Journal
FEBS LETTERS
Volume 582, Issue 2, Pages 319-326Publisher
ELSEVIER SCIENCE BV
DOI: 10.1016/j.febslet.2007.12.024
Keywords
Toll-like receptor; inflammation and innate immunity; HIF-1 alpha; apoptosis; MAP kinase cascade
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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-1 alpha and ASK1 in THP-1 human myeloid monocytic leukaemia cells. Both pathways are activated via redox-dependent mechanism associated with tyrosine kinase/phospholipase C-1 gamma-mediated activation of protein kinase C alpha/beta, which are known to activate NADPH oxidase and the production of reactive oxygen species that activate both HIF-1 alpha and ASK1. ASK1 contributes to the stabilisation of HIF-1 alpha, most likely via activation of p38 MAP kinase. (C) 2007 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.
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