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Genome-wide fork-collapse sites in MEFs from ATR inhibition
Transient obstruction of DNA polymerase progression activates the ATR checkpoint kinase, which suppresses fork breakage, strand resection, and RPA accumulation. Herein, we use RPA ChIP-Seq to identify replication-problematic loci (RPLs) across the mammalian genome from ATR inhibition.
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.
Deposited / produced by
Nishita K ShastriYu-Chen TsaiEric J Brown
Reused by
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
Data type / assay
ChIP-seq
Organism
Mus musculus
Instrument
Illumina HiSeq 2500
Platform
ILLUMINA
Read type
short-read
Files available
FASTQ (raw reads)
N numbers (samples, groups)
21 / 21 runs
Completeness
100%
Metrics (value · how obtained)
checksum ok
yes
reported
total bases
96570524263
reported
total reads
964775033
reported
supplementary file types
NARROWPEAK
reported
QC cost
6 s compute
measured = computed from the data · extrapolated/reported = derived or from the repository · dq-1.0 · provisional — verify independently