publication . Article . Other literature type . 2019

N-terminal degradation activates the NLRP1B inflammasome.

Darren C. Johnson; Andrew R. Griswold; Kuo Gai; Brooke A. Vittimberga; Marian C. Okondo; Cornelius Y. Taabazuing; Ashley J. Chui; Daniel P. Ball; Sahana D. Rao; Elizabeth L. Orth; ...
Open Access
  • Published: 14 Mar 2019 Journal: Science, volume 364, pages 82-85 (issn: 0036-8075, eissn: 1095-9203, Copyright policy)
  • Publisher: American Association for the Advancement of Science (AAAS)
Abstract
<jats:p>Intracellular pathogens and danger signals trigger the formation of inflammasomes, which activate inflammatory caspases and induce pyroptosis. The anthrax lethal factor metalloprotease and small-molecule DPP8/9 inhibitors both activate the NLRP1B inflammasome, but the molecular mechanism of NLRP1B activation is unknown. In this study, we used genome-wide CRISPR-Cas9 knockout screens to identify genes required for NLRP1B-mediated pyroptosis. We discovered that lethal factor induces cell death via the N-end rule proteasomal degradation pathway. Lethal factor directly cleaves NLRP1B, inducing the N-end rule–mediated degradation of the NLRP1B N terminus and ...
Subjects
free text keywords: Multidisciplinary, Article, Cell biology, HEK 293 cells, Chemistry, Pyroptosis, Programmed cell death, Intracellular parasite, Proteolysis, medicine.diagnostic_test, medicine, Innate immune system, Inflammasome, medicine.drug, Caspase, biology.protein, biology
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Europe PubMed Central
Other literature type . 2019
http://dx.doi.org/10.1126/scie...
Other literature type . 2019
Provider: Datacite
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