The SPRY domain of Pyrin, mutated in familial Mediterranean fever patients, interacts with inflammasome components and inhibits proIL-1β processing-Reference-Cited by-同舟云学术

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The SPRY domain of Pyrin, mutated in familial Mediterranean fever patients, interacts with inflammasome components and inhibits proIL-1β processing

Published:2007-04-13 Issue:8 Volume:14 Page:1457-1466
ISSN:1350-9047
Container-title:Cell Death & Differentiation
language:en
Short-container-title:Cell Death Differ

Author:

Papin S,Cuenin S,Agostini L,Martinon F,Werner S,Beer H-D,Grütter C,Grütter M,Tschopp J

Publisher

Springer Science and Business Media LLC

Subject

Cell Biology,Molecular Biology

Link

http://www.nature.com/articles/4402142.pdf

Reference41 articles.

1. McDermott MF, Aksentijevich I . The autoinflammatory syndromes. Curr Opin Allergy Clin Immunol 2002; 2: 511–516.

2. Grateau G, Drenth JP, Delpech M . Hereditary fevers. Curr Opin Rheumatol 1999; 11: 75–78.

3. Stojanov S, Kastner DL . Familial autoinflammatory diseases: genetics, pathogenesis and treatment. Curr Opin Rheumatol 2005; 17: 586–599.

4. Agostini L, Martinon F, Burns K, McDermott MF, Hawkins PN, Tschopp J . NALP3 forms an IL-1beta-processing inflammasome with increased activity in Muckle–Wells autoinflammatory disorder. Immunity 2004; 20: 319–325.

5. Hoffman HM, Mueller JL, Broide DH, Wanderer AA, Kolodner RD . Mutation of a new gene encoding a putative pyrin-like protein causes familial cold autoinflammatory syndrome and Muckle–Wells syndrome. Nat Genet 2001; 29: 301–305.

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