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).

• Application of alternative de novo motif recognition models for analysis of structural heterogeneity of transcription factor binding sites: a case study of FOXA2 binding sites.

  PMID 34547062 · PMC8408018 · Vavilovskii zhurnal genetiki i selektsii · 2021 · 6 claims · 7 setups

  Has reproduction · 62

  Combining four de novo models (PWM, diPWM, BaMM, InMoDe) significantly increases the fraction of recognized peaks versus PWM alone (by 26.3%).

  hg38 foxa2 pwm whole-genome chip-seq pwm dipwm

• Identification of functional SNPs in the 5-prime flanking sequences of human genes.

  PMID 15717931 · PMC550646 · BMC genomics · 2005 · 6 claims · 5 setups

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  7 of 10 candidate SNPs tested by EMSA showed reproducible allele-specific differences in TF-DNA complex binding/stability

  flanking synthetic genomic cloned comparative electrophoretic rflp

• CTCF binding site classes exhibit distinct evolutionary, genomic, epigenomic and transcriptomic features.

  PMID 19922652 · PMC3091324 · Genome biology · 2009 · 8 claims · 8 setups

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  CTCF binding sites can be classified into three occupancy-based classes (LowOc, MedOc, HighOc) based on similarity to the CTCF PWM motif

  cd4+ hela imr90 embryonic chip-seq computational gene

• Interpretable prediction models for widespread m6A RNA modification across cell lines and tissues.

  PMID 37995291 · PMC10697738 · Bioinformatics (Oxford, England) · 2023 · 7 claims · 6 setups

  Has reproduction · 79

  CLSM6A, a CNN-based model set, predicts single-nucleotide-resolution m6A RNA modification sites across eight cell lines and three tissues in H. sapiens

  clsm6a learned last-layer computational model-based propagation-based

• Severe combined immunodeficiency (SCID) and attention deficit hyperactivity disorder (ADHD) associated with a Coronin-1A mutation and a chromosome 16p11.2 deletion.

  PMID 19097825 · PMC2692687 · Clinical immunology (Orlando, Fla.) · 2009 · 8 claims · 7 setups

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  CORO1A deficiency, caused by a paternal 2bp frameshift mutation combined with a maternal de novo 600kb deletion at chromosome 16p11.2, is the molecular cause of this patient's T-B+NK+ SCID

  ebv-transformed genomic father peripheral intracellular snp sequencing