ArticleCell reports2020
WRNIP1 Is Recruited to DNA Interstrand Crosslinks and Promotes Repair.
Article in Cell reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 23 citations in OpenAlex.
- The function of Mgs1/WRNIP1 in genome maintenance.Frontiers in molecular biosciences · 2026Review
- Research progress on the role of the NEIL family in cancer.Frontiers in cell and developmental biology · 2025Review
- PP2A licenses the FANCD2/FANCI complex for chromosome loading.Cell reports · 2024Article
- Repair of genomic interstrand crosslinks.DNA repair · 2024Review
- Werner helicase interacting protein 1 contributes to G-quadruplex processing in human cells.Scientific reports · 2024Article
- Article
- Implications of ubiquitination and the maintenance of replication fork stability in cancer therapy.Bioscience reports · 2023Review
- NEIL3-mediated proteasomal degradation facilitates the repair of cisplatin-induced DNA damage in human cells.Scientific reports · 2023Article
- Banp regulates DNA damage response and chromosome segregation during the cell cycle in zebrafish retina.eLife · 2022Article
- RNF166 plays a dual role for Lys63-linked ubiquitination and sumoylation of its target proteins.Journal of neural transmission (Vienna, Austria : 1996) · 2022Article
- Article
- The rarA gene as part of an expanded RecFOR recombination pathway: Negative epistasis and synthetic lethality with ruvB, recG, and recQ.PLoS genetics · 2021Article
- Focal Point of Fanconi Anemia Signaling.International journal of molecular sciences · 2021Review
- Purification of DNA repair protein complexes from mammalian cells.STAR protocols · 2021Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 2 countries.
Funding
Abstract
The Fanconi anemia (FA) pathway repairs DNA interstrand crosslinks (ICLs). Many FA proteins are recruited to ICLs in a timely fashion so that coordinated repair can occur. However, the mechanism of this process is poorly understood. Here, we report the purification of a FANCD2-containing protein complex with multiple subunits, including WRNIP1. Using live-cell imaging, we show that WRNIP1 is recruited to ICLs quickly after their appearance, promoting repair. The observed recruitment facilitates subsequent recruitment of the FANCD2/FANCI complex. Depletion of WRNIP1 sensitizes cells to ICL-forming drugs. We find that ubiquitination of WRNIP1 and the activity of its UBZ domain are required to facilitate recruitment of FANCD2/FANCI and promote repair. Altogether, we describe a mechanism by which WRNIP1 is recruited rapidly to ICLs, resulting in chromatin loading of the FANCD2/FANCI complex in an unusual process entailing ubiquitination of WRNIP1 and the activity of its integral UBZ domain.
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Registered trials
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.