (2019): 19652–58. http://dx.doi.org/10.1073/pnas.1903798116.

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Helicobacter pylori-induced gastritis is the strongest risk factor for gastric adenocarcinoma, a malignancy preceded by a series of well-defined histological stages, including metaplasia. One microbial constituent that augments cancer risk is the cag type 4 secretion system (T4SS), which translocates the oncoprotein CagA into host cells. Aberrant stem cell activation is linked to carcinogenesis, and Lrig1 (leucine-rich repeats and Ig-like domains 1) marks a distinct population of progenitor cells. We investigated whether microbial effectors with carcinogenic potential influence Lrig1 progenito

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15

Andrzejewska, Joanna, Sae Kyung Lee, Patrick Olbermann, et al. "Characterization of the Pilin Ortholog of the Helicobacter pylori Type IV cag Pathogenicity Apparatus, a Surface-Associated Protein Expressed during Infection." Journal of Bacteriology 188, no. 16 (2006): 5865–77. http://dx.doi.org/10.1128/jb.00060-06.

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ABSTRACT The Helicobacter pylori cag pathogenicity island (cag PAI) encodes components of a type IV secretion system (T4SS) involved in host interaction and pathogenicity. Previously, seven cag PAI proteins were identified as homologs of Agrobacterium tumefaciens Vir proteins, which form a paradigm T4SS. The T pilus composed of the processed VirB2 pilin is an external structural part of the A. tumefaciens T4SS. In H. pylori, cag-dependent assembly of pili has not been observed so far, nor has a pilin (VirB2) ortholog been characterized. We have here identified, using a motif-based search, an H

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16

Kumari, Rajesh, Mohd Shariq, Shivani Sharma, Ajay Kumar, and Gauranga Mukhopadhyay. "CagW, a VirB6 homologue interacts with Cag-type IV secretion system substrate CagA in Helicobacter pylori." Biochemical and Biophysical Research Communications 515, no. 4 (2019): 712–18. http://dx.doi.org/10.1016/j.bbrc.2019.06.013.

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17

Lu, Jacky, Kathryn P. Haley, Jamisha D. Francis, et al. "The Innate Immune Glycoprotein Lactoferrin Represses the Helicobacter pylori cag Type IV Secretion System." ChemBioChem 22, no. 18 (2021): 2783–90. http://dx.doi.org/10.1002/cbic.202100249.

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18

Rohde, Manfred, Jürgen Püls, Renate Buhrdorf, Wolfgang Fischer, and Rainer Haas. "A novel sheathed surface organelle of the Helicobacter pylori cag type IV secretion system." Molecular Microbiology 49, no. 1 (2003): 219–34. http://dx.doi.org/10.1046/j.1365-2958.2003.03549.x.

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19

Gaddy, J. A., and T. L. Cover. "High Resolution Electron Microscopy Analysis of the Helicobacter pylori Cag Type IV Secretion System." Microscopy and Microanalysis 19, S2 (2013): 224–25. http://dx.doi.org/10.1017/s1431927613003115.

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20

Bourzac, Kevin M., Laura A. Satkamp, and Karen Guillemin. "The Helicobacter pylori cag Pathogenicity Island Protein CagN Is a Bacterial Membrane-Associated Protein That Is Processed at Its C Terminus." Infection and Immunity 74, no. 5 (2006): 2537–43. http://dx.doi.org/10.1128/iai.74.5.2537-2543.2006.

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ABSTRACT Helicobacter pylori infects nearly half the world's population and is associated with a spectrum of gastric maladies. Infections with cytotoxin-associated gene pathogenicity island (cag PAI)-containing strains are associated with an increased risk for gastric cancer. The cag PAI contains genes encoding a type IV secretion system (T4SS) and a delivered effector, CagA, that becomes tyrosine phosphorylated upon delivery into host cells and initiates changes in cell signaling. Although some cag PAI genes have been shown to be required for CagA delivery, a subset of which are homologues of

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21

Sierra, Johanna C., Stuart Hobbs, Rupesh Chaturvedi, et al. "Induction of COX-2 expression by Helicobacter pylori is mediated by activation of epidermal growth factor receptor in gastric epithelial cells." American Journal of Physiology-Gastrointestinal and Liver Physiology 305, no. 2 (2013): G196—G203. http://dx.doi.org/10.1152/ajpgi.00495.2012.

