When Degradation Elicits the Alarm: N-Terminal Degradation of NLRP1B Unleashes Its Inflammasome Activity

Mohamed A Eldeeb; Richard P Fahlman; Mansoore Esmaili; Edward A Fon

doi:10.1016/j.molcel.2019.04.032

When Degradation Elicits the Alarm: N-Terminal Degradation of NLRP1B Unleashes Its Inflammasome Activity

Mol Cell. 2019 May 16;74(4):637-639. doi: 10.1016/j.molcel.2019.04.032.

Authors

Mohamed A Eldeeb¹, Richard P Fahlman², Mansoore Esmaili², Edward A Fon³

Affiliations

¹ McGill Parkinson Program, Neurodegenerative Diseases Group, Department of Neurology and Neurosurgery, Montreal Neurological Institute, McGill University, Montreal, QC, Canada. Electronic address: eldeeb@ualberta.ca.
² Department of Biochemistry, University of Alberta, Edmonton, AB, Canada.
³ McGill Parkinson Program, Neurodegenerative Diseases Group, Department of Neurology and Neurosurgery, Montreal Neurological Institute, McGill University, Montreal, QC, Canada.

PMID: 31100244
DOI: 10.1016/j.molcel.2019.04.032

Abstract

Despite being among the first discovered mammalian innate immune sensor, NLRP1B (NLR pyrin domain-containing1B) activation and its molecular basis have remained elusive. Two recent studies have unveiled N-terminal degradation as a common mechanism for pathogen-mediated NLRP1B inflammasome activation in mammals.

MeSH terms

Animals
Apoptosis Regulatory Proteins / genetics*
Humans
Immunity, Innate / genetics*
Inflammasomes / genetics*
Inflammasomes / immunology
Interleukin-1beta / genetics
Macrophages / immunology
Macrophages / metabolism
Macrophages / microbiology
Mice
Proteolysis
RAW 264.7 Cells
Shigella flexneri / immunology
Shigella flexneri / pathogenicity

Substances

Apoptosis Regulatory Proteins
Inflammasomes
Interleukin-1beta
Nalp1b protein, mouse