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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Has reproduction · 62
CASK loss of function differentially regulates neuronal maturation and synaptic function in human induced cortical excitatory neurons.
PMID 36262316 · PMC9574418 · iScience · 2022 · 7 claims · 8 setups
Immature (day 7) CASK KO induced neurons show increased dendritic complexity/neurite overgrowth and upregulated gene networks for cell adhesion, neurite outgrowth, and cytoskeletal organization.
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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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Mutations in alpha-tubulin cause abnormal neuronal migration in mice and lissencephaly in humans.
PMID 17218254 · PMC1885944 · Cell · 2007 · 8 claims · 8 setups
A semidominant ENU-induced S140G mutation in α-1 tubulin (Tuba1) causes hyperactivity and impaired neuronal migration in Jna/+ mice
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Has reproduction · 86
Single-cell transcriptome maps of myeloid blood cell lineages in Drosophila.
PMID 32900993 · PMC7479620 · Nature communications · 2020 · 8 claims · 8 setups
Single-cell RNA-seq of developing Drosophila lymph glands resolves heterogeneity of hemocytes and identifies major and sub cell types.
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New genes, new dilemmas: FTLD genetics and its implications for families.
PMID 18166610 · PMC10846215 · American journal of Alzheimer's disease and other dementias · 2007 · 8 claims · 8 setups
MAPT and PGRN mutations account for the largest number of familial FTLD cases and differ fundamentally in disease mechanism