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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Using structural bioinformatics to investigate the impact of non synonymous SNPs and disease mutations: scope and limitations.
PMID 19758473 · PMC2745591 · BMC bioinformatics · 2009 · 8 claims · 8 setups
None of 39 tested structural properties can be used as a sole classification criterion to separate neutral SNPs from disease mutations.
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The European Bioinformatics Institute's data resources: towards systems biology.
PMID 15608238 · PMC539980 · Nucleic acids research · 2005 · 8 claims · 5 setups
Since 2003 the EBI has launched new databases covering protein-protein interactions (IntAct), pathways (Reactome) and small molecules (ChEBI)
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Crystal structure of the HSV-1 Fc receptor bound to Fc reveals a mechanism for antibody bipolar bridging.
PMID 16646632 · PMC1450327 · PLoS biology · 2006 · 8 claims · 5 setups
The C-terminal domain of the gE ectodomain (CgE) is the minimal Fc-binding domain of gE-gI
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In silico screening of mutational effects on enzyme-proteic inhibitor affinity: a docking-based approach.
PMID 17559675 · PMC1913526 · BMC structural biology · 2007 · 8 claims · 4 setups
A rigid-body docking-based approach can predict mutational effects on binding energetics for three structurally distinct enzyme-proteic inhibitor systems (hRI-Ang, Bn-Bs, BPTI-β-Trypsin)
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Prediction of specificity-determining residues for small-molecule kinase inhibitors.
PMID 19032760 · PMC2655090 · BMC bioinformatics · 2008 · 8 claims · 5 setups
S-Filter is a novel method combining sequence and structural information (within PFAAT) to predict specificity-determining residues and selectivity profiles for small-molecule kinase inhibitors
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Assembling a jigsaw puzzle with 20,000 parts.
PMID 12801408 · PMC193613 · Genome biology · 2003 · 8 claims · 8 setups
Re-routing the intracellular interaction domains of receptor tyrosine kinases can redirect their signaling output, e.g. converting a growth signal into an apoptosis signal.