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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8925219 | PMC |
| http://dx.doi.org/10.1186/s13024-022-00527-x | DOI Listing |
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Calcium release from damaged lysosomes triggers stress granule formation for cell survival.
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Center for Global Health, Department of Internal Medicine, University of New Mexico Health Sciences Center, Albuquerque, NM, USA.
Lysosomes are essential membrane-bound organelles that integrate intracellular needs and external signals through multiple functions, including autophagy-mediated degradation and MTORC1 signaling. The integrity of the lysosomal membrane is therefore crucial for maintaining cellular homeostasis. Various endogenous and exogenous factors can damage lysosomes, contributing to diseases such as infections, cancer, and neurodegeneration.
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Introduction: Alzheimer's disease (AD) and other tauopathies are characterized by intracellular aggregates of microtubule-associated protein tau that are actively released and promote proteopathic spread. Microglia engulf pathological proteins, but how they endocytose tau is unknown.
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Calcium signaling from damaged lysosomes induces cytoprotective stress granules.
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Center for Global Health, Department of Internal Medicine, University of New Mexico Health Sciences Center, Albuquerque, NM, 87106, USA.
Lysosomal damage induces stress granule (SG) formation. However, the importance of SGs in determining cell fate and the precise mechanisms that mediate SG formation in response to lysosomal damage remain unclear. Here, we describe a novel calcium-dependent pathway controlling SG formation, which promotes cell survival during lysosomal damage.
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The microtubule-associated protein Tau is a driver of neuronal dysfunction in Alzheimer's disease and other tauopathies. In this process, Tau initially undergoes subtle changes to its abundance, subcellular localization and a vast array of post-translational modifications including phosphorylation that progressively result in the protein's somatodendritic accumulation and dysregulation of multiple Tau-dependent cellular processes. Given the various loss- and gain-of-functions of Tau in disease and the brain-wide changes in the proteome that characterize tauopathies, we asked whether targeting Tau would restore the alterations in proteostasis observed in disease.
View Article and Find Full Text PDFA mechanism that transduces lysosomal damage signals to stress granule formation for cell survival.
bioRxiv
April 2024
Center for Global Health, Department of Internal Medicine, University of New Mexico Health Sciences Center, Albuquerque, NM 87106, USA.
Lysosomal damage poses a significant threat to cell survival. Our previous work has reported that lysosomal damage induces stress granule (SG) formation. However, the importance of SG formation in determining cell fate and the precise mechanisms through which lysosomal damage triggers SG formation remains unclear.
View Article and Find Full Text PDF