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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Adaptive optics scanning laser ophthalmoscopy images in a family with the mitochondrial DNA T8993C mutation.
PMID 18997096 · PMC4836613 · Investigative ophthalmology & visual science · 2009 · 7 claims · 8 setups
High T8993C mutant load (>77%) is associated with severe neurologic and/or retinal abnormalities, while low mutant load (42-54%) causes no detectable abnormalities.
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Large-scale identification and characterization of alternative splicing variants of human gene transcripts using 56,419 completely sequenced and manually annotated full-length cDNAs.
PMID 16914452 · PMC1557807 · Nucleic acids research · 2006 · 8 claims · 8 setups
Analysis of 56,419 full-length cDNAs identified 6877 alternative splicing genes encoding 18,297 alternative splicing variants made of 37,670 exons.
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A distinct clinical, neuropsychological and radiological phenotype is associated with progranulin gene mutations in a large UK series.
PMID 18234697 · PMC2577762 · Brain : a journal of neurology · 2008 · 8 claims · 7 setups
Five different pathogenic GRN mutations (frameshift/premature termination) were identified in 25 affected members of a large UK FTLD cohort, with no whole-gene deletions detected
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Structural evolution of the protein kinase-like superfamily.
PMID 16244704 · PMC1261164 · PLoS computational biology · 2005 · 8 claims · 5 setups
All kinases in the superfamily share a 'universal core' domain consisting only of the regions required for ATP binding and the phosphotransfer reaction.
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Comparative genomics search for losses of long-established genes on the human lineage.
PMID 18085818 · PMC2134963 · PLoS computational biology · 2007 · 8 claims · 6 setups
A novel comparative genomics method (TransMap-based syntenic mapping of gene structures between human, mouse, and dog) can detect losses of well-established single-copy genes without relying on sequence homology to a parental gene, distinguishing them from typical duplication- or retrotransposition-derived pseudogenes.