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. 2010 Feb 23;1(2):109–113. doi: 10.4161/gmic.1.2.11587

Figure 1.

Figure 1

H. pylori activation of NFκB via CagA-dependent and CagA-independent pathways. (A) CagA-dependent activation of NFκB. CagA is injected into host epithelial cells where it interacts with TRAF6 and TAK1 or Met to activate NFκB through TAK1 or Akt, respectively. Akt then activates IKK directly or indirectly via TAK1. Akt could also activate NFκB by indirect phosphorylation of RelA. (B) CagA-independent activation of NFκB. Host immune cells are stimulated by H. pylori products, such as LPS, via TLR pathways for the activation of NFκB. Alternatively, peptidoglycan injected into cells via the T4SS stimulates Nod1 activity leading to NFκB activation. Solid arrow: known interaction or activation; solid arrow with question mark: proposed interaction or activation; dashed arrow: activation through multiple steps.