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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Mutational analysis of human CEACAM1: the potential of receptor polymorphism in increasing host susceptibility to bacterial infection.
PMID 16953805 · PMC1859983 · Cellular microbiology · 2007 · 7 claims · 8 setups
Ile-91 is the primary docking residue required for binding of all tested Nm and Hi strains to CEACAM1, despite structural diversity of bacterial ligands
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Fabry disease: identification of 50 novel alpha-galactosidase A mutations causing the classic phenotype and three-dimensional structural analysis of 29 missense mutations.
PMID 16595074 · PMC3500179 · Human genomics · 2006 · 8 claims · 7 setups
50 novel α-Gal A mutations were identified in 49 of 66 unrelated families with classic Fabry disease.
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Cancer biomarker AKR1B10 and carbonyl metabolism.
PMID 19028477 · PMC6193474 · Chemico-biological interactions · 2009 · 8 claims · 6 setups
AKR1B10 reduces the anticancer drug daunorubicin to daunorubicinol, decreasing its chemotherapeutic effectiveness
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Disruption of the EGFR E884-R958 ion pair conserved in the human kinome differentially alters signaling and inhibitor sensitivity.
PMID 19015641 · PMC2633425 · Oncogene · 2009 · 8 claims · 8 setups
E884K works in concert with L858R in-cis, in a dominant fashion, to differentially alter EGFR downstream signaling and inhibitor sensitivity in an inhibitor-specific manner
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Mutations in the formin gene INF2 cause focal segmental glomerulosclerosis.
PMID 20023659 · PMC2980844 · Nature genetics · 2010 · 8 claims · 8 setups
Mutations in INF2, a formin family actin-regulating protein, cause autosomal dominant focal segmental glomerulosclerosis (FSGS)
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An efficient method for the prediction of deleterious multiple-point mutations in the secondary structure of RNAs using suboptimal folding solutions.
PMID 18445289 · PMC2386494 · BMC bioinformatics · 2008 · 8 claims · 6 setups
Using RNAsubopt suboptimal solutions computed once for the wild-type sequence, specific multiple-point mutations likely to cause conformational rearrangement can be selected without brute-force enumeration.