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Chronic infection of the gastric mucosa by Helicobacter pylori is associated with an increased risk of developing gastric cancer; however, the vast majority of infected individuals never develop this disease. One H. pylori virulence factor that increases gastric cancer risk is the cag pathogenicity island, which encodes a bacterial type IV secretion system. Cyclooxygenase-2 (COX-2) expression is induced by proinflammatory stimuli, leading to increased prostaglandin E2 (PGE2) secretion by gastric epithelial cells. COX-2 expression is increased in gastric tissue from H. pylori -infected persons.

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22

Pham, Kieu Thuy, Evelyn Weiss, Luisa F. Jiménez Soto, Ute Breithaupt, Rainer Haas, and Wolfgang Fischer. "CagI Is an Essential Component of the Helicobacter pylori Cag Type IV Secretion System and Forms a Complex with CagL." PLoS ONE 7, no. 4 (2012): e35341. http://dx.doi.org/10.1371/journal.pone.0035341.

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23

Mane, S. P., M. G. Dominguez-Bello, M. J. Blaser, et al. "Host-Interactive Genes in Amerindian Helicobacter pylori Diverge from Their Old World Homologs and Mediate Inflammatory Responses." Journal of Bacteriology 192, no. 12 (2010): 3078–92. http://dx.doi.org/10.1128/jb.00063-10.

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ABSTRACT Helicobacter pylori is the dominant member of the gastric microbiota and has been associated with an increased risk of gastric cancer and peptic ulcers in adults. H. pylori populations have migrated and diverged with human populations, and health effects vary. Here, we describe the whole genome of the cag-positive strain V225d, cultured from a Venezuelan Piaroa Amerindian subject. To gain insight into the evolution and host adaptation of this bacterium, we undertook comparative H. pylori genomic analyses. A robust multiprotein phylogenetic tree reflects the major human migration out o

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24

Tegtmeyer, Nicole, Silja Wessler, and Steffen Backert. "Role of the cag-pathogenicity island encoded type IV secretion system in Helicobacter pylori pathogenesis." FEBS Journal 278, no. 8 (2011): 1190–202. http://dx.doi.org/10.1111/j.1742-4658.2011.08035.x.

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25

Feeshan, Ahmed, Kumar Ramnani Vijay, and A. khan Aleem. "Expression Analysis of Genes of Type IV Secretory System of H. Pylori in Different Gastrointestinal Diseases." International Journal of Pharmaceutical and Clinical Research 15, no. 12 (2023): 1247–54. https://doi.org/10.5281/zenodo.11200655.

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Helicobacter pylori (H. pylori) has been classified as a class I carcinogen which infects approximately half of the world’s population with certain geographical variations. This has made H. pylori infection as a global public health issue. Differential disease outcome has further led more interest in understanding the molecular pathogenesis of H.pylori. Advancements in the proteomics, transcriptomics and accessibility to partial or complete H. pylori genome sequences helped in understanding the complex gene regulation networks of H. pylori. Yet, the precise molecular mechanism through wh

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26

Gaddy, Jennifer A., Jana N. Radin, John T. Loh, et al. "The Host Protein Calprotectin Modulates the Helicobacter pylori cag Type IV Secretion System via Zinc Sequestration." PLoS Pathogens 10, no. 10 (2014): e1004450. http://dx.doi.org/10.1371/journal.ppat.1004450.

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27

Johnson, Elizabeth M., Jennifer A. Gaddy, Bradley J. Voss, Ewa E. Hennig, and Timothy L. Cover. "Genes Required for Assembly of Pili Associated with the Helicobacter pylori cag Type IV Secretion System." Infection and Immunity 82, no. 8 (2014): 3457–70. http://dx.doi.org/10.1128/iai.01640-14.

