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30 results
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mitochondria contacts affecting calcium homeostasis, but the specific molecular mechanisms
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mitochondria avoid triggering innate immune responses or metabolic disruption in recipient
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mitochondria have functions beyond aerobic energy production (referencing Ca regulation
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mitochondria removal, actually depletes healthy mitochondria from synapses in tauopathy
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mitochondria following DNAJC6 paucity, but doesn't explain the organelle
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mitochondria from AD or other neurodegenerative disease contexts retain dysfunction
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mitochondria requiring clearance from functional ones. This selectivity mechanism is crucial
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mitochondria-mediated apoptosis, remain unknown. Understanding these mechanisms is critical
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mitochondria-ER contact sites linked to vascular calcification but doesn
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mitochondria are taken up, integrated into cellular networks, or maintain
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mitochondria contact sites and modulate Ca2+ signaling, but the precise
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mitochondria tethering is a common hallmark of many neurodegenerative diseases
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mitochondria moving anterogradely and accumulating in distal axons, but the mechanisms
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mitochondria accumulate reactive oxygen species leading to recipient cell damage
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mitochondria contacts and calcium homeostasis. (2021, Cell Death Differ, PMID
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mitochondria, ER, ribosomes, etc.), it's unclear how dysfunction in specific
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mitochondria. Understanding these mechanisms is essential for therapeutic targeting. Source
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mitochondria accumulate reactive oxygen species leading to recipient cell damage
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- Gap How do Aβ and tau differentially trigger mitochondrial DNA release to activate cGAS-STING signaling?
mitochondria and triggers DNA leakage remain undefined. This mechanistic gap prevents
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mitochondria represents a poorly understood aspect of mitochondrial quality control
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mitochondria tethering complex VAPB-PTPIP51: Novel therapeutic targets for aging
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Mitochondria-Associated Endoplasmic Reticulum Membranes. (2026, Pharmacol Res, PMID:41932666)
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- Gap What determines the cell-type specificity of ABCA7 variant effects despite widespread expression?
impact phosphatidylcholine and mitochondria in neurons. (2025, Nature, PMID:40931065)
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impact phosphatidylcholine and mitochondria in neurons. (2025, Nature, PMID:40931065)
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mitochondria remains poorly characterized. Understanding this regulation could identify new intervention
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mitochondria interactions. Gap type: contradiction Source paper: Cytosolic calcium regulates
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The abstract reports a striking near-universal defect in Miro1
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mitochondria but this study reveals it binds cytoplasmic mtDNA as an autophagy
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role of mitochondria in autism spectrum disorder. (None, None, PMID:39223276)
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The abstract acknowledges that HE occurs under 'synergistic effect of
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