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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Hierarchical modeling of activation mechanisms in the ABL and EGFR kinase domains: thermodynamic and mechanistic catalysts of kinase activation by cancer mutations.
PMID 19714203 · PMC2722018 · PLoS computational biology · 2009 · 8 claims · 8 setups
Cancer mutations in ABL and EGFR activate kinases via a common multi-stage mechanism involving hydrophobic spine assembly, formation of a Src-like intermediate structure, and cooperative breakage/formation of characteristic salt bridges
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A novel breast cancer-associated BRIP1 (FANCJ/BACH1) germ-line mutation impairs protein stability and function.
PMID 18628483 · PMC2561321 · Clinical cancer research : an official journal of the American Association for Cancer Research · 2008 · 6 claims · 7 setups
A novel heterozygous BRIP1 germline mutation (c.2992-2995delAAGA) was identified in a breast cancer patient, causing a frameshift and premature stop codon in exon 20.
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Disease-causing mutations in the CLRN1 gene alter normal CLRN1 protein trafficking to the plasma membrane.
PMID 19753315 · PMC2742642 · Molecular vision · 2009 · 8 claims · 5 setups
Wild-type HA-tagged CLRN1 is correctly trafficked to the plasma membrane in transfected BHK-21 cells
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Prediction by graph theoretic measures of structural effects in proteins arising from non-synonymous single nucleotide polymorphisms.
PMID 18654622 · PMC2447880 · PLoS computational biology · 2008 · 8 claims · 5 setups
Bongo identifies mutations causing local and global structural effects with a remarkably low false positive rate
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Has reproduction · 90
Evolutionary repair: Changes in multiple functional modules allow meiotic cohesin to support mitosis.
PMID 32155147 · PMC7138332 · PLoS biology · 2020 · 8 claims · 8 setups
Replacing the mitotic kleisin Scc1 with the meiotic kleisin Rec8 impairs sister chromosome cohesion, advances genome replication timing, and reduces reproductive fitness by 45%.
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Has reproduction · 71
Spatial organization shapes the turnover of a bacterial transcriptome.
PMID 27198188 · PMC4874777 · eLife · 2016 · 7 claims · 6 setups
The E. coli transcriptome is spatially organized genome-wide: mRNAs encoding inner-membrane proteins are enriched at the membrane, while mRNAs encoding cytoplasmic, periplasmic and outer-membrane proteins are distributed throughout the cytoplasm.
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Has reproduction
αPIX Is a Trafficking Regulator that Balances Recycling and Degradation of the Epidermal Growth Factor Receptor.
PMID 26177020 · PMC4503440 · PloS one · 2015 · 8 claims · 8 setups
αPIX interacts with c-Cbl, including as endogenous proteins
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Paroxysmal exercise-induced dyskinesia and epilepsy is due to mutations in SLC2A1, encoding the glucose transporter GLUT1.
PMID 18577546 · PMC2442425 · Brain : a journal of neurology · 2008 · 8 claims · 8 setups
Co-occurring PED and epilepsy can be caused by autosomal dominant heterozygous mutations in SLC2A1, encoding the glucose transporter GLUT1
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The loss of transcriptional inhibition by the photoreceptor-cell specific nuclear receptor (NR2E3) is not a necessary cause of enhanced S-cone syndrome.
PMID 17438525 · PMC2669504 · Molecular vision · 2007 · 8 claims · 8 setups
NR2E3 LBD fused to a heterologous Gal4 DBD mediates dose-dependent transcriptional repression on Gal4-responsive reporters.
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Mutation analysis of TMC1 identifies four new mutations and suggests an additional deafness gene at loci DFNA36 and DFNB7/11.
PMID 18616530 · PMC4732719 · Clinical genetics · 2008 · 8 claims · 8 setups
TMC1 mutations were identified in seven of the families/patients segregating hearing loss linked to DFNA36/DFNB7-11
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Prediction and assessment of splicing alterations: implications for clinical testing.
PMID 18951448 · PMC2832470 · Human mutation · 2008 · 8 claims · 5 setups
Bioinformatic prediction alone is insufficient; in vitro analysis is needed to confirm or establish splicing aberrations for clinical variant classification