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ABSTRACTHelicobacter pyloricauses numerous alterations in gastric epithelial cells through processes that are dependent on activity of thecagtype IV secretion system (T4SS). Filamentous structures termed “pili” have been visualized at the interface betweenH. pyloriand gastric epithelial cells, and previous studies suggested that pilus formation is dependent on the presence of thecagpathogenicity island (PAI). Thus far, there has been relatively little effort to identify specific genes that are required for pilus formation, and the role of pili in T4SS function is unclear. In this study, we sel

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28

Roberts, Jacquelyn R., Sirena C. Tran, Arwen E. Frick-Cheng, et al. "Subdomains of theHelicobacter pyloriCag T4SS outer membrane core complex exhibit structural independence." Life Science Alliance 7, no. 6 (2024): e202302560. http://dx.doi.org/10.26508/lsa.202302560.

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TheHelicobacter pyloriCag type IV secretion system (Cag T4SS) has an important role in the pathogenesis of gastric cancer. The Cag T4SS outer membrane core complex (OMCC) is organized into three regions: a 14-fold symmetric outer membrane cap (OMC) composed of CagY, CagX, CagT, CagM, and Cag3; a 17-fold symmetric periplasmic ring (PR) composed of CagY and CagX; and a stalk with unknown composition. We investigated how CagT, CagM, and a conserved antenna projection (AP) region of CagY contribute to the structural organization of the OMCC. Single-particle cryo-EM analyses showed that complexes p

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Ogura, Keiji, Shin Maeda, Masafumi Nakao, et al. "Virulence Factors of Helicobacter pylori Responsible for Gastric Diseases in Mongolian Gerbil." Journal of Experimental Medicine 192, no. 11 (2000): 1601–10. http://dx.doi.org/10.1084/jem.192.11.1601.

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Helicobacter pylori infection induces various gastroduodenal diseases. We examined the role of two genes, vacA and cagE, in the gastric pathogenesis induced by H. pylori using a long-term (62 wk) animal model. Reportedly, both genes are associated with the virulence of H. pylori: vacA encodes vacuolating cytotoxin, and cagE, with other genes in the cag pathogenicity islands, encodes a type IV secretion system. Mongolian gerbils were challenged in this study by a wild-type TN2 strain and its isogenic mutants of cagE or vacA. The wild-type and vacA mutants induced severe gastritis, whereas cagE

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30

Hilleringmann, Markus, Werner Pansegrau, Michael Doyle та ін. "Inhibitors of Helicobacter pylori ATPase Cagα block CagA transport and cag virulence". Microbiology 152, № 10 (2006): 2919–30. http://dx.doi.org/10.1099/mic.0.28984-0.

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With the steadily increasing occurrence of antibiotic resistance in bacteria, there is a great need for new antibacterial compounds. The approach described here involves targeting virulence-related bacterial type IV secretion systems (TFSSs) with small-molecule inhibitors. The cag TFSS of Helicobacter pylori was chosen as a model, and novel inhibitors directed against the cag VirB11-type ATPase Cagα were identified. The cag genes encode proteins that are components of a contact-dependent secretion system used by the bacterium to translocate the effector molecule CagA into host cells. Transloca

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31

Rieder, Gabriele, Juanita L. Merchant, and Rainer Haas. "Helicobacter pylori cag-Type IV Secretion System Facilitates Corpus Colonization to Induce Precancerous Conditions in Mongolian Gerbils." Gastroenterology 128, no. 5 (2005): 1229–42. http://dx.doi.org/10.1053/j.gastro.2005.02.064.

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32

Noto, Jennifer M., Jennifer Gaddy, Josephine Y. Lee, et al. "617 Iron Deficiency Amplifies the Pathogenic Potential of Carcinogenic cag+ Helicobacter pylori via Enhancing Function of the cag Type IV Secretion System." Gastroenterology 142, no. 5 (2012): S—121. http://dx.doi.org/10.1016/s0016-5085(12)60457-0.

