TNF-dependent hyperactivation of RIPK1-dependent cytotoxic signaling during embryogenesis and inflammation

• Type of Material: Article
• Authors: Edward Mocarski, Emory University; Pratyusha Mandal, Emory University
• Language: English
• Date: 2021-08-01
• Publisher: PUBLIC LIBRARY SCIENCE
• Publication Version: Final Published Version
• Copyright Statement: © 2021 Mocarski, Mandal
• License: Creative Commons Attribution 4.0 International
• Final Published Version (URL): http://dx.doi.org/10.1371/journal.pbio.3001371
• Title of Journal or Parent Work: PLOS BIOLOGY
• Volume: 19
• Issue: 8
• Start Page: e3001371
• End Page: e3001371
• Grant/Funding Information: This work was funded by United States Public Health Service Extramural Grant R01AI020211 to ESM provided by National Institutes of Health National Institute of Allergy and Infectious Diseases. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
• Keywords: Life Sciences & Biomedicine - Other Topics; Biochemistry & Molecular Biology; Science & Technology; Biology; DEATH; Life Sciences & Biomedicine; CLEAVAGE
• Research Categories: Health Sciences, Immunology; Biology, Microbiology; Health Sciences, Medicine and Surgery

Abstract

In this issue of PLOS Biology, Zhang and colleagues unveil a complex midgestational death during embryogenesis of mice harboring caspase-8 cleavage-resistant receptor-interacting protein (RIP) kinase (RIPK)1. Tumor necrosis factor (TNF) receptor (TNFR)1-dependent signaling drives cell death through a novel pathway requiring synergism between apoptotic and pyroptotic caspases.