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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Activating mutations in ALK provide a therapeutic target in neuroblastoma.
PMID 18923525 · PMC2587486 · Nature · 2008 · 8 claims · 8 setups
Non-synonymous ALK kinase domain mutations occur in 8% of primary neuroblastomas, with F1174L being the most frequent
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The many uses of a genome sequence.
PMID 11423005 · PMC138940 · Genome biology · 2001 · 8 claims · 8 setups
Solved protein structures from structural genomics efforts can be used to model many other proteins by homology, aiding function prediction
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Filtering high-throughput protein-protein interaction data using a combination of genomic features.
PMID 15833142 · PMC1127019 · BMC bioinformatics · 2005 · 8 claims · 8 setups
A combination of three genomic features (interacting Pfam domains, GO annotations, sequence homology) using naive Bayesian networks predicts true protein-protein interactions with high sensitivity and good specificity.
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Novel mutations in TARDBP (TDP-43) in patients with familial amyotrophic lateral sclerosis.
PMID 18802454 · PMC2527686 · PLoS genetics · 2008 · 8 claims · 6 setups
Three heterozygous missense mutations (p.M337V, p.N345K, p.I383V) in exon 6 of TARDBP were identified in familial ALS patients
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Protein structure and function by the sea.
PMID 11983051 · PMC139342 · Genome biology · 2002 · 8 claims · 8 setups
High-throughput structural genomics (X-ray crystallography and NMR) can rapidly expand the number of solved protein structures far beyond what is currently in the Protein Data Bank.
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Bladder tumour-derived somatic TSC1 missense mutations cause loss of function via distinct mechanisms.
PMID 18397877 · PMC2427143 · Human molecular genetics · 2008 · 8 claims · 8 setups
All six somatic TSC1 missense mutations found in bladder tumours cause loss of TSC1 function, but via distinct molecular mechanisms.