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33

Höppner, Christoph, Zhenying Liu, Natalie Domke, Andrew N. Binns, and Christian Baron. "VirB1 Orthologs from Brucella suis and pKM101 Complement Defects of the Lytic Transglycosylase Required for Efficient Type IV Secretion from Agrobacterium tumefaciens." Journal of Bacteriology 186, no. 5 (2004): 1415–22. http://dx.doi.org/10.1128/jb.186.5.1415-1422.2004.

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ABSTRACT Type IV secretion systems mediate conjugative plasmid transfer as well as the translocation of virulence factors from various gram-negative pathogens to eukaryotic host cells. The translocation apparatus consists of 9 to 12 components, and the components from different organisms are believed to have similar functions. However, orthologs to proteins of the prototypical type IV system, VirB of Agrobacterium tumefaciens, typically share only 15 to 30% identical amino acids, and functional complementation between components of different type IV secretion systems has not been achieved. We

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Buhrdorf, Renate, Cornelia Förster, Rainer Haas, and Wolfgang Fischer. "Topological analysis of a putative virB8 homologue essential for the cag type IV secretion system in Helicobacter pylori." International Journal of Medical Microbiology 293, no. 2-3 (2003): 213–17. http://dx.doi.org/10.1078/1438-4221-00260.

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Koelblen, Thomas, Célia Bergé, Mickaël V. Cherrier та ін. "Molecular dissection of protein-protein interactions between integrin α5β1 and the Helicobacter pylori Cag type IV secretion system". FEBS Journal 284, № 23 (2017): 4143–57. http://dx.doi.org/10.1111/febs.14299.

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36

Varga, Matthew G., M. Blanca Piazuelo, Judith Romero-Gallo, et al. "TLR9 activation suppresses inflammation in response to Helicobacter pylori infection." American Journal of Physiology-Gastrointestinal and Liver Physiology 311, no. 5 (2016): G852—G858. http://dx.doi.org/10.1152/ajpgi.00175.2016.

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Helicobacter pylori ( H. pylori) induces chronic gastritis in humans, and infection can persist for decades. One H. pylori strain-specific constituent that augments disease risk is the cag pathogenicity island. The cag island encodes a type IV secretion system (T4SS) that translocates DNA into host cells. Toll-like receptor 9 (TLR9) is an innate immune receptor that detects hypo-methylated CpG DNA motifs. In this study, we sought to define the role of the H. pylori cag T4SS on TLR9-mediated responses in vivo. H. pylori strain PMSS1 or its cagE − mutant, which fails to assemble a T4SS, were use

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Lu, Jacky, Kathryn P. Haley, Jamisha D. Francis, et al. "Cover Feature: The Innate Immune Glycoprotein Lactoferrin Represses the Helicobacter pylori cag Type IV Secretion System (ChemBioChem 18/2021)." ChemBioChem 22, no. 18 (2021): 2737. http://dx.doi.org/10.1002/cbic.202100349.

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Varga, M. G., C. L. Shaffer, J. C. Sierra, et al. "Pathogenic H elicobacter pylori strains translocate DNA and activate TLR9 via the cancer-associated cag type IV secretion system." Oncogene 35, no. 48 (2016): 6262–69. http://dx.doi.org/10.1038/onc.2016.158.

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39

Bauer, Bianca, Stefan Moese, Sina Bartfeld, Thomas F. Meyer, and Matthias Selbach. "Analysis of Cell Type-Specific Responses Mediated by the Type IV Secretion System of Helicobacter pylori." Infection and Immunity 73, no. 8 (2005): 4643–52. http://dx.doi.org/10.1128/iai.73.8.4643-4652.2005.

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ABSTRACT Helicobacter pylori persistently infects the human stomach and can cause gastritis, gastric ulceration, and gastric cancer. The type IV secretion system (TFSS) of virulent H. pylori strains translocates the CagA protein, inducing the dephosphorylation of host cell proteins and leading to changes in the morphology or shape of AGS gastric epithelial cells. Furthermore, the TFSS is involved in the induction of proinflammatory cytokines. While the H. pylori genes required for TFSS function have been investigated systematically, little is known about possible host cell factors involved. We

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40

Tran, Cong Tri, Magali Garcia, Martine Garnier, Christophe Burucoa, and Charles Bodet. "Inflammatory signaling pathways induced by Helicobacter pylori in primary human gastric epithelial cells." Innate Immunity 23, no. 2 (2016): 165–74. http://dx.doi.org/10.1177/1753425916681077.

