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Regulation of Toll-like receptor 4 signalling by A20 zinc finger protein.

Abstract：

:A20 is a zinc finger protein that renders cells resistant to apoptosis. However, the recent demonstration that A20-deficient mice develop severe inflammation and are hyper-responsive to LPS suggests that A20 may play a key role in regulating the inflammatory response. This study, for the first time, explores the likely mechanism by which A20 can regulate the pro-inflammatory effects of LPS. More specifically it characterises the ability of A20 to modulate TLR-4 signalling since TLR-4 acts as the signalling receptor system for LPS. Full length A20 inhibited the ability of TLR-4 to activate the transcription factors, NF-kappa B and AP-1, and induce the chemokine IL-8. The inhibitory capacity of A20 on NF-kappa B was localised to the C-terminal zinc finger domain of A20 whereas full length A20 was required to effect inhibition of AP-1 and IL-8. Furthermore full length and C-terminal A20 showed similar regulatory effects on MEKK-1 activation of NF-kappa B and AP-1 and induction of IL-8. The findings increase our mechanistic understanding of the anti-inflammatory effects of A20 and suggest that it modulates TLR-4 signalling at or downstream of MEKK-1.

journal_name

Biochem Biophys Res Commun

journal_title

Biochemical and biophysical research communications

authors

O'Reilly SM,Moynagh PN

doi

10.1016/s0006-291x(03)00389-9

subject

Has Abstract

pub_date

2003-04-04 00:00:00

pages

586-93

issue

2

eissn

0006-291X

issn

1090-2104

pii

S0006291X03003899

journal_volume

303

pub_type

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