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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Inference of transcriptional regulation using gene expression data from the bovine and human genomes.
PMID 17683551 · PMC1978505 · BMC genomics · 2007 · 7 claims · 8 setups
Using human reference promoter sequences is a useful approach for studying gene expression regulation in species with limited or non-existing genomic sequence, such as cattle.
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A novel matrix metalloproteinase 2 (MMP2) terminal hemopexin domain mutation in a family with multicentric osteolysis with nodulosis and arthritis with cardiac defects.
PMID 18985071 · PMC2721823 · European journal of human genetics : EJHG · 2009 · 7 claims · 8 setups
A novel homozygous frameshift mutation (1732delA) in exon 11 of MMP2 causes MONA in this Turkish family by deleting the terminal (third and fourth) hemopexin domains.
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Human-zebrafish non-coding conserved elements act in vivo to regulate transcription.
PMID 16179648 · PMC1236720 · Nucleic acids research · 2005 · 8 claims · 4 setups
Deeply conserved human-zebrafish non-coding elements are enriched for in vivo cis-acting transcriptional regulatory activity.
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Has reproduction · 64
Comprehensive bioinformatics analysis and experimental verification identify mitochondrial gene Dgat2 as a novel therapeutic biomarker for myocardial ischemia-reperfusion.
PMID 40510478 · PMC12159077 · Frontiers in endocrinology · 2025 · 8 claims · 8 setups
Dgat2 is a hub mitochondria-related differentially expressed gene (MitoDEG) that can serve as a novel biomarker and therapeutic target in MI/RI
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Chromosomal phenotypes and submicroscopic abnormalities.
PMID 15601540 · PMC3525070 · Human genomics · 2004 · 8 claims · 8 setups
Microdeletion syndromes are flanked by region-specific low-copy repeats (LCRs), and non-allelic homologous recombination (NAHR) between these LCRs, via interchromosomal or intrachromosomal mechanisms, causes the deletions.