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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Proteomic identification of heterogeneous nuclear ribonucleoprotein L as a novel component of SLM/Sam68 Nuclear Bodies.
PMID 19912651 · PMC2784748 · BMC cell biology · 2009 · 7 claims · 7 setups
hnRNP L is a novel Sam68-interacting protein partner identified by proteomics and confirmed by co-immunoprecipitation
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Proteomics-based identification of novel factor inhibiting hypoxia-inducible factor (FIH) substrates indicates widespread asparaginyl hydroxylation of ankyrin repeat domain-containing proteins.
PMID 18936059 · PMC2649815 · Molecular & cellular proteomics : MCP · 2009 · 8 claims · 5 setups
DMOG pretreatment acts as a pharmacological 'substrate trap' that stabilizes transient FIH-substrate interactions, enabling their identification by SILAC-based proteomics
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Raf-1 activation disrupts its binding to keratins during cell stress.
PMID 15314064 · PMC2172217 · The Journal of cell biology · 2004 · 8 claims · 8 setups
Raf-1 kinase associates directly with keratin K8 (not K18), independent of Raf kinase activity and independent of Ras-Raf interaction
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Proteomics identification of nuclear Ran GTPase as an inhibitor of human VRK1 and VRK2 (vaccinia-related kinase) activities.
PMID 18617507 · PMC2577208 · Molecular & cellular proteomics : MCP · 2008 · 8 claims · 8 setups
Nuclear Ran GTPase was identified by mass spectrometry as a novel interacting partner of VRK1 and VRK2B
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Functional effects of KCNE3 mutation and its role in the development of Brugada syndrome.
PMID 19122847 · PMC2585750 · Circulation. Arrhythmia and electrophysiology · 2008 · 7 claims · 5 setups
A missense R99H mutation in KCNE3 was identified in a Brugada Syndrome proband and cosegregates with the phenotype in the family (4/4 phenotype-positive, 0/3 phenotype-negative members carried it)
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CHEK2 mutations affecting kinase activity together with mutations in TP53 indicate a functional pathway associated with resistance to epirubicin in primary breast cancer.
PMID 18725978 · PMC2518116 · PloS one · 2008 · 7 claims · 6 setups
TP53 mutations, especially those affecting the L2/L3 DNA-binding domains, are associated with resistance (progressive disease) to epirubicin therapy