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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No evidence of a Neanderthal contribution to modern human diversity.
PMID 18304371 · PMC2374707 · Genome biology · 2008 · 8 claims · 7 setups
There is no evidence of any Neanderthal contribution to modern human genetic diversity
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Metabolism as a complex genetic trait, a systems biology approach: implications for inborn errors of metabolism and clinical diseases.
PMID 18836848 · PMC4319114 · Journal of inherited metabolic disease · 2008 · 7 claims · 8 setups
Synergistic heterozygosity — cumulative heterozygous mutations at multiple loci in functionally related metabolic pathways — can cause physiologically relevant reduction of pathway flux and disease.
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Evolutionary history of the UCP gene family: gene duplication and selection.
PMID 18980678 · PMC2584656 · BMC evolutionary biology · 2008 · 8 claims · 8 setups
The UCP gene family arose through two ancestral gene duplications early in vertebrate evolution, producing the UCP1, UCP2 and UCP3 lineages.
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Has reproduction · 67
Optimal scaling of digital transcriptomes.
PMID 24223126 · PMC3819321 · PloS one · 2013 · 8 claims · 8 setups
Fifteen existing and novel transcript-count normalization algorithms can be compared with two novel, mutually independent metrics: the number of "uniform" genes (sufficiently low coefficient of variation after normalization) and low average Spearman correlation between normalized expression profiles of gene pairs.
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Current and future directions in genomics of amyotrophic lateral sclerosis.
PMID 18625410 · PMC3524513 · Physical medicine and rehabilitation clinics of North America · 2008 · 8 claims · 8 setups
Familial ALS (FALS, 5-10% of cases) follows Mendelian autosomal dominant inheritance, with 20% caused by SOD1 mutations and 80% by unknown mutations