Abstract
Helicobacter pylori Suppresses Glycogen Synthase Kinase 3β to Promote β-Catenin Activity
Highlights
-Catenin is a multifunctional protein that (i) participates in cell adhesion by bridging E-cadherin to ␣-catenin and (ii) mediates transcriptional regulation by forming a complex with LEF/ TCF2 transcription factors [11, 12]. -Catenin redistribution in
We report that 1) H. pylori suppresses GSK3 activity in a CagA-independent manner, 2) H. pylori-induced suppression of GSK3 leads to inhibition of Ser/Thr phosphorylation, ubiquitinylation, and degradation of -catenin, and 3) H. pylori stimulates -catenin-dependent lymphoid enhancer-binding factor/T cell factor (LEF/TCF) transactivation activity and causes up-regulation of cyclin D1
LEF/TCF transcription factors are known to bind to cyclin D1 promoter and regulate gene expression [20]
Summary
-Catenin is a multifunctional protein that (i) participates in cell adhesion by bridging E-cadherin to ␣-catenin and (ii) mediates transcriptional regulation by forming a complex with LEF/ TCF2 transcription factors [11, 12]. -Catenin redistribution in. We report that 1) H. pylori suppresses GSK3 activity in a CagA-independent manner, 2) H. pylori-induced suppression of GSK3 leads to inhibition of Ser/Thr phosphorylation, ubiquitinylation, and degradation of -catenin, and 3) H. pylori stimulates -catenin-dependent LEF/TCF transactivation activity and causes up-regulation of cyclin D1. H. pylori stimulates -catenin-dependent LEF/TCF transactivation activity and causes an increase of cyclin D1 level in MDCK cells.
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