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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Systems biology approaches for the study of multiple sclerosis.
PMID 18505469 · PMC3865652 · Journal of cellular and molecular medicine · 2008 · 8 claims · 8 setups
The MHC locus on chromosome 6p21 is the strongest genetic region linked to MS susceptibility.
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Serum S100A6 concentration predicts peritoneal tumor burden in mice with epithelial ovarian cancer and is associated with advanced stage in patients.
PMID 19888321 · PMC2765613 · PloS one · 2009 · 8 claims · 8 setups
Serum S100A6 concentration correlates with peritoneal tumor burden in a mouse OVCA xenograft model, based on inverse regression calibration against bioluminescent imaging data.
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Has reproduction · 69
JunB Is Critical for Survival of T Helper Cells.
PMID 35837408 · PMC9273772 · Frontiers in immunology · 2022 · 7 claims · 7 setups
JunB is required for clonal expansion of Th1, Th2, and Th17 cells
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Asthma investigators begin to reap the fruits of genomics.
PMID 14611649 · PMC329104 · Genome biology · 2003 · 7 claims · 8 setups
Microarray profiling of animal models of allergic asthma can identify novel differentially expressed candidate genes involved in inflammation and airway remodeling.
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Has reproduction · 83
De novo identification of CD4(+) T cell epitopes.
PMID 38658646 · PMC11093748 · Nature methods · 2024 · 7 claims · 8 setups
SABR-IIs (chimeric receptors linking a covalently attached peptide-MHC-II to CD28-CD3ζ signaling domains) present epitopes to CD4+ T cells and induce a readable NFAT-GFP/CD69 signal upon cognate TCR recognition
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Tipping the balance in autoimmune disease.
PMID 18001485 · PMC2246277 · Genome biology · 2007 · 8 claims · 8 setups
Human autoimmune diseases are fundamentally diseases of immune dysfunction, evidenced by predisposing genes being immune-function genes, some shared and some unique across MS, T1D, SLE, CD and RA