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Gene Review

cagE  -  DNA transfer protein

Helicobacter pylori J99

 
 
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Disease relevance of cagE

 

High impact information on cagE

  • A mutant lacking cagE, which encodes a structural component of the TFSS, failed to up-regulate a superset of host genes, including the cagA-dependent genes, and many of the immune response genes [5].
  • Mutants of the four OMPs, as well as cagE and galE from H. pylori from the U.S. and Japan, were constructed by inserting a chloramphenicol-resistant cassette into the gene [6].
  • Compared with the parental 60190 strain, the picB- mutant attenuated cell cycle progression at 6 h (P < or = 0.05), and decreased apoptosis with enhanced AGS cell viability at 24 h (P < or = 0.04) [7].
  • The responses of human cell lines and mouse embryonic fibroblasts to infection with wild-type H. pylori or cagE mutant were investigated [8].
  • H. pylori isogenic mutants specifically lacking picA or picB, which are responsible for cytokine production by gastric cells, were less effective in the up-regulation of cyclooxygenase-2 mRNA expression and in the stimulation of prostaglandin E2 release compared with the parental wild-type strain [9].
 

Chemical compound and disease context of cagE

 

Biological context of cagE

  • Mongolian gerbils were challenged with wild-type H. pylori strain TN2, which has a functional cag pathogenicity island or isogenic mutants with disrupted cagA (DeltacagA) or cagE (DeltacagE) genes [11].
  • In contrast, apoptosis was not detected following infection with cagA-negative, cagE-negative, VacA-negative clinical isolates or a Campylobacter jejuni strain [12].
  • All 36 strains were found to contain cagA and cagE gene and to induce CagA phosphorylation upon infection [13].
  • In coculture with isogenic cagE-negative mutant ((Delta)cagE), which encodes a type IV secretion system with other genes in the cag PAI, no significant up-regulation was found [14].
  • The cagE locus was detected in most isolates and RFLP analysis of a 1.52-kb internal fragment showed interstrain diversity with 12 combined (MboI/NlaIII) types [10].
 

Anatomical context of cagE

  • An isogenic cagE mutant of H. pylori lost about 50% of its IL-12-inducing ability, suggesting a role for the cag type IV secretion system in the stimulation of dendritic cells [15].
  • In summary, cagE presence appears to be essential for H. pylori-induced apoptosis of gastric parietal cells, and this effect is dependent on the activation of NF-kappaB and production of nitric oxide [16].
  • METHODS: Two gastric cancer-derived epithelial cell lines were infected with H. pylori organisms of previously defined cagE and cagA status for periods of up to 24 h [17].
  • Neutrophil infiltration in gastric mucosa was significantly more severe in patients infected with cagE-positive strains than in patients infected with negative strains [18].
  • The role of cagPAI on cultured cells was also investigated using isogenic mutant cagE, which carries non-functional cagPAI [19].
 

Associations of cagE with chemical compounds

  • H. pylori isolated from gastric biopsies over a 4-year period were screened by specific PCR assays for the presence of cagA, cagD, cagE and virD4 genes in the cag PAI, and for the presence of IS605 in the PAI and elsewhere in the genome [20].
  • In contrast, expression of xylE in urea or picB decreased after parallel exposure to acid pH (pH 7 > 6 > 5 > 4), regardless of the growth phase [21].
 

Other interactions of cagE

 

