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MEKK3 and TAK1 synergize to activate IKK complex in Helicobacter pylori infection.
- Source :
-
BBA - Molecular Cell Research . Apr2014, Vol. 1843 Issue 4, p715-724. 10p. - Publication Year :
- 2014
-
Abstract
- Abstract: Helicobacter pylori colonises the gastric epithelial cells of half of the world's population and represents a risk factor for gastric adenocarcinoma. In gastric epithelial cells H. pylori induces the immediate early response transcription factor nuclear factor of kappa light polypeptide gene enhancer in B-cells (NF-κB) and the innate immune response. We show that H. pylori induces in a type IV secretion system-dependent (T4SS) and cytotoxin associated gene A protein (CagA)-independent manner a transient activation of the inhibitor of NF-κB (IκBα) kinase (IKK)-complex. IKKα and IKKβ expression stabilises the regulatory IKK complex subunit NF-κB essential modulator (NEMO). We provide evidence for an intimate mutual control of the IKK complex by mitogen-activated protein kinase kinase kinase 3 (MEKK3) and transforming growth factor β activated kinase 1 (TAK1). TAK1 interacts transiently with the E3 ubiquitin ligase tumor necrosis factor receptor-associated factor 6 (TRAF6). Protein modifications in the TAK1 molecule, e.g. TAK1 autophosphorylation and K63-linked ubiquitinylation, administer NF-κB signalling including transient recruitment of the IKK-complex. Overall, our data uncover H. pylori-induced interactions and protein modifications of the IKK complex, and its upstream regulatory factors involved in NF-κB activation. [Copyright &y& Elsevier]
Details
- Language :
- English
- ISSN :
- 01674889
- Volume :
- 1843
- Issue :
- 4
- Database :
- Academic Search Index
- Journal :
- BBA - Molecular Cell Research
- Publication Type :
- Academic Journal
- Accession number :
- 94686961
- Full Text :
- https://doi.org/10.1016/j.bbamcr.2014.01.006