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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Has reproduction · 73
RSK1 is an exploitable dependency in myeloproliferative neoplasms and secondary acute myeloid leukemia.
PMID 39820365 · PMC11739599 · Nature communications · 2025 · 8 claims · 8 setups
RSK1 is a conserved, exploitable therapeutic dependency across MPN and secondary AML
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Genomics: applications in mechanism elucidation.
PMID 19166886 · PMC2698023 · Advanced drug delivery reviews · 2009 · 8 claims · 8 setups
Genomic tools require no a priori knowledge of a compound's mode of action and can reveal biological pathways (metabolism, distribution, off-target effects) in addition to the precise mechanism of action.
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Prevalence and functional analysis of sequence variants in the ATR checkpoint mediator Claspin.
PMID 19737971 · PMC2994259 · Molecular cancer research : MCR · 2009 · 8 claims · 8 setups
CLSPN is a mediator protein essential for the ATR- and CHK1-dependent checkpoint response to replicative stress or single-stranded DNA
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Has reproduction · 84
Single-cell protein activity analysis reveals aberrant myogenesis and IGF2-PI3K pathway dependencies in MYOD1-mutant rhabdomyosarcoma.
PMID 41758938 · PMC12947870 · Science advances · 2026 · 7 claims · 8 setups
MYOD1 L122R-mutant SRMS comprises three coexisting tumor cell states (MYOD1-enriched progenitor-like, proliferative transition, and partially differentiated with reduced MYOD1 activity) reflecting disrupted myogenic differentiation.
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MPLW515L is a novel somatic activating mutation in myelofibrosis with myeloid metaplasia.
PMID 16834459 · PMC1502153 · PLoS medicine · 2006 · 8 claims · 8 setups
A somatic activating mutation in MPL (W515L, transmembrane domain) is present in 9% (4/45) of JAK2V617F-negative myelofibrosis (MF) patients
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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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Proteomic and genetic approaches identify Syk as an AML target.
PMID 19800574 · PMC2803063 · Cancer cell · 2009 · 8 claims · 8 setups
EGFR inhibitors (e.g., gefitinib) induce AML differentiation through a non-EGFR, off-target mechanism