BRCA1 suppresses microhomology-mediated tandem duplications at Tus/Ter-stalled replication forks
Small ~10 kb microhomology-mediated tandem duplications (“Group 1 TDs”) are abundant in BRCA1-linked but not BRCA2-linked breast cancer genomes. Here, we define the mechanism underlying this rearrangement signature. We show that BRCA1, but not BRCA2, suppresses TDs at a Tus/Ter site-specific chromosomal replication fork barrier in primary mammalian cells. BRCA1 has no equivalent role at chromosomal double strand breaks, indicating specificity for the stalled fork response. Two motor proteins—FAN...
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.
- Mechanism of tandem duplication formation in BRCA1-mutant cells 2017 · 141 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
No quantitative QC rubric exists for this data type yet, so it is deliberately left unscored — this is an honest "not applicable", not a poor rating.
measured = computed from the data · extrapolated/reported = derived or from the repository · dq-1.0 · provisional — verify independently