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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Solving structures of protein complexes by molecular replacement with Phaser.
PMID 17164524 · PMC2483468 · Acta crystallographica. Section D, Biological crystallography · 2007 · 7 claims · 4 setups
Maximum-likelihood MR functions enable complex asymmetric units to be built up from individual components using a 'tree search with pruning' approach implemented in Phaser's automated MR mode.
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A restricted spectrum of NRAS mutations causes Noonan syndrome.
PMID 19966803 · PMC3118669 · Nature genetics · 2010 · 8 claims · 6 setups
Germline NRAS mutations (T50I, G60E) cause a subset of Noonan syndrome cases via enhanced MAPK activation
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What have we learned from the congenital myasthenic syndromes.
PMID 19688192 · PMC3050586 · Journal of molecular neuroscience : MN · 2010 · 8 claims · 8 setups
CMS have been traced to mutations in at least 11 disease genes encoding proteins at the neuromuscular junction
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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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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)