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Table 1 CagA-positive H.pylori mediates dysregulation of multiple signaling pathways

From: Helicobacter pylori virulence factor CagA promotes tumorigenesis of gastric cancer via multiple signaling pathways

Dysregulation of signaling pathway Molecular mechanism Proposed function References
Wnt/β-catenin signaling pathway Competitive binding E-cadherin Release of β-catenin from the E-cadherin/β-catenin complex [22]
Phosphorylation of LRP6 Activation of Dvl [34]
Phosphorylation of Akt Inactivation of GSK-3β and activation of downstream β-catenin [37]
Direct binding GSK-3β Degradation of GSK-3β and activation of downstream β-catenin [38]
P13K/Akt signaling pathway Phosphorylation of EGFR Activation of the P13K p85 subunit and downstream Akt [37, 48]
Interaction with c-met Activation of P13K/Akt, the downstream β-catenin and NF-κB [21]
Interaction with P13K p85 Activation of the P13K p85 subunit and downstream Akt [20, 50]
NF-κB signaling pathway Activation of MEK/ERK Phosphorylation of p65, induced the release of IL-8 [56, 57]
Autophosphorylation of TAK1 Synergy with phosphorylation of MEKK3 Recruitment and activation of IKK complex [60]
Shh signaling pathway Activation of NF-κB Overexpression of Shh  
JNK signaling pathway Activation of TNF homolog Eiger or overexpression of Rhol Upregulation of JNK signaling, induced apoptosis and compensatory proliferation [68, 69]
JAK/STAT3 signaling pathway Induced IL-6, IL-10 Phosphorylation of STAT3, nuclear translocation of STAT3 [7073]
ERK/MAPK signaling pathway Interaction with SHP2, Grb2 and Crk/Crk-L Activation of ERK/MAPK signaling, induced cell scattering [19, 20, 76]