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LPS‐induced Toll‐like receptor 4 signalling triggers cross‐talk of apoptosis signal‐regulating kinase 1 (ASK1) and HIF‐1α protein
Author(s) -
Sumbayev Vadim V.
Publication year - 2008
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2007.12.024
Subject(s) - ask1 , microbiology and biotechnology , tlr4 , toll like receptor , signal transduction , p38 mitogen activated protein kinases , map kinase kinase kinase , tropomyosin receptor kinase c , receptor tyrosine kinase , mitogen activated protein kinase kinase , innate immune system , protein kinase a , biology , kinase , chemistry , receptor , platelet derived growth factor receptor , biochemistry , growth factor
Toll‐like receptor 4 (TLR4) is required for recognition of lipopolysaccharide (LPS) of Gram‐negative bacteria and induction of the innate immune response to them. Nevertheless, the involvement of some crucial pathways in TLR4 signalling is poorly understood. Here, we report that LPS‐induced TLR4 signalling triggers cross talk of HIF‐1α and ASK1 in THP‐1 human myeloid monocytic leukaemia cells. Both pathways are activated via redox‐dependent mechanism associated with tyrosine kinase/phospholipase C‐1γ‐mediated activation of protein kinase C α/β, which are known to activate NADPH oxidase and the production of reactive oxygen species that activate both HIF‐1α and ASK1. ASK1 contributes to the stabilisation of HIF‐1α, most likely via activation of p38 MAP kinase.