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).

• Genome-wide siRNA-based functional genomics of pigmentation identifies novel genes and pathways that impact melanogenesis in human cells.

  PMID 19057677 · PMC2585813 · PLoS genetics · 2008 · 7 claims · 8 setups

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  Genome-wide siRNA screening identified 92 novel genes that support melanin production in human melanocytes with a low false discovery rate.

  mnt-1 melanocyte melanocytes genome-wide secondary quantitative

• Nitrosative stress-induced s-glutathionylation of protein disulfide isomerase leads to activation of the unfolded protein response.

  PMID 19773442 · PMC2756322 · Cancer research · 2009 · 7 claims · 8 setups

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  PABA/NO treatment causes S-glutathionylation (not S-nitrosylation) of PDI in cells and in vitro

  skov3 recombinant mtt daf-fm-da immunoprecipitation

• ChIP-seq guidelines and practices of the ENCODE and modENCODE consortia.

  PMID 22955991 · PMC3431496 · Genome research · 2012 · 8 claims · 8 setups

  Has reproduction · 74

  ENCODE/modENCODE define a set of working standards and guidelines for ChIP-seq covering antibody validation, experimental replication, sequencing depth, data/metadata reporting, and data quality assessment.

  small-genome nuclear whole-cell encode chip-seq chip-chip immunoblot

• Global sequencing of proteolytic cleavage sites in apoptosis by specific labeling of protein N termini.

  PMID 18722006 · PMC2566540 · Cell · 2008 · 7 claims · 8 setups

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  A subtiligase-based N-terminal biotinylation and enrichment method enables global identification and sequencing of protease cleavage sites in complex mixtures

  jurkat computational immunoblotting structural protein-protein

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

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

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  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