Article in Nucleic acids research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
2 · The registry
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
5 · Who and what money
Authors and funding
12 authors.
Tong WuDepartment of Molecular and Cell Biology, The Scripps Research Institute, La Jolla, CA 92037,United States.
Youhang LiDepartment of Molecular and Cell Biology, The Scripps Research Institute, La Jolla, CA 92037,United States.
Yuqin ZhaoDepartment of Molecular and Cell Biology, The Scripps Research Institute, La Jolla, CA 92037,United States.
Elodie BourniqueDepartment of Biological Chemistry, School of Medicine, University of California Irvine, Irvine, CA 92697, United States.
Pedro OrtegaDepartment of Biological Chemistry, School of Medicine, University of California Irvine, Irvine, CA 92697, United States.
Minghua NieDepartment of Molecular and Cell Biology, The Scripps Research Institute, La Jolla, CA 92037,United States.ORCID 0000-0003-0222-7615
Yiqing WangCenter for Chromosome Stability, Department of Cellular and Molecular Medicine, University of Copenhagen, Blegdamsvej 3B, 2200 Copenhagen N, Denmark.
Hailong WangCollege of Life Science, Capital Normal University, Beijing 100037, China.ORCID 0009-0000-1656-110X
Rémi BuissonDepartment of Biological Chemistry, School of Medicine, University of California Irvine, Irvine, CA 92697, United States.ORCID 0000-0002-7196-8209
Ian D HicksonCenter for Chromosome Stability, Department of Cellular and Molecular Medicine, University of Copenhagen, Blegdamsvej 3B, 2200 Copenhagen N, Denmark.ORCID 0000-0002-0583-566X
Michael N BoddyDepartment of Molecular and Cell Biology, The Scripps Research Institute, La Jolla, CA 92037,United States.
Xiaohua WuDepartment of Molecular and Cell Biology, The Scripps Research Institute, La Jolla, CA 92037,United States.ORCID 0000-0003-4947-3047
Funding
Defining Genome Stability Mechanisms and their Regulation by SUMO and UbiquitinR35GM136273 · NIGMS · SCRIPPS RESEARCH INSTITUTE, THE · PI MICHAEL N BODDY · 2020 to 2026
$4.3M
Study the mechanisms underlying common fragile site protectionR01CA187052 · NCI · SCRIPPS RESEARCH INSTITUTE, THE · PI WU, XIAOHUA · 2015 to 2025
$4.2M
Investigating DNA polymerase O in replication stress and cancer therapyR01CA294646 · NCI · SCRIPPS RESEARCH INSTITUTE, THE · PI Xiaohua Wu · 2024 to 2026
$3.0M
S-phase checkpoint and rereplication in mammalian cellsR01GM080677 · NIGMS · SCRIPPS RESEARCH INSTITUTE, THE · PI WU, XIAOHUA · 2010 to 2018
$2.9M
Molecular Mechanisms of APOBEC-Induced Mutagenesis in CancerR37CA252081 · NCI · UNIVERSITY OF CALIFORNIA-IRVINE · PI Remi Buisson · 2021 to 2026
$2.5M
Investigating DNA double-strand break repair mechanisms in mammalian cellsR35GM141868 · NIGMS · SCRIPPS RESEARCH INSTITUTE, THE · PI WU, XIAOHUA · 2021 to 2025
$2.5M
Study of Break-induced Replication in Mammalian CellsR01CA244912 · NCI · SCRIPPS RESEARCH INSTITUTE, THE · PI WU, XIAOHUA · 2020 to 2024
$2.5M
Role of the Mre11 complex in the maintenance of genome stabilityR01CA197995 · NCI · SCRIPPS RESEARCH INSTITUTE, THE · PI WU, XIAOHUA · 2015 to 2019
$2.2M
NF-KB regulation by the DNA damage responseR21ES036190 · NIEHS · UNIVERSITY OF CALIFORNIA-IRVINE · PI BUISSON, REMI · 2025 to 2025
$432k
Role of APOBEC3B in the Innate Immune ResponseR21AI185033 · NIAID · UNIVERSITY OF CALIFORNIA-IRVINE · PI Remi Buisson · 2025 to 2026
$425k
American Cancer Society RSG-24-1249960-01-DMCCalifornia Institute for Regenerative Medicine ALTF 213-2023California Institute for Regenerative Medicine TG2-01152Danish National Research FoundationNCI NIH HHS R01 CA187052NCI NIH HHS R01 CA197995NCI NIH HHS R01 CA244912NCI NIH HHS R01 CA294646NCI NIH HHS R37 CA252081NIAID NIH HHS R21 AI185033NIEHS NIH HHS R21 ES036190NIGMS NIH HHS R01 GM080677NIGMS NIH HHS R35 GM136273NIGMS NIH HHS R35 GM141868NIH HHS CA187052NIH HHS CA197995NIH HHS CA294646NIH HHS GM080677NIH HHS GM136273NIH HHS R21-AI185033NIH HHS R21-ES036190NIH HHS R37-CA252081NIH HHS R37-CA252081-S2State Key Laboratory of Radiation Medicine and Protection CA294646State Key Laboratory of Radiation Medicine and Protection SD2501
6 · The paper itself
Abstract
R-loops play essential physiological roles but also pose a significant threat to genome stability, particularly during replication, by exacerbating transcription-replication conflicts (TRCs). In this study, we have uncovered a critical role of the SMC5/6 complex in resolving TRCs to preserve fork integrity. We identified the SMC5/6 complex as a synthetic lethal partner of senataxin (SETX), an RNA/DNA helicase critical for removing R-loops that arise during replication. We demonstrated that in SETX-deficient cells, the SMC5/6 complex is recruited to TRCs in response to the buildup of DNA supercoiling and facilitates the recruitment of the BLM/TOP3A/RMI1/RMI2 complex (BTRR). Once recruited, BTRR acts to resolve the TRCs in a manner dependent on the catalytic activity of TOP3A. BTRR is also required for FANCM accumulation at TRCs, which activates the FANCD2 pathway to resolve TRCs. These studies underscore the role of SMC5/6 in sensing TRCs and define the SMC5/6-BTRR-FANCM-FANCD2 axis as an important player in mitigating TRC-induced genome instability. Our findings also provide therapeutic opportunities for targeting this axis for effective treatment of SETX-deficient tumors.
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.
The SMC5/SMC6 complex is critical for resolving R-loop-induced transcription-replication conflicts. · full record | OpenQuestion