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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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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Proteomics and genomics: perspectives on drug and target discovery.
PMID 18302945 · PMC2386992 · Current opinion in chemical biology · 2008 · 8 claims · 8 setups
Protein kinases account for approximately 25% of research and development projects in biotechnology and pharma
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Structural proteomics of the SARS coronavirus: a model response to emerging infectious diseases.
PMID 17680348 · PMC7088133 · Journal of structural and functional genomics · 2007 · 8 claims · 8 setups
Structures of 16 SARS-CoV proteins or functional domains have been determined, and 8 of these have novel folds
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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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The role of medical structural genomics in discovering new drugs for infectious diseases.
PMID 19855826 · PMC2756625 · PLoS computational biology · 2009 · 8 claims · 6 setups
Structure-based drug design using X-ray/NMR protein structures has contributed to the development of numerous approved and improved therapeutics.
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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.
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Structural genomics and drug discovery for infectious diseases.
PMID 19860716 · PMC2789569 · Infectious disorders drug targets · 2009 · 7 claims · 4 setups
CSGID applies high-throughput X-ray crystallography structural genomics to NIAID category A-C pathogen proteins to enable structure-aided drug discovery, with a goal of 400 protein/protein-ligand structures
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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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An emerging cyberinfrastructure for biodefense pathogen and pathogen-host data.
PMID 17984082 · PMC2239001 · Nucleic acids research · 2008 · 8 claims · 7 setups
The Biodefense Proteomics Resource Center (RC) is a public cyberinfrastructure that stores, integrates, and disseminates experimental data from seven Proteomics Research Centers (PRCs) on biodefense pathogens and host interactions
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Discovery and hypothesis generation through bioinformatics.
PMID 16522224 · PMC1431734 · Genome biology · 2006 · 8 claims · 8 setups
Bioinformatics should be used as a tool for discovery and hypothesis generation, not merely to manage biological data
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Has reproduction
An attenuated phenotype of Costello syndrome in three unrelated individuals with a HRAS c.179G>A (p.Gly60Asp) mutation correlates with uncommon functional consequences.
PMID 25914166 · PMC4830354 · American journal of medical genetics. Part A · 2015 · 7 claims · 8 setups
HRAS c.179G>A (p.Gly60Asp) causes an attenuated Costello syndrome phenotype without severe failure-to-thrive, intellectual disability, or cancer predisposition
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Mutations in TRPV4 cause Charcot-Marie-Tooth disease type 2C.
PMID 20037586 · PMC2812627 · Nature genetics · 2010 · 8 claims · 8 setups
Heterozygous missense mutations in TRPV4 (c.805C>T/R269C and c.806G>A/R269H) cause CMT2C