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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 Alpha-Beta Oscillation Coupling Enhances lncRNA-9969-Mediated Autophagy Through SST Interneuron-Specific ceRNA Networks rel 2.60

Autophagy Through SST Interneuron-Specific ceRNA Networks starts from the claim

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Hypothesis Alpha-Theta Oscillation Modulation Enhances lncRNA-9969-Mediated Autophagy Through SST Interneuron-Specific ceRNA Networks rel 2.40

Autophagy Through SST Interneuron-Specific ceRNA Networks starts from the claim

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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 VCP/p97 ATPase mutations impair extraction of ubiquitinated autophagy substrates, causing proteasome-autophagy flux obstruction rel 1.80

autophagy substrates, causing proteasome-autophagy flux obstruction starts from the claim

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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 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 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 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 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 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 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 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 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 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 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 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 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 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 Liquid-Liquid Phase Separation (LLPS) Saturation Partitioning Excludes Autophagy Receptors from SG Core rel 1.10

Autophagy Receptors from SG Core 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 Gamma-Entrained PV Interneuron Networks Enable Precision p-tau217-Guided lncRNA Exosome Therapy in AD rel 1.00

autophagy pathways critical for tau clearance. The gamma-entrained PV interneuron

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Hypothesis G3BP1 NTF2L Domain-Mediated mRNP Scaffold Creates Core Exclusion Zone for Autophagy Receptors rel 1.00

Autophagy Receptors starts from the claim that modulating G3BP1 within

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