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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IgVH genes from different anatomical regions, with different histopathological patterns, of a rheumatoid arthritis patient suggest cyclic re-entry of mature synovial B-cells in the hypermutation process.
PMID 11056671 · PMC17813 · Arthritis research · 2000 · 8 claims · 5 setups
Somatically mutated IgVH genes with amino acid deletions and mixed IgV molecules were found in all three anatomical regions, suggesting a novel pathway for generating (auto)antibody specificities
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Prediction and assessment of splicing alterations: implications for clinical testing.
PMID 18951448 · PMC2832470 · Human mutation · 2008 · 8 claims · 5 setups
Bioinformatic prediction alone is insufficient; in vitro analysis is needed to confirm or establish splicing aberrations for clinical variant classification
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Has reproduction · 88
Transcriptome-wide analyses of piRNA binding sites suggest distinct mechanisms regulate piRNA binding and silencing in C. elegans.
PMID 36737102 · PMC10158993 · RNA (New York, N.Y.) · 2023 · 8 claims · 7 setups
C. elegans piRNAs preferentially bind the coding regions (CDS) of target mRNAs in vivo, rather than 3' UTRs.
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Intricate targeting of immunoglobulin somatic hypermutation maximizes the efficiency of affinity maturation.
PMID 15867095 · PMC2213188 · The Journal of experimental medicine · 2005 · 7 claims · 6 setups
IgVH genes have evolved precise placement of coding-strand Cs so that AID-induced C-to-T mutations are predominantly silent, especially in the CDRs.
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Genomic analysis of the clonal origins of relapsed acute lymphoblastic leukemia.
PMID 19039135 · PMC2746051 · Science (New York, N.Y.) · 2008 · 8 claims · 7 setups
Diagnosis and relapse ALL samples show different patterns of CNAs, with relapse-acquired abnormalities preferentially affecting cell cycle regulation and B-cell development genes