Helicobacter pylori induces AGS cell motility and elongation via independent signaling pathways.
Helicobacter pylori induces motogenic and cytoskeletal responses in gastric epithelial cells. We demonstrate that these responses can be induced via independent signaling pathways that often occur in parallel. The cag pathogenicity island appears to be nonessential for induction of motility, whereas the elongation phenotype depends on translocation and phosphorylation of CagA.
Moese
Stefan
S
Department of Molecular Biology, Max Planck Institute for Infection Biology, Berlin, Germany.
Selbach
Matthias
M
Kwok
Terry
T
Brinkmann
Volker
V
König
Wolfgang
W
Meyer
Thomas F
TF
Backert
Steffen
S
D000942:Antigens, Bacterial / Q000235:genetics / Q000378:metabolism; D001426:Bacterial Proteins / Q000235:genetics / Q000378:metabolism; D002465:Cell Movement; D002478:Cells, Cultured; D003599:Cytoskeleton / Q000378:metabolism; D004847:Epithelial Cells / Q000382:microbiology* / Q000648:ultrastructure; D005753:Gastric Mucosa / Q000166:cytology / Q000382:microbiology*; D015964:Gene Expression Regulation, Bacterial; D016480:Helicobacter pylori / Q000235:genetics / Q000472:pathogenicity*; D006801:Humans; D015398:Signal Transduction; D014162:Transfection; D014774:Virulence
D000942:Antigens, Bacterial; D001426:Bacterial Proteins; C080866:cagA protein, Helicobacter pylori