Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Expression of CEACAM1 or CEACAM5 in AZ-521 cells restores the type IV secretion deficiency for translocation of CagA byHelicobacter pylori

15 Oct 2018

Abstract excerpt

Helicobacter pylori represents an important pathogen involved in diseases ranging from gastritis, peptic ulceration, to gastric malignancies. Prominent virulence factors comprise the vacuolating cytotoxin VacA and the cytotoxin-associated genes pathogenicity island (cagPAI)-encoded type IV secretion system (T4SS). The T4SS effector protein CagA can be translocated into AGS and other gastric epithelial cells...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Helicobacter pylori-related gastroenterology studies
Share to Peptidase Inhibition and Analysis
Share to Veterinary medicine and infectious diseases

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Source

Identifiers

PMID: 30321907
DOI: 10.1111/cmi.12965

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Expression of CEACAM1 or CEACAM5 in AZ-521 cells restores the type IV secretion deficiency for translocation of CagA byHelicobacter pyloriPMID 30321907Read ↗

Role of the cag ‐pathogenicity island encoded type IV secretion system in Helicobacter pylori pathogenesisSemantic proximity Read ↗

Molecular mechanisms of gastric epithelial cell adhesion and injection of CagA by Helicobacter pyloriSemantic proximity Read ↗

Role of type IV secretion in<i>Helicobacter pylori</i>pathogenesisSemantic proximity Read ↗

A novel inhibitory domain of Helicobacter pylori protein CagA reduces CagA effects on host cell biology.Semantic proximity Read ↗

<i>Helicobacter pylori</i> CagA—a bacterial intruder conspiring gastric carcinogenesisSemantic proximity Read ↗

Disruption of gastric mucous granule exocytosis by Helicobacter pylori virulence factor CagASemantic proximity Read ↗

Signaling by epithelial members of the CEACAM family – mucosal docking sites for pathogenic bacteriaSemantic proximity Read ↗

Inhibitors of Helicobacter pylori ATPase Cagα block CagA transport and cag virulenceSemantic proximity Read ↗

Helicobacter pylori cytotoxin-associated gene A (CagA) subverts the apoptosis-stimulating protein of p53 (ASPP2) tumor suppressor pathway of the host.Semantic proximity Read ↗

<i>Helicobacter pylori</i> CagA: a new paradigm for bacterial carcinogenesisSemantic proximity Read ↗

The Helicobacter pylori CagA protein disrupts matrix adhesion of gastric epithelial cells by dephosphorylation of vinculin.Semantic proximity Read ↗

Complex Cellular Responses of Helicobacter pylori-Colonized Gastric Adenocarcinoma CellsSemantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.