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✓ Hypotheses 1 ✓ Papers 1 + Wikis 1 ✓ Gaps 1 + Colliders 0 + Debates 1 + Bounties 0 + Missions 1 + Work packets 1 + Genes 0 + Diseases 0 ✓ Phenotypes 0 + Gene ontology 0

30 results

Hypothesis Mitochondrial SPM Synthesis Platform Engineering rel 1.60

mitochondria to overexpress key enzymes in the SPM biosynthetic pathway

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Hypothesis TRPML1-PINK1/Parkin Axis Coordinates Mitophagy with Lysosomal Biogenesis rel 1.60

mitochondria, PINK1 is imported and degraded. In damaged mitochondria with

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Paper Mitochondria transfer-based therapies reduce the morbidity and mortality of Leigh syndrome. rel 1.50

mitochondria to acceptor cells1-3. One possible consequence of mitochondria

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Hypothesis NLRP3/Mitophagy Coupling Modulation rel 1.40

Mitochondria serve as critical platforms for this secondary activation, with

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Hypothesis Mitochondrial Transfer Pathway Enhancement rel 1.40

mitochondria from neuroprotective A2 astrocytes to dysfunctional A1 astrocytes. MIRO1

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Paper Mitochondria-lysosome contacts regulate mitochondrial Ca(2+) dynamics via lysosomal TRPML1. rel 1.20

mitochondria, which was mediated by tethering of mitochondria-lysosome contact

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Paper Human iPSCs derived astrocytes rescue rotenone-induced mitochondrial dysfunction and dopaminergic neurodegeneration in vitro by donating functional mitochondria. rel 1.20

mitochondria with normal function. In addition, the half-life of mitochondria

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Hypothesis AMPK hypersensitivity in astrocytes creates enhanced mitochondrial rescue responses rel 1.20

mitochondria - **ULK1**: Initiates autophagy for energy mobilization Astrocytes express high

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Paper Manipulation of Mitochondria Dynamics Reveals Separate Roles for Form and Function in Mitochondria Distribution. rel 1.10

Mitochondria shape is controlled by membrane fusion and fission mediated

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Hypothesis Differential Calpain-Mediated Cleavage of Apoptotic vs. Autophagic Substrates rel 1.00

mitochondria. Calpain activation is consistently associated with necrotic and apoptotic

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Hypothesis Drp1-S616 Phosphorylation Fission Priming Enables t-Bid-Driven MPTP Amplification rel 1.00

mitochondria to mPTP opening. [PMID:25478730]. 3. tBid translocates to mitochondria

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Paper Stress triggers gut dysbiosis via CRH-CRHR1-mitochondria pathway. rel 0.90

mitochondria respiration conferred resilience against stress-induced mitochondria damaging and epithelium

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Paper Photoreceptor inner segments in monkey and human retina: mitochondrial density, optics, and regional variation. rel 0.90

mitochondria, inner segment dimensions, and optical properties, as a basis

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Paper Autophagosomes form at ER-mitochondria contact sites. rel 0.90

mitochondria-associated ER membrane fraction under starvation conditions. Disruption of the ER-mitochondria

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Paper Presequence protease reverses mitochondria-specific amyloid-β-induced mitophagy to protect mitochondria. rel 0.90

mitochondria and has been shown to play a central role

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Paper Increased calpain-1 in mitochondria induces dilated heart failure in mice: role of mitochondrial superoxide anion. rel 0.90

mitochondria, respectively. Transgenic up-regulation of mitochondria-targeted CAPN1 dose

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Paper Optineurin is an autophagy receptor for damaged mitochondria in parkin-mediated mitophagy that is disrupted by an ALS-linked mutation. rel 0.90

mitochondria for degradation by autophagosomes. We examined the role of optineurin

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Paper Role of Mitochondria-ER Contact Sites in Mitophagy. rel 0.90

mitochondria-ER contact sites (MERCS). Upon damage, mitochondria produce reactive

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Paper PINK1 is selectively stabilized on impaired mitochondria to activate Parkin. rel 0.90

mitochondria to trigger their autophagy. How Parkin recognizes damaged mitochondria

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Paper The multifaceted role of mitochondria in autism spectrum disorder. rel 0.90

mitochondria. Failure to supply a sufficient amount of energy, seen

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Hypothesis Dose-Response Framework: PINK1/Parkin Mitophagy as the Critical Mediator Linking HBOT Parameters to Tau Clearance rel 0.90

mitochondria. Under physiological conditions, PINK1 accumulates on the outer membrane

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Hypothesis MFN2-PACS2 Axis at MAMs Coordinates Mitophagy-ER-Phagy Sync rel 0.90

mitochondria and decreased recruitment of autophagy machinery as quantified by LC3-mitochondria

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Hypothesis Mitochondrial-Nuclear Epigenetic Cross-Talk Restoration rel 0.80

mitochondria from Alzheimer's patients) demonstrate that mitochondrial dysfunction precedes

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Hypothesis SIRT3-Mediated Mitochondrial Deacetylation Failure with PINK1/Parkin Mitophagy Dysfunction rel 0.80

mitochondria for autophagic degradation. PINK1 (PTEN-induced kinase 1) accumulates

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Hypothesis CX43 hemichannel engineering enables size-selective mitochondrial transfer rel 0.80

mitochondria, with diameters ranging from 0.5-1.0 micrometers, are orders

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Hypothesis PINK1/PARK2-Mediated Mitophagy Enhancement for Neuroinflammation Control rel 0.80

mitochondria via the TOM/TIM complex, where it undergoes proteolytic cleavage

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Hypothesis Designer TRAK1-KIF5 fusion proteins accelerate therapeutic mitochondrial delivery rel 0.80

mitochondria to the kinesin-1 motor complex through direct interactions

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Hypothesis RAB27A-dependent extracellular vesicle engineering for mitochondrial cargo delivery rel 0.80

mitochondria to microtubules via kinesin and dynein motor proteins. The process

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Paper Fragmented mitochondria released from microglia trigger A1 astrocytic response and propagate inflammatory neurodegeneration rel 0.70

mitochondria into the neuronal milieu. The amount of damaged mitochondria

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Paper Super mitochondria-enriched extracellular vesicles enable enhanced mitochondria transfer. rel 0.70

Mitochondria transfer is a spontaneous process that releases functional mitochondria

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