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All 6 Hypotheses 1 Papers 1 Wikis 1 Gaps 0 Colliders 0 Debates 1 Bounties 0 Missions 1 Work packets 1 Genes 0 Diseases 0 Phenotypes 0 Gene ontology 0

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30 results

Hypothesis LRP1-Autophagy BBB Permeabilization for Antibody Transport rel 3.90

autophagy pathway in BMECs. [PMID:31504123]. 2. Pharmacological autophagy induction

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Hypothesis H2: Impaired Autophagy Receptor Recruitment Traps G3BP1 Granules rel 2.10

autophagy. TBK1 phosphorylates key autophagy receptors including p62/SQSTM1 (sequestosome 1) at Ser403

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Hypothesis Autophagy-Lysosomal Degradation of IBA1 in Stressed Microglia rel 2.00

autophagy in astrocytes. [PMID:25715680]. 2. Microglia upregulate autophagy in neurodegeneration

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Hypothesis TBK1-OPTN-NDP52 Phospho-Cascade Coordinates Multi-Organelle Autophagy rel 1.90

Autophagy starts from the claim that modulating TBK1, OPTN (TBC1D7

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Hypothesis C9orf72 DPRs Impair Autophagy Receptor Docking on Stress Granules rel 1.70

autophagy receptor function through steric occlusion of critical ubiquitin-binding

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Hypothesis VPS34 Complex I Subunit Heterogeneity Dictates Organelle-Specific vs. Bulk Autophagy rel 1.70

Autophagy starts from the claim that modulating PIK3C3/VPS34, ATG14L, UVRAG

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Hypothesis p21^Cip1 Phospho-State as Autophagy Responsiveness Predictor rel 1.60

autophagy-mediated survival. This hypothesis proposes that distinct phosphorylation states

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Hypothesis H7: mTOR Hyperactivity Blocks Autophagy, Permitting Tau Seeding rel 1.60

autophagy in response to metabolic demands. In cortical layer II neurons

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Hypothesis P2RY12-mediated autophagy inhibition in cerebral VSMCs impairs CAA clearance rel 1.50

autophagy through phosphorylation of UNC-51-like autophagy activating kinase

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Hypothesis GDF15-GFRAL Axis as Systemic Autophagy-Senescence Integrator rel 1.50

Autophagy-Senescence Integrator starts from the claim that modulating GDF15

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Hypothesis Autophagic Flux Enhancement Synergizes With Chaperones to Clear High-Molecular-Weight Tau Seeds rel 1.50

autophagy receptor that bridges ubiquitinated protein aggregates to the autophagy

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Hypothesis Autophagosome-Lysosome Fusion Defects as Primary Driver of α-Synuclein Propagation rel 1.40

autophagy through precise membrane fusion events. VPS41 functions as a key component

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Hypothesis P2RY12-driven autophagy impairment in cerebral VSMCs mediates BBB breakdown and neurovascular unit dysfunction rel 1.40

autophagy flux through mTOR pathway engagement, ultimately compromising blood-brain

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Hypothesis p62 Liquid-Liquid Phase Separation Nucleates Cross-Organelle Cargo for Coordinated Autophagy rel 1.40

Autophagy starts from the claim that modulating SQSTM1/p62 (SQSTM1), ULK1/FIP200

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Hypothesis MFN2-PACS2 Axis at MAMs Coordinates Mitophagy-ER-Phagy Sync rel 1.30

autophagy receptor through its LC3-interacting region (LIR) motif located

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Hypothesis Chaperone-Autophagy Coupling Prevents Aggregate Persistence by Directing Seeds to Selective Autophagy rel 1.30

autophagy pathways, particularly chaperone-mediated autophagy (CMA) and aggrephagy. The mechanism

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Hypothesis Autophagy-Epigenetic Feedback Loop Creates a Compounding Biomarker Signal — Autophagy Flux Methylation as an AD Stage Chronometer rel 1.30

autophagy regulatory genes, which further suppresses autophagy in a self

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Hypothesis Pharmacological P2RY12 inhibition (ticagrelor/clopidogrel) as repurposing probe for neurovascular outcomes rel 1.20

autophagy activating kinase 1) at Ser757, effectively blocking autophagy initiation

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Hypothesis FUS Mutations Alter Stress Granule Material Properties to Confer Autophagy Resistance rel 1.20

autophagy-mediated clearance through multiple mechanisms. The autophagy machinery, including

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Hypothesis ALS-Linked OPTN/TBK1 Mutations Impair Phosphorylation Cascade Required for Pathological SG Recognition rel 1.20

autophagy axis. TBK1 (TANK-binding kinase 1) functions as a central

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Hypothesis Autophagy-Lysosomal Flux Impairment Preventing Pathological TDP-43 Clearance rel 1.10

Autophagy-Lysosomal Flux Impairment Preventing Pathological TDP-43 Clearance starts

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Hypothesis mTORC1 Reactivation as Autophagy-Senescence Divergence Point Marker rel 1.10

Autophagy-Senescence Divergence Point Marker starts from the claim that

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Hypothesis TFEB-Dependent Lysosome Biogenesis rel 1.10

autophagy through their coordinated control of the Coordinated Lysosomal Expression

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Hypothesis ALS-Associated G3BP1/2 Mutations Disrupt TRIM21 Binding Interfaces rel 1.10

autophagy flux is reflected in CSF levels of autophagy-related

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Hypothesis P2RY12 rs2046934 polymorphism modifies neurodegeneration risk by altering cerebral vascular autophagy capacity rel 0.90

autophagy capacity starts from the claim that modulating P2RY12 (rs2046934

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Hypothesis Lamin B1 Degradation as Irreversibility Gate rel 0.90

Autophagy-dependent degradation of nuclear lamina components (LMNB1, LMNB2) occurs

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Hypothesis TFEB/TFE3 Parallel Activation Drives Coordinated Organelle Clearance via CLEAR Network rel 0.90

autophagy-lysosomal pathways, including small molecule autophagy enhancers (nilotinib, trehalose

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Hypothesis CHIP-mediated K63-linked ubiquitination redirects oligomeric pathologic conformers to selective autophagy through p62/SQSTM1 rel 0.80

autophagy pathways rather than proteasomal degradation for clearance of large

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Hypothesis Chaperone-Autophagy Coupling Prevents Aggregate Persistence by Shunting Seeds to Selective Autophagy rel 0.80

autophagy coupling hypothesis centers on the critical interaction between p62/SQSTM1

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Hypothesis Autophagic Receptor Sequestration via K63-Ub 'Signalone' Recognition rel 0.80

autophagy. Under cellular stress conditions, G3BP1 undergoes liquid-liquid phase

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