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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Female monozygotic twins discordant for hemophilia A due to nonrandom X-chromosome inactivation.
PMID 18645989 · PMC5715470 · American journal of hematology · 2008 · 7 claims · 8 setups
Monozygotic twin A (severe hemophilia A, FVIII:C <1%) shows complete nonrandom X-inactivation skewed toward the paternal (normal factor VIII) X-chromosome
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Severe insulin resistance and intrauterine growth deficiency associated with haploinsufficiency for INSR and CHN2: new insights into synergistic pathways involved in growth and metabolism.
PMID 19720790 · PMC2780873 · Diabetes · 2009 · 7 claims · 8 setups
INSR is disrupted by the chromosome 19 breakpoint, causing INSR haploinsufficiency (monoallelic expression) that explains the insulin resistance/dysglycemia phenotype
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Has reproduction · 86
Multi-INTACT: integrative analysis of the genome, transcriptome, and proteome identifies causal mechanisms of complex traits.
PMID 39901160 · PMC11789355 · Genome biology · 2025 · 8 claims · 2 setups
Multi-INTACT achieves higher power than existing single-gene-product methods while maintaining calibrated false discovery rates in simulations.
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Genotype-phenotype associations: modulation by diet and obesity.
PMID 19037211 · PMC2771769 · Obesity (Silver Spring, Md.) · 2008 · 8 claims · 7 setups
Obesity modulates the association between APOE genotype and fasting insulin/glucose levels in men, with obese APOE4 carriers showing higher insulin and glucose than other obese genotype groups.
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Novel integrative genomics strategies to identify genes for complex traits.
PMID 16886998 · PMC2367618 · Animal genetics · 2006 · 8 claims · 7 setups
Forward genetics is restricted to genes harboring mutations, systematically missing network genes that causally influence disease without themselves being mutated.