Mixed lineage kinase domain-like protein mediates necrosis signaling downstream of RIP3 kinase.

By Liming Sun, Huayi Wang, Zhigao Wang, Sudan He, She Chen, Daohong Liao, Lai Wang, Jiacong Yan, Weilong Liu, Xiaoguang Lei and 1 more. Cell, 2012

2,549 citations recorded by the source corpus.

Subfields: Cancer Research, Immunology, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/0739c5fda77b5307cc0925154ffa0ac0c349254e

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Citations in the corpus

MLKL compromises plasma membrane integrity by binding to phosphatidylinositol phosphates. (2014, background): “, 2013), which subsequently leads to MLKL activation by RIPK3-mediated phosphorylation (Sun et al., 2012; Murphy et al., 2013).”
Essential versus accessory aspects of cell death: recommendations of the NCCD 2015 (2014, positive): “Upon phosphorylation by RIPK3, MLKL has a critical, non-redundant role in necroptosis.(177,179) Phosphorylated MLKL forms indeed oligomers that translocate to cellular membranes (including the plasma membrane) and bind Cell death: causes versus correlates L Galluzzi et al”
Molecular mechanisms of cell death: recommendations of the Nomenclature Committee on Cell Death 2018 (2018, background): “that are required for MLKL recruitment and necroptosis activation [437, 438, 442, 471].”
Targeting cell death pathways for cancer therapy: recent developments in necroptosis, pyroptosis, ferroptosis, and cuproptosis research (2022, background): “This process eventually leads to cell death characterized by permeabilization of the plasma membrane, cell swelling, and loss of cellular and organelle integrity [31, 32].”
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].”
From pyroptosis, apoptosis and necroptosis to PANoptosis: A mechanistic compendium of programmed cell death pathways (2021, background): “Necroptosis is executed by formation of mixed lineage kinase domain-like pseudokinase (MLKL) pores following MLKL phosphorylation downstream of the receptor-interacting protein kinase 1 (RIPK1) and RIPK3 signaling axis [17–21].”
Necroptosis: Mechanisms and Relevance to Disease (2016, neutral): “As mentioned above, RIPK3 operates immediately upstream of MLKL in the signal transduction cascade that precipitates necroptosis (9), in a manner that depends strictly on RIPK3 kinase activity (31).”
Regulation of tumour necrosis factor signalling: live or let die (2015, background): “A similar block in TNF-induced necroptosis can be achieved by knocking down MLKL expression using RNA interference 115 .”
Toll-like Receptor 3-mediated Necrosis via TRIF, RIP3, and MLKL* (2013, background): “Following preparation of cell extracts, immunoprecipitation, and electrophoretic separation on denaturing polyacrylamide gels followed by transfer (4, 9), immunoblot analysis was performed on the following antibodies: mouse anti-(cid:2) -actin (clone AC-74; Sigma); rabbit anti-Casp8 (Cell Signaling)”
Mixed lineage kinase domain-like protein MLKL causes necrotic membrane disruption upon phosphorylation by RIP3. (2014, methodology): “To see if the phospho-MLKL dots were overlapping with those of RIP3, we coimmunostained these two proteins under normal or necrosis-inducing conditions in the presence or absence of NSA, which arrests RIP3 conjugates at a smaller size (Sun et al., 2012).”
The pseudokinase MLKL mediates necroptosis via a molecular switch mechanism. (2013, background): “Recent evidence suggests that necroptosis is dependent on the RIP kinases RIPK1 and RIPK3 (Cho et al., 2009; Degterev et al., 2005; Duprez et al., 2011; He et al., 2009); the MLKL pseudokinase has also been implicated as a keymediator downstream of RIPK3 (Sun et al., 2012; Zhao et al., 2012).”