The pseudokinase MLKL mediates necroptosis via a molecular switch mechanism.

By James M. Murphy, P. Czabotar, Joanne M. Hildebrand, I. Lucet, Jian‐guo Zhang, Silvia Álvarez-Díaz, Rowena S. Lewis, N. Lalaoui, D. Metcalf, A. Webb and 13 more. Immunity, 2013

1,171 citations recorded by the source corpus.

Subfields: Molecular Biology

View Paper: https://www.semanticscholar.org/paper/ffde9a62885f1c5d336715d0882c9589a454bb5b

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Citations in the corpus

Synergism of TNF-α and IFN-γ Triggers Inflammatory Cell Death, Tissue Damage, and Mortality in SARS-CoV-2 Infection and Cytokine Shock Syndromes (2020, neutral): “Necroptosis is executed by RIPK3-mediated MLKL oligomerization (Dhuriya and Sharma, 2018; Giampietri et al., 2014; Murphy et al., 2013).”
Regulation of tumour necrosis factor signalling: live or let die (2015, background): “The importance of MLKL in TNF signalling that leads to necrop tosis has been confirmed by studies of a gene-deficient mouse model, which showed that ablation of Mlkl abrogates cellular necroptosis but not apoptosis 116,117 .”
Mixed lineage kinase domain-like protein MLKL causes necrotic membrane disruption upon phosphorylation by RIP3. (2014, background): “Consistent with this hypothesis, mutation of S345 to aspartic acid and mutation on either K219 or Q343 leads to constitutively active MLKL (Murphy et al., 2013).”
Essential versus accessory aspects of cell death: recommendations of the NCCD 2015 (2014, background): “Moreover, contrary to initial beliefs,(190) the lethal activity of RIPK3 is not influenced by the absence of phosphoglycerate mutase family member 5 (PGAM5) and dynamin 1 like (DNM1L, best known as dynamin-related protein 1, DRP1).(104,172,176) Based on these results, the NCCD proposes here to redef”
Molecular mechanisms of cell death: recommendations of the Nomenclature Committee on Cell Death 2018 (2018, background): “Moreover, it has also been reported that MLKL oligomerization promotes a cascade of intracellular events involving (1) Ca2+ influx, which is presumably mediated by the MLKL target transient receptor potential cation channel subfamily M member 7 (TRPM7) [449]; and (2) PS exposure, which seems to be d”
Glutaminolysis and Transferrin Regulate Ferroptosis (2015, background): “However, mounting evidence suggests that it may benefit the organism under various infectious or inflammatory conditions (Cho et al., 2009; He et al., 2009; Murphy et al., 2013; Sun et al., 2012).”
Molecular mechanisms of cell death in neurological diseases (2021, background): “RIPK3 then phosphorylates and thereby activates the pseudokinase MLKL, the terminal effector of necroptosis that causes lysis of the plasma membrane [58, 59].”
MLKL compromises plasma membrane integrity by binding to phosphatidylinositol phosphates. (2014, background): “MLKL consists of an N-terminal 4HBD fused by a brace region (BR) to a C-terminal inactive KLD (Murphy et al., 2013).”
Necroptosis: a regulated inflammatory mode of cell death (2018, background): “Although RIPK3 and MLKL is necessary for programmed cell death [10, 14, 15], necroptosis is confined to certain types of tissue that express RIPK3/MLKL.”
Necroptosis: Mechanisms and Relevance to Disease (2016, neutral): “Irrespective of this unknown, phosphorylated MLKL exposes an N-terminal 4-helix bundle (NB) domain and a central brace region, hence forming homo-oligomers and acquiring the ability to bind phosphatidylinositol phosphate (PIP) species of the inner leaflet of the plasma membrane (15–19).”