MyD88 Death-Domain Oligomerization Determines Myddosome Architecture: Implications for Toll-like Receptor Signaling-Reference-Cited by-同舟云学术

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MyD88 Death-Domain Oligomerization Determines Myddosome Architecture: Implications for Toll-like Receptor Signaling

Published:2020-03 Issue:3 Volume:28 Page:281-289.e3
ISSN:0969-2126
Container-title:Structure
language:en
Short-container-title:Structure

Author:

Moncrieffe Martin C.,Bollschweiler Daniel,Li Bing,Penczek Pawel A.,Hopkins Lee,Bryant Clare E.,Klenerman David,Gay Nicholas J.

Funder

Wellcome Trust

National Institutes of Health

Royal Society

University of Cambridge

Publisher

Elsevier BV

Subject

Molecular Biology,Structural Biology

Reference48 articles.

1. PHENIX: a comprehensive Python-based system for macromolecular structure solution;Adams;Acta Crystallogr. D Biol. Crystallogr.,2010

2. Pathogen recognition and innate immunity;Akira;Cell,2006

3. Activation of lymphoma-associated MyD88 mutations via allostery-induced TIR-domain oligomerization;Avbelj;Blood,2014

4. Inferences, questions and possibilities in Toll-like receptor signalling;Beutler;Nature,2004

5. Receptor clustering as a cellular mechanism to control sensitivity;Bray;Nature,1998

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1. TIR domains of TLR family-from the cell culture to the protein sample for structural studies;PLOS ONE;2024-07-05

2. Molecular definition of the endogenous Toll-like receptor signalling pathways;Nature;2024-07-03

3. Progress in mass spectrometry approaches to profiling protein–protein interactions in the studies of the innate immune system;Journal of Proteins and Proteomics;2024-06-28

4. The delayed kinetics of Myddosome formation explains why amyloid-beta aggregates trigger Toll-like receptor 4 less efficiently than lipopolysaccharide;eLife;2024-06-12

5. The delayed kinetics of Myddosome formation explains why amyloid-beta aggregates trigger Toll-like receptor 4 less efficiently than lipopolysaccharide;eLife;2024-06-12

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