MAPK signaling in inflammation-associated cancer development.
10.1007/s13238-010-0019-9
- Author:
Pengyu HUANG
1
;
Jiahuai HAN
;
Lijian HUI
Author Information
1. Laboratory of Molecular Cell Biology, Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai 200031, China.
- Publication Type:Journal Article
- MeSH:
Animals;
Extracellular Signal-Regulated MAP Kinases;
metabolism;
Humans;
Inflammation;
complications;
enzymology;
JNK Mitogen-Activated Protein Kinases;
metabolism;
MAP Kinase Signaling System;
Mice;
Neoplasms;
enzymology;
etiology;
p38 Mitogen-Activated Protein Kinases;
metabolism
- From:
Protein & Cell
2010;1(3):218-226
- CountryChina
- Language:English
-
Abstract:
Mitogen-activated protein (MAP) kinases comprise a family of protein-serine/threonine kinases, which are highly conserved in protein structures from unicellular eukaryotic organisms to multicellular organisms, including mammals. These kinases, including ERKs, JNKs and p38s, are regulated by a phosphorelay cascade, with a prototype of three protein kinases that sequentially phosphorylate one another. MAPKs transduce extracellular signals into a variety of cellular processes, such as cell proliferation, survival, death, and differentiation. Consistent with their essential cellular functions, MAPKs have been shown to play critical roles in embryonic development, adult tissue homeostasis and various pathologies. In this review, we discuss recent findings that reveal the profound impact of these pathways on chronic inflammation and, particularly, inflammation-associated cancer development.
