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Plasma membrane translocation of trimerized MLKL protein is required for TNF-induced necroptosis (vol 16, pg 55, 2014)

NATURE CELL BIOLOGY (2014)

Journal

NATURE CELL BIOLOGY

Volume 16, Issue 2, Pages 200-200

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NATURE PUBLISHING GROUP

DOI: 10.1038/ncb2908

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Understanding Necroptosis in Pancreatic Diseases

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Summary: This article introduces the role and molecular mechanisms of necroptosis in pancreatic diseases and explores its potential as a new therapeutic target.

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Inhibition of MLKL-dependent necroptosis via downregulating interleukin-1R1 contributes to neuroprotection of hypoxic preconditioning in transient global cerebral ischemic rats

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Summary: This study elucidates the molecular mechanism by which hypoxic preconditioning inhibits MLKL-dependent neuronal necroptosis after transient global cerebral ischemia (tGCI). The findings suggest that downregulation of IL-1R1 and disruption of the RIP3-p-MLKL interaction contribute to neuroprotection against tGCI.

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The Many Faces of MLKL, the Executor of Necroptosis

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Summary: Necroptosis is a regulated cell death pathway characterized by disruption of plasma membrane integrity and release of intracellular content. The protein MLKL plays a crucial role in mediating the final step of plasma membrane permeabilization in this pathway. Despite progress in understanding necroptosis and MLKL biology, the precise mechanism of MLKL function is still unclear. This review discusses key steps in MLKL activation, potential models for its role as a "death executor" in necroptosis, and its emerging alternative functions. It also summarizes the current understanding of MLKL in human disease and provides an overview of strategies targeting MLKL for intervention in necroptosis.

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Ferroptotic pores induce Ca2+ fluxes and ESCRT-III activation to modulate cell death kinetics

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Summary: Ferroptosis is a form of regulated necrosis that depends on iron ions and is associated with lipid peroxidation. An increase in cytosolic Ca2+ precedes cell bursting in ferroptosis, and membrane nanopores are linked to plasma membrane damage in this process. Activation of ESCRT-III serves as a general protective mechanism, counterbalancing cell death kinetics during ferroptosis.

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Resveratrol inhibits necroptosis by mediating the TNF-α/RIP1/RIP3/MLKL pathway in myocardial hypoxia/reoxygenation injury

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TNF-α-dependent neuronal necroptosis regulated in Alzheimer's disease by coordination of RIPK1-p62 complex with autophagic UVRAG

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The Lck inhibitor, AMG-47a, blocks necroptosis and implicates RIPK1 in signalling downstream of MLKL

Annette Jacobsen, Catia L. Pierotti, Kym N. Lowes, Amanda E. Au, Ying Zhang, Nima Etemadi, Cheree Fitzgibbon, Wilhelmus J. A. Kersten, Andre L. Samson, Mark F. van Delft, David C. S. Huang, Helene Jousset Sabroux, Guillaume Lessene, John Silke, James M. Murphy

Summary: The Lck inhibitor AMG-47a has been identified as an inhibitor of necroptosis, particularly effective in human cells. Additionally, RIPK1 is found to play a complete dependence in cell death caused by activated MLKL, with some involvement from RIPK3.

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Proteomic analysis of necroptotic extracellular vesicles

Inbar Shlomovitz, Ziv Erlich, Gali Arad, Liat Edry-Botzer, Sefi Zargarian, Hadar Cohen, Tal Manko, Yifat Ofir-Birin, Tomer Cooks, Neta Regev-Rudzki, Motti Gerlic

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Protein acylation by saturated very long chain fatty acids and endocytosis are involved in necroptosis

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Summary: Research has shown that during Necroptosis, protein acylation occurs on key players like MLKL and phosphoMLKL, with VLCFAs playing a crucial role in membrane recruitment. Additionally, disruption of endosomal trafficking may contribute to increased cell viability during Necroptosis.

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Plasma membrane translocation of trimerized MLKL protein is required for TNF-induced necroptosis (vol 16, pg 55, 2014)

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