The N-end rule pathway mediates the degradation of proteins through their destabilizing amino-terminal residues. While previously implicated in apoptosis regulation, N-end rule degradation has now recently been shown to fine-tune pyroptotic cellular demise through the amino-terminal degradation of the inflammasome component NLRP1B.
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http://dx.doi.org/10.1016/j.cub.2019.05.004 | DOI Listing |
mBio
August 2021
Department of Biochemistry, University of Lausannegrid.9851.5, Epalinges, Switzerland.
Inflammasomes are cytosolic multiprotein signaling complexes that are activated upon pattern recognition receptor-mediated recognition of pathogen-derived ligands or endogenous danger signals. Their assembly activates the downstream inflammatory caspase-1 and caspase-4/5 (human) or caspase-11 (mouse), which induces cytokine release and pyroptotic cell death through the cleavage of the pore-forming effector gasdermin D. Pathogen detection by host cells also results in the production and release of interferons (IFNs), which fine-tune inflammasome-mediated responses.
View Article and Find Full Text PDFBiochem J
March 2020
Department of Biochemistry and Biomedical Sciences, McMaster University, 1200 Main St. W., Hamilton, Ontario, Canada L8N 3Z5.
Adipose tissue regulates metabolic homeostasis by participating in endocrine and immune responses in addition to storing and releasing lipids from adipocytes. Obesity skews adipose tissue adipokine responses and degrades the coordination of adipocyte lipogenesis and lipolysis. These defects in adipose tissue metabolism can promote ectopic lipid deposition and inflammation in insulin-sensitive tissues such as skeletal muscle and liver.
View Article and Find Full Text PDFCurr Biol
June 2019
McGill Parkinson Program, Neurodegenerative Diseases Group, Department of Neurology and Neurosurgery, Montreal Neurological Institute, McGill University, Montreal, Quebec, Canada. Electronic address:
The N-end rule pathway mediates the degradation of proteins through their destabilizing amino-terminal residues. While previously implicated in apoptosis regulation, N-end rule degradation has now recently been shown to fine-tune pyroptotic cellular demise through the amino-terminal degradation of the inflammasome component NLRP1B.
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