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).
-
Full-text index only
Endotoxin-tolerant mice have mutations in Toll-like receptor 4 (Tlr4).
PMID 9989976 · PMC2192941 · The Journal of experimental medicine · 1999 · 8 claims · 8 setups
The Lps locus was fine-mapped to a 0.9-cM interval spanning a 1.7-Mb genomic contig on mouse chromosome 4.
-
Full-text index only
Genomic views of distant-acting enhancers.
PMID 19741700 · PMC2923221 · Nature · 2009 · 8 claims · 8 setups
Meta-analysis of ~1200 top GWAS SNPs found that in 40% of cases (472/1170) no known exons overlap the linked SNP or its haplotype block, implying noncoding variation causally contributes to many traits.
-
Full-text index only
Modeling chromosomes in mouse to explore the function of genes, genomic disorders, and chromosomal organization.
PMID 16839184 · PMC1500809 · PLoS genetics · 2006 · 8 claims · 8 setups
Cre/loxP recombination in ES cells can generate megabase-scale deletions, duplications, and inversions depending on loxP orientation, cis/trans configuration, and cell cycle stage
-
Full-text index only
Immunopathogenic interaction of environmental triggers and genetic susceptibility in diabetes: is epigenetics the missing link?
PMID 19033405 · PMC2584121 · Diabetes · 2008 · 8 claims · 3 setups
Epigenetic modification of histones and DNA provides a plausible common mechanism linking environmental triggers to genetic susceptibility regions in autoimmune type 1 diabetes.
-
Full-text index only
Cardiovascular genomics, personalized medicine, and the National Heart, Lung, and Blood Institute: part I: the beginning of an era.
PMID 20031542 · PMC3097376 · Circulation. Cardiovascular genetics · 2008 · 7 claims · 8 setups
Rare Mendelian mutations (e.g., in sarcomere genes, ion channels, FBN1, LMNA) cause specific rare cardiovascular conditions (hypertrophic/dilated cardiomyopathy, long-QT syndrome, thoracic aortic aneurysm, progeria) but explain little of common CVD risk.