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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Massively parallel reporter assay for mapping gene-specific regulatory regions at single-nucleotide resolution.
PMID 41738738 · PMC12935429 · eLife · 2026 · 8 claims · 8 setups
LS-MPRA (BAC-based) and d-MPRA (systematic mutagenesis) are complementary methods for unbiased, high-resolution mapping of cis-regulatory modules.
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Nonsense-mediated mRNA decay orchestrates neuronal migration and cortical lamination while modulating Reelin and ciliary gene regulatory networks.
PMID 41746809 · PMC13042203 · Cell reports · 2026 · 8 claims · 8 setups
UPF2-mediated NMD is required for proper cortical lamination; conditional Upf2 deletion in radial glia disrupts layering of TBR1+/SATB2+ and CTIP2+/CUX1+ neurons.
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Has reproduction · 82
Temporal control of progenitor competence shapes maturation in GABAergic neuron development in mice.
PMID 40629142 · PMC12321585 · Nature neuroscience · 2025 · 8 claims · 8 setups
Ganglionic eminence (ventral) progenitors maintain stable differentiation competence throughout neurogenesis, generating a consistent set of postmitotic precursor states at all stages, unlike dorsal cortical progenitors whose differentiation competence changes gradually.
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CITED2 is a druggable epigenetic switch coupling neuronal maturation to regenerative decline.
PMID 41731079 · PMC13083982 · EMBO molecular medicine · 2026 · 8 claims · 8 setups
The transition from immature non-polarized to mature polarized DRG neurons (E12.5-E17.5) is associated with loss of gene expression signatures needed for regenerative growth competence.
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Dominant clones leverage developmental epigenomic states to drive ependymoma.
PMID 41882368 · PMC13102692 · Nature · 2026 · 8 claims · 8 setups
Chromatin accessibility patterns in neural progenitor cells are pre-established during normal development and are subsequently commissioned (not created) by ZR binding to drive oncogene expression