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).

Publications 1.3k Datasets 392.5k Experiments 6

System / cell line: induced ✕ Assay: nuclear ✕ Clear

The pseudo-mitochondrial genome influences mistakes in heteroplasmy interpretation.

PMID 16859552 · PMC1538596 · BMC genomics · 2006 · 7 claims · 7 setups

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Numts co-amplified with mtDNA during PCR generate false heteroplasmic signals at specific nucleotide positions.

143b ffpe blood cloned southern pcr rt-pcr
Alexander Meissner: learning the reprogramming code.

PMID 19704017 · PMC2733751 · The Journal of cell biology · 2009 · 8 claims · 6 setups

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A defined set of factors present in oocytes and embryonic stem (ES) cells can reprogram a somatic cell to pluripotency, as shown by nuclear transfer and ES cell/somatic cell fusion experiments

blastocysts somatic fused genomic nuclear inducible fusion
Transcriptional and proteomic profiling in a cellular model of DYT1 dystonia.

PMID 19665049 · PMC2774817 · Neuroscience · 2009 · 8 claims · 7 setups

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Accumulation of mutant torsinA(ΔE) in the nuclear envelope is not sufficient to cause transcriptional dysregulation

pc6-3 hek293 microarray 2-dige mass
Gli1-expressing stromal cells are highly reparative precursors of long-lived chondroprogenitors in the fetal murine limb.

PMID 41253754 · PMC12627582 · Nature communications · 2025 · 7 claims · 8 setups

Has reproduction · 10

Fetal Gli1+ cells (including cells outside the cartilage) are the precursors of postnatal long-lived chondroprogenitors and give rise to most growth-plate chondrocytes juvenile/adult.

fetal left-cart-p21moe growth gli1creer single-nuclei bulk cre-based
Mutations in pericentrin cause Seckel syndrome with defective ATR-dependent DNA damage signaling.

PMID 18157127 · PMC2397541 · Nature genetics · 2008 · 8 claims · 8 setups

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Homozygous truncating mutations in PCNT cause Seckel syndrome

consanguineous genomic lymphoblastoid lcls snp-microarray sanger immunofluorescence
Novel point mutation in the extracellular domain of the granulocyte colony-stimulating factor (G-CSF) receptor in a case of severe congenital neutropenia hyporesponsive to G-CSF treatment.

PMID 10449521 · PMC2195597 · The Journal of experimental medicine · 1999 · 7 claims · 8 setups

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A novel C→A point mutation at nucleotide 850 of GCSFR cDNA causes a Pro→His substitution at position 206 (P206H) in the proline-rich hinge of the CRH domain of the G-CSF receptor extracellular domain in an SCN patient hyporesponsive to G-CSF.

bone fibroblast 32d.cl8.6 32d rt-pcr genomic flow

Experiments

The pseudo-mitochondrial genome influences mistakes in heteroplasmy interpretation.

Alexander Meissner: learning the reprogramming code.

Transcriptional and proteomic profiling in a cellular model of DYT1 dystonia.

Gli1-expressing stromal cells are highly reparative precursors of long-lived chondroprogenitors in the fetal murine limb.

Mutations in pericentrin cause Seckel syndrome with defective ATR-dependent DNA damage signaling.

Novel point mutation in the extracellular domain of the granulocyte colony-stimulating factor (G-CSF) receptor in a case of severe congenital neutropenia hyporesponsive to G-CSF treatment.