NDLI: Helicobacter pylori infection of AZ-521 cells reveals a type IV secretion defect and VacA-independent CagA phosphorylation

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Helicobacter pylori infection of AZ-521 cells reveals a type IV secretion defect and VacA-independent CagA phosphorylation

Content Provider	Semantic Scholar
Author	Tegtmeyer, Nicole Backert, Steffen
Copyright Year	2017
Abstract	We refer to the recent publication by Nakano and co-workers in Disease Models & Mechanisms ([Nakano et al., 2016][1]). This report claims that the Helicobacter pylori vacuolating cytotoxin (VacA) is the crucial factor inducing the activation of the host cell kinase for translocated CagA, Src, via a
Starting Page	1539
Ending Page	1540
Page Count	2
File Format	PDF HTM / HTML
Alternate Webpage(s)	http://dmm.biologists.org/content/dmm/10/12/1539.full.pdf
Alternate Webpage(s)	http://dmm.biologists.org/content/dmm/10/12/1541.full.pdf
PubMed reference number	29259027v1
Alternate Webpage(s)	https://doi.org/10.1242/dmm.032813
DOI	10.1242/dmm.032813
Journal	Disease models & mechanisms
Volume Number	10
Language	English
Access Restriction	Open
Subject Keyword	AICARDI-GOUTIERES SYNDROME 1 Bacterial Fimbria Bands Cell Proliferation Clarify Conflict (Psychology) Cultured Cell Line Cytotoxin Duodenal Cancer Duodenum EGFR protein, human Helicobacter pylori Ab:ACnc:Pt:Ser:Qn Helicobacter pylori infection Immunoprecipitation Integrin alpha5beta1 Ion Channel Pathogenicity Phosphatidylserines Positive Regulation of Apoptosis Protein S100-A8 Protein Tyrosine Phosphatase Quantitation S100A8 gene S100A8 wt Allele Sphingomyelins Sulfate measurement Tissue membrane Toxin Ulcer Virulence Factors heparin multiplicity mutant negative regulation of type IV pilus biogenesis pilus assembly receptor
Content Type	Text
Resource Type	Article

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