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XIAP restricts TNF- and RIP3-dependent cell death and inflammasome activation.

Abstract:

X-linked inhibitor of apoptosis protein (XIAP) has been identified as a potent regulator of innate immune responses, and loss-of-function mutations in XIAP cause the development of the X-linked lymphoproliferative syndrome type 2 (XLP-2) in humans. Using gene-targeted mice, we show that loss of XIAP or deletion of its RING domain lead to excessive cell death and IL-1β secretion from dendritic cells triggered by diverse Toll-like receptor stimuli. Aberrant IL-1β secretion is TNF dependent and ...

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Authors


Müller, N More by this author
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Publisher:
Elsevier
Journal:
Cell reports
Volume:
7
Issue:
6
Pages:
1796-1808
Publication date:
2014-06-05
DOI:
EISSN:
2211-1247
ISSN:
2211-1247
URN:
uuid:83f388d9-1ae1-4134-8154-d1b0e5d8d8f3
Source identifiers:
466967
Local pid:
pubs:466967
Language:
English

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