Evidence map›Paper›PMID 27382024›Full record

ArticleInfection and immunity2016

CagA Phosphorylation in Helicobacter pylori-Infected B Cells Is Mediated by the Nonreceptor Tyrosine Kinases of the Src and Abl Families.

Linda M Krisch, Gernot Posselt, Peter Hammerl, Silja Wessler

Open access · hybridAbstract read
In one paragraph

Article in Infection and immunity, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed, 1 pooled it
5.0field-weighted citation impact, top 5% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

25 citing papers in PubMed, 1 synthesis or guideline pooled it, 43 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Frontiers in cell and developmental biology · 2025
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  5. Review
  6. Implications of silver nanoparticles forFrontiers in cellular and infection microbiology · 2024
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  7. High-Salt Diet ExacerbatesJournal of personalized medicine · 2023
    Review
  8. Article
  9. Influence of the Microbiome Metagenomics and Epigenomics on Gastric Cancer.International journal of molecular sciences · 2022
    Review
  10. Inflammation and Gastric Cancer.Diseases (Basel, Switzerland) · 2022
    Review
  11. Article
  12. Review
  13. Toxins · 2021
    Article
  14. Microorganisms · 2020
    Review
  15. MAP Kinases Pathways in Gastric Cancer.International journal of molecular sciences · 2020
    Review
  16. Tyrosine Kinases inToxins · 2019
    Review
  17. Article
  18. Article
  19. Review
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 1 institution in 1 country.

Linda M KrischCancer Cluster Salzburg, Department of Molecular Biology, Division of Microbiology, Paris-Lodron University, Salzburg, Austria.
Gernot PosseltCancer Cluster Salzburg, Department of Molecular Biology, Division of Microbiology, Paris-Lodron University, Salzburg, Austria.
Peter HammerlDepartment of Molecular Biology, Division of Allergy and Immunology, Paris-Lodron University, Salzburg, Austria.
Silja WesslerCancer Cluster Salzburg, Department of Molecular Biology, Division of Microbiology, Paris-Lodron University, Salzburg, Austria silja.wessler@sbg.ac.at.
University of Salzburg · AT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

CagA is one of the most important virulence factors of the human pathogen Helicobacter pylori CagA expression can be associated with the induction of severe gastric disorders such as gastritis, ulceration, gastric cancer, or mucosa-associated lymphoid tissue (MALT) lymphoma. After translocation through a type IV secretion system into epithelial cells, CagA is tyrosine phosphorylated by kinases of the Src and Abl families, leading to drastic cell elongation and motility. While the functional role of CagA in epithelial cells is well investigated, knowledge about CagA phosphorylation and its associated signal transduction pathways in B cells is only marginal. Here, we established the B cell line MEC1 derived from a B cell chronic lymphocytic leukemia (B-CLL) patient as a new infection model to study the signal transduction in B cells controlled by H. pylori We observed that CagA was rapidly injected, strongly tyrosine phosphorylated, and cleaved into a 100-kDa N-terminal and a 40-kDa C-terminal fragment. To identify upstream signal transduction pathways of CagA phosphorylation in MEC1 cells, pharmacological inhibitors were employed to specifically target Src and Abl kinases. We observed that CagA phosphorylation was strongly inhibited upon treatment with an Src inhibitor and slightly diminished when the Abl kinase inhibitor imatinib mesylate (Gleevec) was applied. The addition of dasatinib to block c-Abl and Src kinases led to a complete loss of CagA phosphorylation. In conclusion, these results demonstrate an important role for Src and Abl tyrosine kinases in CagA phosphorylation in B cells, which represent druggable targets in H. pylori-mediated gastric MALT lymphoma.

Indexed as

Antigens, BacterialBacterial ProteinsB-LymphocytesCell Line, TumorGastric MucosaHelicobacter InfectionsHelicobacter pyloriHumansImatinib MesylateLymphoma, B-Cell, Marginal ZonePhosphorylationProtein Kinase InhibitorsProtein-Tyrosine KinasesProto-Oncogene Proteins c-ablSignal Transductionsrc-Family KinasesAntigens, BacterialBacterial ProteinscagA protein, Helicobacter pyloriImatinib MesylateProtein Kinase InhibitorsProtein-Tyrosine KinasesProto-Oncogene Proteins c-ablsrc-Family Kinases

Identifiers

PMID27382024
PMCPMC4995908
OpenAlexW2470376539

What OpenQuestion holds

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LicenceCC BY
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Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.