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30 results
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mitochondria. Calpain activation is consistently associated with necrotic and apoptotic
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mitochondria to mPTP opening. [PMID:25478730]. 3. tBid translocates to mitochondria
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mitochondria and decreased recruitment of autophagy machinery as quantified by LC3-mitochondria
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mitochondria via the TOM/TIM complex, where it undergoes proteolytic cleavage
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mitochondria to the nuclear compartment, thereby influencing epigenetic programming relevant
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mitochondria-associated membranes (MAMs), where the endoplasmic reticulum (ER) and mitochondria
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mitochondria preferentially uses mitochondria-generated ATP (rather than cytoplasmic ATP) for glycolysis
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mitochondria that serve as danger signals for NLRP3 inflammasome activation
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mitochondria, resulting in accumulation of dysfunctional organelles with compromised respiratory
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mitochondria to the microtubule motor complex; under normal conditions, Miro1
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mitochondria-ER contact sites, enabling condition-specific switching between mitophagy
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mitochondria contact sites (MAMs) via Mfn2/GRP75/VDAC1 mislocalization, causing dysregulated calcium
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mitochondria, misfolded proteins, and lipid droplets within cerebral VSMCs. The compromised
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- Hypothesis p62 Liquid-Liquid Phase Separation Nucleates Cross-Organelle Cargo for Coordinated Autophagy
mitochondria, ER, protein aggregates) into a single autophagosomal capture event
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mitochondria. This phosphorylation event increases the binding affinity by approximately
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mitochondria and phosphorylates ubiquitin and the E3 ligase PARK2 (Parkin
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mitochondria released would likely be damaged with degraded mtDNA. Identifier
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mitochondria specifically. [PMID:38245738]. ## Clinical and Translational Relevance From a translational
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mitochondria and cytochrome c release. [PMID:12082527]. 3. Trehalose upregulates
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mitochondria for mitophagy. When TBK1 function is lost, defective mitochondria
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mitochondria, requires NAD+ as a cofactor for its deacetylase activity
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- Hypothesis TBK1 Deficiency Disrupts Microglial Metabolic Reprogramming, Promoting Glycolytic SASP in ALS
mitochondria and compensatory upregulation of glycolysis through HIF-1α stabilization
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mitochondria toward MOMP rather than autophagosomal engulfment. Simultaneously, calcineurin promotes
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mitochondria in neurons via its LC3-interacting region. TBK1 phosphorylates
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mitochondria, impairing their trafficking along axons and disrupting normal mitochondrial
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mitochondria would be efficiently cleared before membrane rupture occurs. This
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mitochondria exhibit enhanced membrane potential and ATP production, restoring neuronal
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mitochondria with compromised membrane integrity. Additionally, hyperphosphorylated tau interferes with
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mitochondria. ## Clinical and Translational Relevance From a translational perspective, this
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mitochondria that cannot efficiently meet neuronal ATP demands. Simultaneously, MFN2
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