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Cell Rep2024;43(6):114335.June 25, 2024Journal Article

The interaction between RIPK1 and FADD controls perinatal lethality and inflammation.

Diego A Rodriguez1, Bart Tummers2, Jeremy J P Shaw1, Giovanni Quarato3, Ricardo Weinlich4, James Cripps5, Patrick Fitzgerald1, Laura J Janke6, Stephane Pelletier7, Jeremy Chase Crawford1, Douglas R Green8
1Department of Immunology, St. Jude Children's Research Hospital, 262 Danny Thomas Place, Memphis, TN 38105, USA.
2Centre for Inflammation Biology & Cancer Immunology (CIBCI), Department of Inflammation Biology, School of Immunology & Microbial Sciences, King's College London, London SE1 1UL, UK. Electronic address: bart.tummers@kcl.ac.uk.
3Department of Immunology, St. Jude Children's Research Hospital, 262 Danny Thomas Place, Memphis, TN 38105, USA; Treeline Biosciences, San Diego, CA 92121, USA.
4Hospital Israelita Albert Einstein, São Paulo, Brazil.
5Center for Cancer Immunology and Immunotherapy, Brown Cancer Center, University of Louisville School of Medicine, Louisville, KY, USA.
6Department of Pathology, St. Jude Children's Research Hospital, 262 Danny Thomas Place, Memphis, TN 38105, USA.
7Department of Medical and Molecular Genetics, Indiana University Genome Editing Center, Indiana University School of Medicine, Indiana University, Indianapolis, IA 46902, USA.
8Department of Immunology, St. Jude Children's Research Hospital, 262 Danny Thomas Place, Memphis, TN 38105, USA. Electronic address: douglas.green@stjude.org.
PubMed PMC DOI PDF

Abstract

Perturbation of the apoptosis and necroptosis pathways critically influences embryogenesis. Receptor-associated protein kinase-1 (RIPK1) interacts with Fas-associated via death domain (FADD)-caspase-8-cellular Flice-like inhibitory protein long (cFLIPL) to regulate both extrinsic apoptosis and necroptosis. Here, we describe Ripk1-mutant animals (Ripk1R588E [RE]) in which the interaction between FA…

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