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30 results

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 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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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 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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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 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 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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Hypothesis Mitochondrial-to-Nuclear Epigenetic Communication via N-formylmethionine rel 0.70

mitochondria to the nuclear compartment, thereby influencing epigenetic programming relevant

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Hypothesis ER-Mitochondria Calcium Microdomains Couple Mitophagy and ER-Phagy Initiation rel 0.70

mitochondria-associated membranes (MAMs), where the endoplasmic reticulum (ER) and mitochondria

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Paper Parvalbumin-Deficiency Accelerates the Age-Dependent ROS Production in Pvalb Neurons <i>in vivo</i>: Link to Neurodevelopmental Disorders. rel 0.70

mitochondria impairment in Pvalb neurons is discussed as an essential

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Hypothesis Metabolic Reprogramming Toward GAPDH Inhibition rel 0.60

mitochondria preferentially uses mitochondria-generated ATP (rather than cytoplasmic ATP) for glycolysis

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Hypothesis PINK1/PARK2-LC3 Mitophagy Enhancement rel 0.60

mitochondria that serve as danger signals for NLRP3 inflammasome activation

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Paper Mouse lines with photo-activatable mitochondria to study mitochondrial dynamics. rel 0.60

mitochondria in tissues. To investigate mitochondrial dynamics in tissues and disease

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Paper Transfer of mitochondria from astrocytes to neurons after stroke. rel 0.60

mitochondria and transfer them to astrocytes for disposal and recycling

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Hypothesis GBA1-Deficiency Disrupts Mitochondrial- Lysosomal Contact Sites by Reducing Miro1 Degradation, Creating a Pink1-Parkin Mitophagy Blockade rel 0.50

mitochondria to the microtubule motor complex; under normal conditions, Miro1

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Paper Targeting mitochondria in dermatological therapy: beyond oxidative damage and skin aging. rel 0.50

mitochondria in oxidative damage and skin aging has been a significant

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Paper Inhibition of mitochondria prevents cell death in kidney epithelial cells by intra- and extracellular acidification. rel 0.50

Mitochondria play a significant role in apoptosis and loss of their

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Paper Mitochondrial function in development and disease. rel 0.50

Mitochondria are organelles with vital functions in almost all eukaryotic

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Paper Parkin regulates amino acid homeostasis at mitochondria-lysosome (M/L) contact sites in Parkinson's disease. rel 0.50

mitochondria-lysosome contacts via destabilization of active Rab7. Subcellular metabolomics

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Paper Melatonin as a Guardian of Mitochondria: Mechanisms and Therapeutic Potential in Neurodegenerative Diseases. rel 0.50

mitochondria represent important therapeutic targets, effective interventions targeting mitochondrial function

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Paper Mitochondria-lysosome contact site dynamics and misregulation in neurodegenerative diseases. rel 0.50

mitochondria-lysosome membrane contact sites have been identified as a key pathway

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Paper New Insights Into the Role of Mitochondria Quality Control in Ischemic Heart Disease. rel 0.50

mitochondria (such as mitophagy, mtROS, and mitochondria-related inflammation) on IHD. In addition

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Paper Stress-induced hyperacetylation of microtubule enhances mitochondrial fission and modulates the phosphorylation of Drp1 at 616Ser. rel 0.50

Mitochondria dynamics results from fission and fusion events that may be unbalanced

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Hypothesis PINK1/PARK2 Mitophagy Enhancement for Microglial Polarization rel 0.40

mitochondria and phosphorylates ubiquitin and the E3 ligase PARK2 (Parkin

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Hypothesis P2RY12-driven autophagy impairment in cerebral VSMCs mediates BBB breakdown and neurovascular unit dysfunction rel 0.40

mitochondria, misfolded proteins, and lipid droplets within cerebral VSMCs. The compromised

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Hypothesis VPS34 Complex I Subunit Heterogeneity Dictates Organelle-Specific vs. Bulk Autophagy rel 0.40

mitochondria-ER contact sites, enabling condition-specific switching between mitophagy

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Hypothesis p62 Liquid-Liquid Phase Separation Nucleates Cross-Organelle Cargo for Coordinated Autophagy rel 0.40

mitochondria, ER, protein aggregates) into a single autophagosomal capture event

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Hypothesis TBK1-OPTN-NDP52 Phospho-Cascade Coordinates Multi-Organelle Autophagy rel 0.40

mitochondria. This phosphorylation event increases the binding affinity by approximately

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Hypothesis MCU Calcium Overload via MFN2/GRP75/VDAC1 MAM Dysfunction rel 0.40

mitochondria contact sites (MAMs) via Mfn2/GRP75/VDAC1 mislocalization, causing dysregulated calcium

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Paper Endoplasmic reticulum-mitochondria contacts: function of the junction. rel 0.40

mitochondria. Increased understanding is being gained of how ER-mitochondria

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