Experiments
Searchable full-text extractions: founding hypothesis, core claims, experimental setups, key results and statistics — pulled out of each paper as structure. Search a cell line, an assay or an entity (e.g. HUH7) and find every paper that worked with it. This corpus stands on its own: most entries carry no reproduction assessment (yet).
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Premature centromere division of the X chromosome in neurons in Alzheimer's disease.
PMID 18624923 · PMC2746937 · Journal of neurochemistry · 2008 · 8 claims · 2 setups
PCD,X frequency is significantly elevated (~3-fold) in frontal cortex neurons of sporadic AD patients compared to age-matched controls
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Genetic analysis of three Korean patients with clinical features of Ehlers-Danlos syndrome type IV.
PMID 17728513 · PMC2693823 · Journal of Korean medical science · 2007 · 7 claims · 6 setups
EDS type IV is genetically heterogeneous; not all clinically/biochemically diagnosed patients carry COL3A1 mutations
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Proteomics of human neurodegenerative diseases.
PMID 18800015 · PMC2710115 · Journal of neuropathology and experimental neurology · 2008 · 8 claims · 8 setups
Proteomic techniques applied to autopsy brain and CSF from patients with neurodegenerative diseases provide insight into pathogenesis and enable biomarker discovery
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Has reproduction · 59
Cell-Type-Specific Gene Modules Related to the Regional Homogeneity of Spontaneous Brain Activity and Their Associations With Common Brain Disorders.
PMID 33958982 · PMC8093778 · Frontiers in neuroscience · 2021 · 8 claims · 6 setups
Fourteen gene modules were consistently (Bonferroni-corrected) associated with ReHo across a discovery sample and two independent replication samples (including one non-Chinese HCP cohort).
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The role of proteomics in depression research.
PMID 19997739 · PMC2940035 · European archives of psychiatry and clinical neuroscience · 2010 · 8 claims · 8 setups
Proteomics offers a complementary, functional-endpoint approach that can elucidate MDD pathophysiological mechanisms and biomarkers beyond transcriptomic/targeted studies
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Paroxysmal exercise-induced dyskinesia and epilepsy is due to mutations in SLC2A1, encoding the glucose transporter GLUT1.
PMID 18577546 · PMC2442425 · Brain : a journal of neurology · 2008 · 8 claims · 8 setups
Co-occurring PED and epilepsy can be caused by autosomal dominant heterozygous mutations in SLC2A1, encoding the glucose transporter GLUT1