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- W2110168699 abstract "Unlike apoptosis, necrotic cell death is characterized by marked loss of plasma membrane integrity. Leakage of cytoplasmic material to the extracellular space contributes to cell demise, and is the cause of acute inflammatory responses, which typically accompany necrosis. The mechanisms underlying plasma membrane damage during necrotic cell death are not well understood. We report that endocytosis is critically required for the execution of necrosis. Depletion of the key endocytic machinery components dynamin, synaptotagmin and endophilin suppresses necrotic neurodegeneration induced by diverse genetic and environmental insults in C. elegans. We used genetically encoded fluorescent markers to monitor the formation and fate of specific types of endosomes during cell death in vivo. Strikingly, we find that the number of early and recycling endosomes increases sharply and transiently upon initiation of necrosis. Endosomes subsequently coalesce around the nucleus and disintegrate during the final stage of necrosis. Interfering with kinesin-mediated endosome trafficking impedes cell death. Endocytosis synergizes with autophagy and lysosomal proteolytic mechanisms to facilitate necrotic neurodegeneration. These findings demonstrate a prominent role for endocytosis in cellular destruction during neurodegeneration, which is likely conserved in metazoans." @default.
- W2110168699 created "2016-06-24" @default.
- W2110168699 creator A5003851453 @default.
- W2110168699 creator A5071420074 @default.
- W2110168699 date "2011-12-09" @default.
- W2110168699 modified "2023-09-30" @default.
- W2110168699 title "Endocytosis and intracellular trafficking contribute to necrotic neurodegeneration in<i>C. elegans</i>" @default.
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- W2110168699 doi "https://doi.org/10.1038/emboj.2011.447" @default.
- W2110168699 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3273398" @default.
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