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MAP kinase activation in macrophages
Author(s) -
Rao K. Murali Krishna
Publication year - 2001
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1189/jlb.69.1.3
Subject(s) - microbiology and biotechnology , biology , kinase , mapk/erk pathway , signal transduction , ask1 , protein kinase a , tradd , mitogen activated protein kinase kinase , programmed cell death , biochemistry , apoptosis , death domain
Stimulation of macrophages by a variety of agents causes activation of mitogen‐activated protein kinases (MAPKs). Activation of MAPKs by lipopolysaccharide involves CD14 and Toll receptors. Subsequent steps still remain to be explored. Tumor necrosis factor‐α (TNF‐α)‐induced activation of MAPKs has been shown to involve the death domain proteins (TRADD, FADD, MADD) and TRAFs. Other molecules involved in this pathway include the protein kinases, ASK1, germinal center kinase (GCK), hematopoietic progenitor kinase 1 (HPK1), and GCK‐related kinase (GCKR). Although, these pathways have been described in various cell types, their role in macrophages remains to be established. The availability of knockout mice and constitutively active and dominant‐negative mutants of MAPKs should greatly enhance our understanding of this field. The activation of MAPKs seems to be different in cell lines compared with primary cells. Among the macrophages, cells from different compartments show different expression of receptors and signal transduction molecules. These differences may account for differences in MAPK activation and other phenotypic differences in macrophages from different compartments. Therefore, it is important to use primary cells for studying MAPK signal‐transduction pathways, and the data from cell lines should not be extrapolated to primary cells.