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).

• Identity rather than 3D position informs splicing of rare introns in the human genome.

  PMID 41561379 · PMC12814444 · iScience · 2026 · 8 claims · 7 setups

  Has reproduction · 98

  Splicing efficiency depends on intron identity rather than nuclear (SPAD) position; despite shared SPAD proximity, major-like and minor-like introns are less efficiently spliced than major and minor introns

  k562 reference intron-class-containing hi-c tsa-seq damid-seq

• An integrative approach to reveal driver gene fusions from paired-end sequencing data in cancer.

  PMID 19881495 · PMC3086882 · Nature biotechnology · 2009 · 8 claims · 8 setups

  Full-text index only

  A 'concept signature' (ConSig) score algorithm ranks genes by association with molecular concepts characteristic of fusion or mutation cancer genes, nominating biologically important fusions from large candidate sets.

  lung known leukemia tumor paired-end computational snp

• IDEAL-Q, an automated tool for label-free quantitation analysis using an efficient peptide alignment approach and spectral data validation.

  PMID 19752006 · PMC2808259 · Molecular & cellular proteomics : MCP · 2010 · 6 claims · 5 setups

  Full-text index only

  IDEAL-Q predicts the elution time of peptides unidentified in a given LC-MS/MS run (but identified in others) using a computation-efficient linear regression plus fragmental refining function, avoiding costly whole-dataset pattern recognition

  standard thp-1 replicate lc-ms manual cross-instrument

• Proteomic and genetic approaches identify Syk as an AML target.

  PMID 19800574 · PMC2803063 · Cancer cell · 2009 · 8 claims · 8 setups

  Full-text index only

  EGFR inhibitors (e.g., gefitinib) induce AML differentiation through a non-EGFR, off-target mechanism

  hl-60 aml molm-14 luciferase-labeled phospho-tyrosine kinome-wide secondary