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
Using random walks to identify cancer-associated modules in expression data.
PMID 24128261 · PMC4015830 · BioData mining · 2013 · 8 claims · 8 setups
Walktrap-GM, a random-walk community detection algorithm adapted with stopping criteria (maximum modularity, maximum size, maximum module score), identifies modules significantly enriched with cancer genes in expression-weighted interaction networks.
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Cell atlases and the developmental foundations of the phenotype.
PMID 41662466 · PMC12904592 · PLoS computational biology · 2026 · 8 claims · 6 setups
There is a proportional relationship between average developmental similarity (⟨simD⟩) and average phenotypic similarity (⟨simP⟩) across genes, supporting the D–P rule on average
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Genomic expression during human myelopoiesis.
PMID 17683550 · PMC2045681 · BMC genomics · 2007 · 8 claims · 5 setups
An integrated myelopoiesis expression dataset of 9,425 genes, each mapped to a unique genomic position, was generated from 24 microarray experiments across 8 myeloid cell types.
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Ultrastructural analyses of deciduous teeth affected by hypocalcified amelogenesis imperfecta from a family with a novel Y458X FAM83H nonsense mutation.
PMID 20160442 · PMC4432877 · Cells, tissues, organs · 2010 · 8 claims · 5 setups
A novel FAM83H nonsense mutation c.1374C>A (p.Y458X) in exon 5 is identified as the cause of AD hypocalcified amelogenesis imperfecta in this family
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Has reproduction · 90
Systematic clustering algorithm for chromatin accessibility data and its application to hematopoietic cells.
PMID 33253153 · PMC7728210 · PLoS computational biology · 2020 · 7 claims · 5 setups
A systematic clustering algorithm for ATAC-seq data can be built by binarizing the genome into open/closed chromatin (1/0) strings and computing Hamming distances between samples for hierarchical clustering.
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What makes species unique? The contribution of proteins with obscure features.
PMID 16859532 · PMC1779552 · Genome biology · 2006 · 7 claims · 8 setups
POFs constitute 18-38% (average 26%) of a typical eukaryotic proteome
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The Princeton Protein Orthology Database (P-POD): a comparative genomics analysis tool for biologists.
PMID 17712414 · PMC1942082 · PloS one · 2007 · 8 claims · 5 setups
P-POD is the first comparative genomics database to combine results from multiple computational ortholog/homolog prediction methods with manually curated literature-derived experimental evidence of functional conservation.
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Identification of genomic regions contributing to etoposide-induced cytotoxicity.
PMID 19089452 · PMC2714550 · Human genetics · 2009 · 7 claims · 6 setups
Etoposide-induced cytotoxicity in CEPH lymphoblastoid cell lines is heritable, with genetics explaining 17-25% of variation
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A common haplotype within the PON1 promoter region is associated with sporadic ALS.
PMID 18618303 · PMC2739087 · Amyotrophic lateral sclerosis : official publication of the World Federation of Neurology Research Group on Motor Neuron Diseases · 2008 · 7 claims · 6 setups
Two SNPs (rs987539 in PON2 intron 6 and rs2074351 upstream of PON1 exon 2) within the paraoxonase gene cluster are significantly associated with susceptibility to sporadic ALS
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A focused antibody library for selecting scFvs expressed at high levels in the cytoplasm.
PMID 18034894 · PMC2241821 · BMC biotechnology · 2007 · 7 claims · 7 setups
A human scFv library was built on the single scFv13R4 framework with CDR3 loops diversified to mimic natural human CDR3 amino-acid distributions.
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ksgA mutations confer resistance to kasugamycin in Neisseria gonorrhoeae.
PMID 19097863 · PMC2723803 · International journal of antimicrobial agents · 2009 · 8 claims · 6 setups
Spontaneous KSG-resistant N. gonorrhoeae mutants arise exclusively through mutations in ksgA, not rpsI