PI3 kinase and direct S-nitrosation are involved in down-regulation of apoptosis signal-regulating kinase 1 during LPS-induced Toll-like receptor 4 signalling

Sumbayev, Vadim V. (2008) PI3 kinase and direct S-nitrosation are involved in down-regulation of apoptosis signal-regulating kinase 1 during LPS-induced Toll-like receptor 4 signalling. Immunology Letters, 115 (2). pp. 126-130. ISSN 0165-2478. (The full text of this publication is not currently available from this repository. You may be able to access a copy if URLs are provided)

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Official URL
http://dx.doi.org/10.1016/j.imlet.2007.10.013

Abstract

Toll-like receptor 4 (TLR4) is the human pattern recognition receptor that detects lipopolysaccharide (LPS) shared by Gram-negative bacteria. TLR4 is expressed in different cell types including myeloid cells, the key effectors of innate immune reactions. Apoptosis signal-regulating kinase 1 (ASK 1), the upstream kinase of MAP kinase-dependent apoptotic pathway has recently been found to be selectively required for p38 MAP kinase activation/cytokine production during TLR4 signalling. However, the activity of this enzyme has to be down-regulated to protect the cells against apoptosis. In the present study we have found that inhibition of PI3 kinase by LY294002 in THP-1 cells exposed to LPS attenuated down-regulation of ASK1 activity followed by programmed cell death. In addition, nitric oxide produced in response to exposure of THP-1 cells to LPS was found to S-nitrosate and therefore, down-regulate ASK1 activity.

Item Type: Article
Uncontrolled keywords: toll-like receptors; inflammation and innate immunity; apoptosis; MAP kinase cascades
Subjects: Q Science > QR Microbiology > QR180 Immunology
Divisions: Faculties > Science Technology and Medical Studies > Medway School of Pharmacy
Depositing User: Louise Dorman
Date Deposited: 20 May 2009 15:18
Last Modified: 06 Jun 2014 08:54
Resource URI: https://kar.kent.ac.uk/id/eprint/15245 (The current URI for this page, for reference purposes)
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