Suppression of GSK3β by ERK mediates lipopolysaccharide induced cell migration in macrophage through β-catenin signaling.
10.1007/s13238-012-2058-x
- Author:
Kai GONG
1
;
Fangfang ZHOU
;
Huizhe HUANG
;
Yandao GONG
;
Long ZHANG
Author Information
1. Department of Biological Sciences and Biotechnology, Tsinghua University, Beijing, China.
- Publication Type:Journal Article
- MeSH:
Animals;
Cell Line;
Cell Movement;
drug effects;
Enzyme Activation;
drug effects;
Extracellular Signal-Regulated MAP Kinases;
metabolism;
Gene Expression Regulation, Enzymologic;
drug effects;
Glycogen Synthase Kinase 3;
metabolism;
Glycogen Synthase Kinase 3 beta;
Lipopolysaccharides;
pharmacology;
Macrophages;
cytology;
drug effects;
enzymology;
metabolism;
Matrix Metalloproteinase 9;
genetics;
Mice;
Proto-Oncogene Proteins c-akt;
metabolism;
Signal Transduction;
drug effects;
Transcription, Genetic;
drug effects;
Wnt Proteins;
metabolism;
beta Catenin;
metabolism
- From:
Protein & Cell
2012;3(10):762-768
- CountryChina
- Language:English
-
Abstract:
We investigate the role of β-catenin signaling in the response of macrophage to lipopolysaccharide (LPS) using RAW264.7 cells. LPS rapidly stimulated cytosolic β-catenin accumulation. β-catenin-mediated transcription was showed to be required for LPS induced gene expression and cell migration. Mechanically, ERK activation-primed GSK3β inactivation by Akt was demonstrated to mediate the LPS induced β-catenin accumulation. Overall, our findings suggest that suppression of GSK3β by ERK stimulates β-catenin signaling therefore contributes to LPS induced cell migration in macrophage activation.