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Inflammatory signaling pathways induced by Helicobacter pylori remain unclear, having been studied mostly on cell-line models derived from gastric adenocarcinoma with potentially altered signaling pathways and nonfunctional receptors. Here, H. pylori-induced signaling pathways were investigated in primary human gastric epithelial cells. Inflammatory response was analyzed on chemokine mRNA expression and production after infection of gastric epithelial cells by H. pylori strains, B128 and B128Δ cagM, a cag type IV secretion system defective strain. Signaling pathway involvement was investigated

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41

Reyes-Leon, Adriana, John C. Atherton, Richard H. Argent, J. L. Puente, and J. Torres. "Heterogeneity in the Activity of Mexican Helicobacter pylori Strains in Gastric Epithelial Cells and Its Association with Diversity in the cagA Gene." Infection and Immunity 75, no. 7 (2007): 3445–54. http://dx.doi.org/10.1128/iai.01951-06.

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ABSTRACT Helicobacter pylori CagA is translocated into gastric epithelial cells by a type IV secretion system and interacts with the Src homology 2 phosphatase, altering cell morphology. Multiple EPIYA motifs in CagA are associated with increased activity in cells and with gastric cancer. The aim of this work was to study the heterogeneity in activity in cells of multiple H. pylori single colonies isolated from a single patient and its association with polymorphism in cagA. The presence of cagA, cagE, cagT, and cag10 was studied with 318 H. pylori isolates from the antra and corpora of 18 pati

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Wroblewski, Lydia, Eunyoung Choi, Christine Petersen, et al. "814 – Helicobacter Pylori Induces Aberrant Lrig1 Stem Cell Activity Within the Stomach in a Cag Type Iv Secretion System-Dependent Manner." Gastroenterology 156, no. 6 (2019): S—171—S—172. http://dx.doi.org/10.1016/s0016-5085(19)37220-8.

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43

Kim, Sung Soo, Dae Young Cheung, and Soo-Heon Park. "Differences of mutation of helicobacter pylori cagA gene isolated from duodenal ulcer and gastric cancer." Journal of Clinical Oncology 33, no. 3_suppl (2015): 69. http://dx.doi.org/10.1200/jco.2015.33.3_suppl.69.

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69 Background: H. pylori is the pathogen of both duodenal ulcer and gastric carcinoma. However, they are markedly different in terms of its physiologic and pathologic basis. CagA is 120-145-kDa protein of H. pylori and located one end of Cag PAI encoding components of type IV secretion system. H. pylori expressing CagA are associated with development of atrophic gastritis, peptic ulcer, and gastric carcinoma. This study was aimed to examine the differences of cagA mutations of H. pylori isolated from duodenal ulcer and gastric carcinoma. Methods: Isolated H. pylori from 29 patients with gastri

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Shrestha, Rejina, Naoko Murata-Kamiya, Satoshi Imai, et al. "Mouse Gastric Epithelial Cells Resist CagA Delivery by the Helicobacter pylori Type IV Secretion System." International Journal of Molecular Sciences 23, no. 5 (2022): 2492. http://dx.doi.org/10.3390/ijms23052492.

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The initial step in bacterial infection is adherence of the bacterium to the target cell surface. Helicobacter pylori exploits the interaction of bacterial adhesin protein HopQ with human epithelial CEACAMs (CEACAM1, 5, and 6) to stably adhere to gastric epithelial cells, which is necessary for delivery of the H. pylori CagA oncoprotein into the epithelial cells via a type IV secretion system. In contrast to human CEACAMs, however, HopQ does not interact with Ceacam1 (mouse CEACAM1) in vitro or in CHO cells ectopically expressing Ceacam1. Since the mouse genome lacks Ceacam5 and Ceacam6, no si

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Guiney, Donald G., Patty Hasegawa, and Sheri P. Cole. "Helicobacter pylori Preferentially Induces Interleukin 12 (IL-12) Rather than IL-6 or IL-10 in Human Dendritic Cells." Infection and Immunity 71, no. 7 (2003): 4163–66. http://dx.doi.org/10.1128/iai.71.7.4163-4166.2003.

