FADD prevents RIP3-mediated epithelial cell necrosis and chronic intestinal inflammation
By P. Welz, A. Wullaert, Katerina Vlantis, Vangelis Kondylis, Vanesa Fernández-Majada, M. Ermolaeva, Petra Kirsch, A. Sterner-Kock, G. van Loo, M. Pasparakis. Nature, 2011
605 citations recorded by the source corpus.
Subfields: Immunology, Molecular Biology
View Paper: https://www.semanticscholar.org/paper/48bae473eeebbb7001c66d0519e19369c9f22d7d
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In Immunology
- Guido Kroemer
- T. Kanneganti
- L. Galluzzi
- L. Zitvogel
- Simone Fulda
- Junying Yuan
- Oliver Kepp
- Douglas R. Green
In Molecular Biology
- Guido Kroemer
- Douglas R. Green
- L. Galluzzi
- Beth Levine
- T. Kanneganti
- Simone Fulda
- D. Tang
- Brent R. Stockwell
Citations in the corpus
- Molecular mechanisms of cell death: recommendations of the Nomenclature Committee on Cell Death 2018 (2018, background): “Thus, the embryonic lethality imposed on mice by the loss of Casp8 or Fadd can be rescued by concurrent ablation of Ripk3 or Mlkl, even though these double knockout animals generally display lymphoproliferative and/or systemic autoimmune disorders as adults [432, 466, 484, 485].”
- Synchronized renal tubular cell death involves ferroptosis (2014, background): “This possibility has been ruled out in non-IRI settings by conditional tissue targeting of proteins involved in the prevention of spontaneously occurring necroptosis, such as RIPK1, and components that regulate its ubiquitinylation status [linear ubiquitinylation chain assembly complex (LUBAC), cell”
- ZBP1 and TAK1: Master Regulators of NLRP3 Inflammasome/Pyroptosis, Apoptosis, and Necroptosis (PAN-optosis) (2019, background): “Studies focused on the RHIM domain-containing proteins (RIPK1 and RIPK3) and their crosstalk with FADD–caspase-8–mediated pathways improved our understanding of the apoptotic and necroptotic pathways and their intricate regulatory mechanisms (Holler et al., 2000; He et al., 2009; Zhang et al., 2009;”
- The RIP1/RIP3 Necrosome Forms a Functional Amyloid Signaling Complex Required for Programmed Necrosis (2012, neutral): “…critical for preventing extensive necrosis during embryonic development in order to ensure proper clonal expansion of lymphocytes and to prevent extensive necrosis and inflammation in skin and intestinal epithelium (Kaiser et al., 2011; Oberst et al., 2011; Welz et al., 2011; Zhang et al., 2011).”