ArticleNature communications2020
The RepID-CRL4 ubiquitin ligase complex regulates metaphase to anaphase transition via BUB3 degradation.
Article in Nature communications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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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.
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.
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Who cites it
23 citing papers in PubMed, 38 citations in OpenAlex.
- PHIP suppresses NuRD to enable the growth of SWI/SNF-mutant cancers.Nature communications · 2026Article
- NUF2 interacts with BUB3 and drives lung adenocarcinoma progression through activation of the NF-κB pathway.World journal of surgical oncology · 2026Article
- RepID promotes metastatic potential in osteosarcoma through regulation of the PRC1-GATA6 axis.Animal cells and systems · 2026Article
- REV1 Loss Triggers a G2/M Cell-Cycle Arrest Through Dysregulation of Mitotic Regulators.Genes · 2025Article
- Leukemia mutated proteins PHF6 and PHIP form a chromatin complex that represses acute myeloid leukemia stemness.Genes & development · 2025Article
- RepID depletion enhances TWS119-induced erythropoiesis through chromatin reprogramming and transcription factor recruitment.Genes & genomics · 2025Article
- RepID as a potential biomarker and therapeutic target for lung neuroendocrine tumor.Scientific reports · 2024Article
- The Relevance of Reperfusion Stroke Therapy for miR-9-3p and miR-9-5p Expression in Acute Stroke-A Preliminary Study.International journal of molecular sciences · 2024Article
- On the Prevalence and Roles of Proteins Undergoing Liquid-Liquid Phase Separation in the Biogenesis of PML-Bodies.Biomolecules · 2023Article
- RepID represses megakaryocytic differentiation by recruiting CRL4A-JARID1A at DAB2 promoter.Cell communication and signaling : CCS · 2023Article
- RepID represses megakaryocytic differentiation by recruiting CRL4A-JARID1A at DAB2 promoter.Research square · 2023Article
- The E3 ubiquitin ligase HECTD1 contributes to cell proliferation through an effect on mitosis.Scientific reports · 2022Article
- PHIP variants associated with Chung-Jansen syndrome disrupt replication fork stability and genome integrity.Cold Spring Harbor molecular case studies · 2022Article
- Convergence of SIRT1 and ATR signaling to modulate replication origin dormancy.Nucleic acids research · 2022Article
- HumanInternational journal of biological sciences · 2022Article
- A trivalent nucleosome interaction by PHIP/BRWD2 is disrupted in neurodevelopmental disorders and cancer.Genes & development · 2021Article
- Cereblon: promise and challenges for combating human diseases.Pflugers Archiv : European journal of physiology · 2021Review
- Molecular double clips within RepID WD40 domain control chromatin binding and CRL4-substrate assembly.Biochemical and biophysical research communications · 2021Article
- SUMO-Targeted Ubiquitin Ligases and Their Functions in Maintaining Genome Stability.International journal of molecular sciences · 2021Review
- DCAF14 promotes stalled fork stability to maintain genome integrity.Cell reports · 2021Article
Corrections and comments
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Authors and funding
13 authors at 3 institutions in 1 country.
Funding
Abstract
The spindle assembly checkpoint (SAC) prevents premature chromosome segregation by inactivating the anaphase promoting complex/cyclosome (APC/C) until all chromosomes are properly attached to mitotic spindles. Here we identify a role for Cullin-RING ubiquitin ligase complex 4 (CRL4), known for modulating DNA replication, as a crucial mitotic regulator that triggers the termination of the SAC and enables chromosome segregation. CRL4 is recruited to chromatin by the replication origin binding protein RepID/DCAF14/PHIP. During mitosis, CRL4 dissociates from RepID and replaces it with RB Binding Protein 7 (RBBP7), which ubiquitinates the SAC mediator BUB3 to enable mitotic exit. During interphase, BUB3 is protected from CRL4-mediated degradation by associating with promyelocytic leukemia (PML) nuclear bodies, ensuring its availability upon mitotic onset. Deficiencies in RepID, CRL4 or RBBP7 delay mitotic exit, increase genomic instability and enhance sensitivity to paclitaxel, a microtubule stabilizer and anti-tumor drug.
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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.