Mixed lineage kinase domain-like is a key receptor interacting protein 3 downstream component of TNF-induced necrosis

By Jie Zhao, Siriporn Jitkaew, Zhenyu Cai, S. Choksi, Qiuning Li, Ji Luo, Zheng-Gang Liu. Proceedings of the National Academy of Sciences of the United States of America, 2012

879 citations recorded by the source corpus.

Subfields: Immunology, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/edb0d565ca70eafb3c6da094e7910d554eb646bf

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Citations in the corpus

Crosstalk between apoptosis, necrosis and autophagy. (2013, background): “Subsequent ﬁ ndings further supported the hypothesis that MLKL is indeed required for TNFa induced necroptosis [39], as MLKL mutants that cannot be phosphorylated at key residues prevented the activation of the necrosome despite still being able to incorporate into the necrosomal complex.”
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).”
Necroptosis: a regulated inflammatory mode of cell death (2018, background): “Papa S, Zazzeroni F, Bubici C, Jayawardena S, Alvarez K, Matsuda S, et al. Gadd45 [beta] mediates the NF-[kappa] B suppression of JNK signalling by targeting MKK7/JNKK2.”
Targeting cell death pathways for cancer therapy: recent developments in necroptosis, pyroptosis, ferroptosis, and cuproptosis research (2022, background): “The data from Wang et al. have revealed that the epigenetic repression of RIPK3 allows NSCLC cell lines to escape from necroptosis, which subsequently increases resistance to chemotherapy [331].”
MLKL compromises plasma membrane integrity by binding to phosphatidylinositol phosphates. (2014, background): “, 2009), and mixed lineage kinase domain-like (MLKL) protein (Sun et al., 2012; Zhao et al., 2012).”
Toll-like Receptor 3-mediated Necrosis via TRIF, RIP3, and MLKL* (2013, background): “These diverse studies resulted in the recognition of RIP3 as the key common mediator of programmed necrosis (10), with adapters such as MLKL and PGAM5 implicated downstream through as yet undefined mechanisms (16–18).”
Cell Death Signaling. (2015, background): “Recent studies have implicated the pseudokinase mixed lineage kinase-like (MLKL) (Sun et al. 2012; Zhao et al. 2012) as a critical player in the execution of RIPdependent necrosis.”