Necroptosis and its role in inflammation
By M. Pasparakis, Peter Vandenabeele. Nature, 2015
1,998 citations recorded by the source corpus.
Subfields: Immunology, Molecular Biology
View Paper: https://www.semanticscholar.org/paper/d7036e32bf0a52198cfd7ebdc3e86594d15c244b
How researchers see this paper
The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.
In Immunology
- T. Kanneganti
- Brent R. Stockwell
- M. Lamkanfi
- R. Malireddi
- S. Kesavardhana
- M. Conrad
- Yan Yu
- Weitong Gao
In Molecular Biology
- Brent R. Stockwell
- M. Conrad
- T. Kanneganti
- F. Ursini
- M. Maiorino
- W. Yang
- R. Malireddi
- S. Kesavardhana
Citations in the corpus
- Ferroptosis: Death by Lipid Peroxidation. (2016, background): “While the mechanisms and physiological relevance of necroptosis have been reviewed recently [3], we focus here on the molecular mechanisms controlling ferroptosis and its relevance to health and disease.”
- Caspases in cell death, inflammation and disease (2019, background): “Under the conditions that also the activation of caspase-8 is hampered (complex IIb), RIPK1 will recruit RIPK3 resulting in the phosphorylation of MLKL and the induction of necroptosis.”
- GPx4, Lipid Peroxidation, and Cell Death: Discoveries, Rediscoveries, and Open Issues (2017, positive): “Since cell death and inflammation are linked by a bi-univocal relationship (83), ferroptosis is a critical player in diseases that are collectively defined as neuro-inflammatory.”
- ZBP1 and TAK1: Master Regulators of NLRP3 Inflammasome/Pyroptosis, Apoptosis, and Necroptosis (PAN-optosis) (2019, background): “Several cell death pathways have been identified with specific genetically encoded requirements; these have collectively been named programmed cell death pathways (Bergsbaken et al., 2009; Lamkanfi and Dixit, 2010; Pasparakis and Vandenabeele, 2015; Man and Kanneganti, 2016).”
- Dendritic Cells and Cancer Immunity (2016, background): “One possibility is cell death via necroptosis, a programed form of necrosis linked to inflammation [48].”
- Caspases in Cell Death, Inflammation, and Gasdermin-Induced Pyroptosis (2020, background): “cFLIPL forms a caspase-8-cFLIPL heteromeric complex in the ripoptosome (complex-II) and inhibits the apoptotic function of caspase-8 (1, 21).”
- GSDMD membrane pore formation constitutes the mechanism of pyroptotic cell death (2016, neutral): “Necroptosis involves the formation of the necrosome, a complex consisting of RIP (receptor serine – threonine – protein kinase)1, RIP3 and MLKL (mixed lineage kinase domain-like) and similarly to pyroptosis it is characterized by cell lysis (Pasparakis & Vandenabeele, 2015).”
- Molecular mechanisms of cell death: recommendations of the Nomenclature Committee on Cell Death 2018 (2018, neutral): “, scaffolding) functions, respectively [4, 517].”
- Autophagy, ferroptosis, pyroptosis, and necroptosis in tumor immunotherapy (2022, positive): “first demonstrated that necroptosis of tumor cells is one of the ICD, through which necroptotic cells can release DAMPs to DC cells to trigger antigen presentation and thus activate cytotoxic CD8+ T lymphocytes.(151,261,262) Furthermore, unlike the study by Aes et al.”
- The Role of Tumor Necrosis Factor Alpha (TNF-α) in Autoimmune Disease and Current TNF-α Inhibitors in Therapeutics (2021, background): “The activation of TNFR1 can trigger the formation of different signaling complexes, referred to as complexes I, IIa, IIb, and IIc, which result in distinct cellular responses [11,12].”