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ABSTRACT Dendritic cells are potent antigen-presenting cells that are present in the gastrointestinal tract and are required for the induction of a Th1 T-cell acquired immune response. Since infection with the gastric pathogen Helicobacter pylori elicits a Th1 cell response, the interaction of these organisms with dendritic cells should reflect the Th1 bias. We incubated H. pylori with cultured human dendritic cells and measured the cytokine induction profile, comparing the response to that induced by Salmonella enterica serovar Typhimurium. We found that H. pylori induced little interleukin 6

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Sharafutdinov, Irshad, Jakob Knorr, Delara Soltan Esmaeili, Steffen Backert, and Nicole Tegtmeyer. "Cortactin Promotes Effective AGS Cell Scattering by Helicobacter pylori CagA, but Not Cellular Vacuolization and Apoptosis Induced by the Vacuolating Cytotoxin VacA." Pathogens 11, no. 1 (2021): 3. http://dx.doi.org/10.3390/pathogens11010003.

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Cortactin is an actin-binding protein and actin-nucleation promoting factor regulating cytoskeletal rearrangements in eukaryotes. Helicobacter pylori is a gastric pathogen that exploits cortactin to its own benefit. During infection of gastric epithelial cells, H. pylori hijacks multiple cellular signaling pathways, leading to the disruption of key cell functions. Two bacterial virulence factors play important roles in this scenario, the vacuolating cytotoxin VacA and the translocated effector protein CagA of the cag type IV secretion system (T4SS). Specifically, by overruling the phosphorylat

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Wroblewski, Lydia, Alberto Delgado, Maria B. Piazuelo, et al. "930 HELICOBACTER PYLORI PROMOTES THE DIFFERENTIATION OF PPAR∂-EXPRESSING EPITHELIAL CELLS FROM LRIG+ STEM CELLS IN A CAG TYPE IV SECRETION SYSTEM-DEPENDENT MANNER." Gastroenterology 158, no. 6 (2020): S—185. http://dx.doi.org/10.1016/s0016-5085(20)31147-1.

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Lai, Chih-Ho, Yun-Chieh Chang, Shin-Yi Du, et al. "Cholesterol Depletion Reduces Helicobacter pylori CagA Translocation and CagA-Induced Responses in AGS Cells." Infection and Immunity 76, no. 7 (2008): 3293–303. http://dx.doi.org/10.1128/iai.00365-08.

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ABSTRACT Infection with Helicobacter pylori cagA-positive strains is associated with gastritis, ulcerations, and gastric cancer. CagA is translocated into infected epithelial cells by a type IV secretion system and can be tyrosine phosphorylated, inducing signal transduction and motogenic responses in epithelial cells. Cellular cholesterol, a vital component of the membrane, contributes to membrane dynamics and functions and is important in VacA intoxication and phagocyte evasion during H. pylori infection. In this investigation, we showed that cholesterol extraction by methyl-β-cyclodextrin r

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Hirata, Yoshihiro, Shin Maeda, Yuzo Mituno, et al. "High prevalence of functional type IV secretion system for CagA protein in Japanese clinical Helicobacter pylori." Gastroenterology 120, no. 5 (2001): A652—A653. http://dx.doi.org/10.1016/s0016-5085(08)83244-1.

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HIRATA, Y., S. MAEDA, Y. MITUNO, et al. "High prevalence of functional type IV secretion system for CagA protein in Japanese clinical Helicobacter pylori." Gastroenterology 120, no. 5 (2001): A652—A653. http://dx.doi.org/10.1016/s0016-5085(01)83244-3.

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