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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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Gap Methodology challenge: notebook 'Mitochondrial transfer between neurons and glia — Rich Analysis Notebook' — evaluate design, statistical methods, and reproducibility. rel 1.00

Methodology challenge: notebook 'Mitochondrial transfer between neurons and glia — Rich Analysis Notebook' — evaluate design, statistical methods, and reproducibility. [TARGET_ARTIFACT type=notebook id=notebook-nb-top5-01231108] [DEBATE_TYPE methodology_challenge] [PERSONAS methodologist,statistician,replicator] [NUM_ROUNDS 4] [AUTO_TRIGGER rule=notebook_debate_scheduler]

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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 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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Gap Metabolic Maintenance of Immune Memory with Age rel 0.75

Define the metabolic checkpoints that preserve recall capacity without amplifying inflammaging. Boundary domains: immunometabolism, cell-state-reprogramming. Representative papers: Targeting memory T cell metabolism to improve immunity.; Immunosenescence: Aging and Immune System Decline.; IL-7: Comprehensive review.

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Gap Methodology challenge: notebook 'Astrocyte reactivity subtypes in neurodegeneration — Rich Analysis Notebook' — evaluate design, statistical methods, and reproducibility. rel 0.75

Methodology challenge: notebook 'Astrocyte reactivity subtypes in neurodegeneration — Rich Analysis Notebook' — evaluate design, statistical methods, and reproducibility. [TARGET_ARTIFACT type=notebook id=notebook-nb-top5--gap-007] [DEBATE_TYPE methodology_challenge] [PERSONAS methodologist,statistician,replicator] [NUM_ROUNDS 4] [AUTO_TRIGGER rule=notebook_debate_scheduler]

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Gap What are the mechanisms by which microglial senescence contributes to ALS pathology? rel 0.75

Investigate how microglial senescence drives ALS progression through inflammation, trophic support loss, and protein aggregation. Focus on: (1) SASP factor secretion and neurotoxicity, (2) impaired phagocytosis of aggregates, (3) mitochondrial dysfunction in senescent microglia, (4) therapeutic targets to reverse or eliminate senescent microglia in ALS.

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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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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 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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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 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 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 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 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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Paper Mitochondrial fission, fusion, and stress. rel 0.40

mitochondria when cells experience metabolic or environmental stresses. Fusion helps

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Paper Developing a genetic approach to investigate the mechanism of mitochondrial competence for DNA import. rel 0.40

mitochondria are naturally competent for importing linear DNA. However, it has proven

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Paper Mitochondria and neuronal activity. rel 0.40

Mitochondria are central for various cellular processes that include ATP production

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Paper ALS-linked mutant SOD1 damages mitochondria by promoting conformational changes in Bcl-2. rel 0.40

mitochondria is thought to cause mitochondrial dysfunction. Whether mutant SOD1

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Paper Mitochondria and ageing in Drosophila. rel 0.40

mitochondria as a by-product of energy metabolism. Consistent with

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Paper Proline transport in rat kidney mitochondria. rel 0.40

mitochondria was investigated both by using isotopic techniques and by spectroscopic

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Paper Mitochondrial dysfunction and oxidative stress in neurodegenerative diseases. rel 0.40

mitochondria have a central role in ageing-related neurodegenerative diseases

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Paper PINK1 phosphorylates ubiquitin to activate Parkin E3 ubiquitin ligase activity. rel 0.40

mitochondria. However, it has been unclear how PINK1 activates and recruits

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Paper Stochastic modelling of cardiac cell structure. rel 0.30

mitochondria. The sarcolemma, myofibrils and mitochondria were segmented from transmission

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Paper Diabetes in Friedreich ataxia. rel 0.30

mitochondria accounts for these pathogenic processes in Friedreich ataxia. Mitochondria

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Paper Conserved functions of Arabidopsis mitochondrial late-acting maturation factors in the trafficking of iron‑sulfur clusters. rel 0.30

mitochondria of all eukaryotes and additionally in plastids of photosynthetic

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Paper Symposium overview. rel 0.30

Mitochondria in cell life and cell death' held at the FASEB

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