Analytical, diagnostic and therapeutic context of cagE

References

  1. Prevalence of Helicobacter pylori vacA, cagA, cagE, iceA, babA2 Genotypes and Correlation with Clinical Outcome in Turkish Patients with Dyspepsia. Erzin, Y., Koksal, V., Altun, S., Dobrucali, A., Aslan, M., Erdamar, S., Dirican, A., Kocazeybek, B. Helicobacter (2006) [Pubmed]
  2. Virulence factors of Helicobacter pylori responsible for gastric diseases in Mongolian gerbil. Ogura, K., Maeda, S., Nakao, M., Watanabe, T., Tada, M., Kyutoku, T., Yoshida, H., Shiratori, Y., Omata, M. J. Exp. Med. (2000) [Pubmed]
  3. Role of interferon-stimulated responsive element-like element in interleukin-8 promoter in Helicobacter pylori infection. Yamaoka, Y., Kudo, T., Lu, H., Casola, A., Brasier, A.R., Graham, D.Y. Gastroenterology (2004) [Pubmed]
  4. cagE is a virulence factor associated with Helicobacter pylori-induced duodenal ulceration in children. Day, A.S., Jones, N.L., Lynett, J.T., Jennings, H.A., Fallone, C.A., Beech, R., Sherman, P.M. J. Infect. Dis. (2000) [Pubmed]
  5. Cag pathogenicity island-specific responses of gastric epithelial cells to Helicobacter pylori infection. Guillemin, K., Salama, N.R., Tompkins, L.S., Falkow, S. Proc. Natl. Acad. Sci. U.S.A. (2002) [Pubmed]
  6. A M(r) 34,000 proinflammatory outer membrane protein (oipA) of Helicobacter pylori. Yamaoka, Y., Kwon, D.H., Graham, D.Y. Proc. Natl. Acad. Sci. U.S.A. (2000) [Pubmed]
  7. Helicobacter pylori strain-specific genotypes and modulation of the gastric epithelial cell cycle. Peek, R.M., Blaser, M.J., Mays, D.J., Forsyth, M.H., Cover, T.L., Song, S.Y., Krishna, U., Pietenpol, J.A. Cancer Res. (1999) [Pubmed]
  8. MyD88 and TNF receptor-associated factor 6 are critical signal transducers in Helicobacter pylori-infected human epithelial cells. Hirata, Y., Ohmae, T., Shibata, W., Maeda, S., Ogura, K., Yoshida, H., Kawabe, T., Omata, M. J. Immunol. (2006) [Pubmed]
  9. Helicobacter pylori up-regulates cyclooxygenase-2 mRNA expression and prostaglandin E2 synthesis in MKN 28 gastric mucosal cells in vitro. Romano, M., Ricci, V., Memoli, A., Tuccillo, C., Di Popolo, A., Sommi, P., Acquaviva, A.M., Del Vecchio Blanco, C., Bruni, C.B., Zarrilli, R. J. Biol. Chem. (1998) [Pubmed]
  10. Investigation of the biological relevance of Helicobacter pylori cagE locus diversity, presence of CagA tyrosine phosphorylation motifs and vacuolating cytotoxin genotype on IL-8 induction in gastric epithelial cells. Owen, R.J., Sharp, S., Lawson, A.J., Durrani, Z., Rijpkema, S., Kidd, M. FEMS Immunol. Med. Microbiol. (2003) [Pubmed]
  11. CagA protein secreted by the intact type IV secretion system leads to gastric epithelial inflammation in the Mongolian gerbil model. Shibata, W., Hirata, Y., Maeda, S., Ogura, K., Ohmae, T., Yanai, A., Mitsuno, Y., Yamaji, Y., Okamoto, M., Yoshida, H., Kawabe, T., Omata, M. J. Pathol. (2006) [Pubmed]
  12. Helicobacter pylori induces gastric epithelial cell apoptosis in association with increased Fas receptor expression. Jones, N.L., Day, A.S., Jennings, H.A., Sherman, P.M. Infect. Immun. (1999) [Pubmed]
  13. Functional variability of cagA gene in Japanese isolates of Helicobacter pylori. Hirata, Y., Yanai, A., Shibata, W., Mitsuno, Y., Maeda, S., Ogura, K., Yoshida, H., Kawabe, T., Omata, M. Gene (2004) [Pubmed]
  14. cDNA microarray analysis of Helicobacter pylori-mediated alteration of gene expression in gastric cancer cells. Maeda, S., Otsuka, M., Hirata, Y., Mitsuno, Y., Yoshida, H., Shiratori, Y., Masuho, Y., Muramatsu , M., Seki, N., Omata, M. Biochem. Biophys. Res. Commun. (2001) [Pubmed]
  15. Helicobacter pylori preferentially induces interleukin 12 (IL-12) rather than IL-6 or IL-10 in human dendritic cells. Guiney, D.G., Hasegawa, P., Cole, S.P. Infect. Immun. (2003) [Pubmed]
  16. Helicobacter pylori induces apoptosis of rat gastric parietal cells. Neu, B., Randlkofer, P., Neuhofer, M., Voland, P., Mayerhofer, A., Gerhard, M., Schepp, W., Prinz, C. Am. J. Physiol. Gastrointest. Liver Physiol. (2002) [Pubmed]
  17. Gastric epithelial cell CXC chemokine secretion following Helicobacter pylori infection in vitro. Sieveking, D., Mitchell, H.M., Day, A.S. J. Gastroenterol. Hepatol. (2004) [Pubmed]
  18. Relationship between nuclear factor-kappaB activation and virulence factors of Helicobacter pylori in Japanese clinical isolates. Maeda, S., Amarsanaa, J., Mitsuno, Y., Hirata, Y., Akanuma, M., Ikenoue, T., Ogura, K., Yoshida, H., Shiratori, Y., Omata, M., Anarsanaa, J. J. Gastroenterol. Hepatol. (2002) [Pubmed]
  19. NF-kappaB and ERK-signaling pathways contribute to the gene expression induced by cag PAI-positive-Helicobacter pylori infection. Shibata, W., Hirata, Y., Yoshida, H., Otsuka, M., Hoshida, Y., Ogura, K., Maeda, S., Ohmae, T., Yanai, A., Mitsuno, Y., Seki, N., Kawabe, T., Omata, M. World J. Gastroenterol. (2005) [Pubmed]
  20. Molecular epidemiology of Helicobacter pylori in England: prevalence of cag pathogenicity island markers and IS605 presence in relation to patient age and severity of gastric disease. Owen, R.J., Peters, T.M., Varea, R., Teare, E.L., Saverymuttu, S. FEMS Immunol. Med. Microbiol. (2001) [Pubmed]
  21. Effect of growth phase and acid shock on Helicobacter pylori cagA expression. Karita, M., Tummuru, M.K., Wirth, H.P., Blaser, M.J. Infect. Immun. (1996) [Pubmed]
  22. The cag pathogenicity island of Helicobacter pylori is disrupted in the majority of patient isolates from different human populations. Kauser, F., Khan, A.A., Hussain, M.A., Carroll, I.M., Ahmad, N., Tiwari, S., Shouche, Y., Das, B., Alam, M., Ali, S.M., Habibullah, C.M., Sierra, R., Megraud, F., Sechi, L.A., Ahmed, N. J. Clin. Microbiol. (2004) [Pubmed]
  23. Helicobacter pylori induced transactivation of SRE and AP-1 through the ERK signalling pathway in gastric cancer cells. Mitsuno, Y., Yoshida, H., Maeda, S., Ogura, K., Hirata, Y., Kawabe, T., Shiratori, Y., Omata, M. Gut (2001) [Pubmed]
  24. Relation of CagA seropositivity to cagPAI phenotype and histological grade of gastritis in patients with Helicobacter pylori infection. Shimoyama, T., Fukuda, S., Nakasato, F., Yoshimura, T., Mikami, T., Munakata, A. World J. Gastroenterol. (2005) [Pubmed]
 
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