Proinflammatory TLR signalling is regulated by a TRAF2-dependent proteolysis mechanism in macrophages
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Title
Proinflammatory TLR signalling is regulated by a TRAF2-dependent proteolysis mechanism in macrophages
Authors
Keywords
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Journal
Nature Communications
Volume 6, Issue 1, Pages -
Publisher
Springer Nature
Online
2015-01-07
DOI
10.1038/ncomms6930
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- Different modes of ubiquitination of the adaptor TRAF3 selectively activate the expression of type I interferons and proinflammatory cytokines
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