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Synthetic viability by BRCA2 and PARP1/ARTD1 deficiencies

https://doi.org/10.1038/ncomms12425
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41/41 checkable references clean · checked 2026-08-19

Every reference with a DOI in the deposited reference list resolved to a known work in Crossref or DataCite at the dated check, and none carried a retraction, withdrawal, or removal notice.

2 without a DOI — not checked. A reference deposited without a DOI is never matched by title or guessed at; it stays outside the checked set, and this line discloses that.

The 41 checked references that resolve
resolves10.1146/annurev.pathol.3.121806.151422
Linking the Cellular Functions of<i>BRCA</i>Genes to Cancer Pathogenesis and Treatment
resolves10.1016/j.cell.2011.03.041
Double-Strand Break Repair-Independent Role for BRCA2 in Blocking Stalled Replication Fork Degradation by MRE11
resolves10.1016/j.ccr.2012.05.015
A Distinct Replication Fork Protection Pathway Connects Fanconi Anemia Tumor Suppressors to RAD51-BRCA1/2
resolves10.1038/nature03443
Specific killing of BRCA2-deficient tumours with inhibitors of poly(ADP-ribose) polymerase
resolves10.1038/nature03445
Targeting the DNA repair defect in BRCA mutant cells as a therapeutic strategy
resolves10.1056/NEJMoa0900212
Inhibition of Poly(ADP-Ribose) Polymerase in Tumors from <i>BRCA</i> Mutation Carriers
resolves10.1038/nrc1691
The Concept of Synthetic Lethality in the Context of Anticancer Therapy
resolves10.1038/nrc2812
PARP inhibition: PARP1 and beyond
resolves10.1093/nar/gkv1383
Readers of poly(ADP-ribose): designed to be fit for purpose
resolves10.1016/j.molcel.2016.01.019
PARP1 Links CHD2-Mediated Chromatin Expansion and H3.3 Deposition to DNA Repair by Non-homologous End-Joining
resolves10.1101/gad.9.5.509
Mice lacking ADPRT and poly(ADP-ribosyl)ation develop normally but are susceptible to skin disease.
resolves10.1158/0008-5472.CAN-12-2753
Trapping of PARP1 and PARP2 by Clinical PARP Inhibitors
resolves10.1073/pnas.1013715108
Nonhomologous end joining drives poly(ADP-ribose) polymerase (PARP) inhibitor lethality in homologous recombination-deficient cells
resolves10.1038/nrc.2015.21
BRCAness revisited
resolves10.1056/NEJMoa1105535
Olaparib Maintenance Therapy in Platinum-Sensitive Relapsed Ovarian Cancer
resolves10.1016/S1470-2045(14)70228-1
Olaparib maintenance therapy in patients with platinum-sensitive relapsed serous ovarian cancer: a preplanned retrospective analysis of outcomes by BRCA status in a randomised phase 2 trial
resolves10.1186/1471-2164-8-41
Loss of Parp-1 affects gene expression profile in a genome-wide manner in ES cells and liver cells
resolves10.1089/scd.2010.0058
Mouse Embryonic Stem Cells, but Not Somatic Cells, Predominantly Use Homologous Recombination to Repair Double-Strand DNA Breaks
resolves10.1038/ncomms3993
Poly(ADP-ribose) binding to Chk1 at stalled replication forks is required for S-phase checkpoint activation
resolves10.1038/nm.1719
Mouse embryonic stem cell–based functional assay to evaluate mutations in BRCA2
resolves10.1038/386804a0
Embryonic lethality and radiation hypersensitivity mediated by Rad51 in mice lacking Brca2
resolves10.1038/emboj.2009.206
PARP is activated at stalled forks to mediate Mre11‐dependent replication restart and recombination
resolves10.1038/nsmb.2258
Topoisomerase I poisoning results in PARP-mediated replication fork reversal
resolves10.1158/0008-5472.CAN-11-3417
Mre11-Dependent Degradation of Stalled DNA Replication Forks Is Prevented by BRCA2 and PARP1
resolves10.1016/j.cell.2010.03.012
53BP1 Inhibits Homologous Recombination in Brca1-Deficient Cells by Blocking Resection of DNA Breaks
resolves10.1084/jem.20131939
CtIP-mediated resection is essential for viability and can operate independently of BRCA1
resolves10.1074/jbc.M706734200
PARP1-dependent Kinetics of Recruitment of MRE11 and NBS1 Proteins to Multiple DNA Damage Sites
resolves10.1101/gad.2053211
Analysis of protein dynamics at active, stalled, and collapsed replication forks
resolves10.1038/nsmb.1831
53BP1 loss rescues BRCA1 deficiency and is associated with triple-negative and BRCA-mutated breast cancers
resolves10.1016/S0300-9084(99)80040-6
Involvement of poly(ADP-ribose) polymerase in base excision repair
resolves10.1073/pnas.92.11.4753
A dominant-negative mutant of human poly(ADP-ribose) polymerase affects cell recovery, apoptosis, and sister chromatid exchange following DNA damage.
resolves10.1101/gad.11.18.2347
PARP is important for genomic stability but dispensable in apoptosis
resolves10.1038/nature18325
Replication fork stability confers chemoresistance in BRCA-deficient cells
resolves10.1101/gad.256214.114
Resistance to therapy in <i>BRCA2</i> mutant cells due to loss of the nucleosome remodeling factor CHD4
resolves10.1038/nprot.2013.143
Genome engineering using the CRISPR-Cas9 system
resolves10.1093/nar/25.6.1317
B lymphocyte-specific, Cre-mediated mutagenesis in mice
resolves10.1038/ng747
Synergistic tumor suppressor activity of BRCA2 and p53 in a conditional mouse model for breast cancer
resolves10.1007/978-1-62703-056-4_12
Laser Capture Microdissection for Protein and NanoString RNA Analysis
resolves10.1016/j.cell.2007.06.016
ATM Prevents the Persistence and Propagation of Chromosome Breaks in Lymphocytes
resolves10.1038/nprot.2012.010
Monitoring the spatiotemporal dynamics of proteins at replication forks and in assembled chromatin using isolation of proteins on nascent DNA
resolves10.1016/j.molcel.2015.07.031
Timeless Interacts with PARP-1 to Promote Homologous Recombination Repair
The 2 references without a DOI — listed, not checked
no DOI — not checkedNagy, A. in Manipulating the Mouse Embryo: A Laboratory Manual 3rd edn Cold Spring Harbor Laboratory Press (2003).
no DOI — not checkedGolubeva, Y. & R. K., in Methods in Molecular Biology ed. Kozlov S. V. Humana (2009).
What this badge says. CiteStamped means the CHECKABLE references of this work were clean at the dated check: each resolved to a known work in a public registry, and none carried a retraction notice at that time. It says nothing about the quality, findings, or importance of the work itself, and nothing about references deposited without a DOI.

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