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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p53 expression and its relationship to DNA alterations in bone and soft tissue sarcomas.
PMID 8260365 · PMC1968651 · British journal of cancer · 1993 · 8 claims · 6 setups
25.7% (29/113) of bone and soft tissue sarcomas show positive p53 immunostaining
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Loss or somatic mutations of hMSH2 occur in hereditary nonpolyposis colorectal cancers with hMSH2 germline mutations.
PMID 8613431 · PMC5921088 · Japanese journal of cancer research : Gann · 1996 · 5 claims · 4 setups
hMSH2 germline mutations were detected in 5 of 36 Japanese HNPCC kindreds (14%)
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Candidate target genes for loss of heterozygosity on human chromosome 17q21.
PMID 15187990 · PMC2409524 · British journal of cancer · 2004 · 8 claims · 5 setups
JUP (plakoglobin) is the only identified gene physically located between the D17S746 and D17S846 markers that define the smallest common region of LOH on chromosome 17q21
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Comparative genomics search for losses of long-established genes on the human lineage.
PMID 18085818 · PMC2134963 · PLoS computational biology · 2007 · 8 claims · 6 setups
A novel comparative genomics method (TransMap-based syntenic mapping of gene structures between human, mouse, and dog) can detect losses of well-established single-copy genes without relying on sequence homology to a parental gene, distinguishing them from typical duplication- or retrotransposition-derived pseudogenes.
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F-SNP: computationally predicted functional SNPs for disease association studies.
PMID 17986460 · PMC2238878 · Nucleic acids research · 2008 · 6 claims · 8 setups
F-SNP is a database integrating functional effect predictions for SNPs from 16 bioinformatics tools/databases across four categories: splicing, transcription, translation, and post-translation
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Mutations in pericentrin cause Seckel syndrome with defective ATR-dependent DNA damage signaling.
PMID 18157127 · PMC2397541 · Nature genetics · 2008 · 8 claims · 8 setups
Homozygous truncating mutations in PCNT cause Seckel syndrome