Mixed lineage kinase domain-like protein MLKL causes necrotic membrane disruption upon phosphorylation by RIP3.

By Huayi Wang, Liming Sun, L. Su, J. Rizo, Lei Liu, Lifeng Wang, Fuxiang Wang, Xiaodong Wang. Molecules and Cells, 2014

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Regulation of tumour necrosis factor signalling: live or let die (2015, background): “It is suggested that oligomerized MLKL forms pores that are essential for the influx of positively charged ions, such as Na + , K + or Ca 2+ , which is known to be an early event in TNF-induced necrop-tosis 120–122 .”
MLKL compromises plasma membrane integrity by binding to phosphatidylinositol phosphates. (2014, background): “Very recently, another paper independently found that the recombinant N-terminal domain of MLKL is able to induce leakage of cardiolipin- or PIP-containing liposomes, suggesting a direct role of MLKL in membrane rupture (Wang et al., 2014).”
Inflammation and aging: signaling pathways and intervention therapies (2023, background): “In addition, immunostaining using antibodies that target phosphorylated MLKL has been identified as a specific marker for necroptosis.(240) Focus on liver, its aging has been linked to an increase in necroptosis, and this process has been found to contribute to chronic liver inflammation, which in t”
Necroptosis: a regulated inflammatory mode of cell death (2018, background): “Experimental studies carried out on mice lacking RIPK3 exhibit impaired virus-induced necroptosis and increased sensitivity to viral infection [8, 13, 77, 79, 80].”