Bulk-ATAC sequencing in RUNX-altered murine lung adenocarcinoma cell lines
Here, we using CRISPR activation and knockout studies to assess the implication of dysregulation of RUNX transcription factors on chromatin accessibility using bulk ATAC-sequencing. Tumor cell lines were derived from primary Kras G12D; p53 mutant mice (KP model) after initiation of tumors with SPC-Cre, resulting in lung adenocarcinoma. Cell lines were then expanded and profiled using bulk ATAC-sequencing.
Provenance — who produced it, who reused it
Linked to 1 papers in the literature. Roles are inferred factual signals (who deposited the data vs who reused it), with counts — never a judgement about any author.
- Epigenomic State Transitions Characterize Tumor Progression in M... 2020 · 234 cites
Deep data QC
metadata only · no data-level QC for this typeStandardized, field-standard QC computed by touching the data — every metric states how it was obtained
measured = computed from the data · extrapolated/reported = derived or from the repository · dq-1.0 · provisional — verify independently