ArticleNature communications2018
The replication initiation determinant protein (RepID) modulates replication by recruiting CUL4 to chromatin.
Article in Nature communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
What it found
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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
33 citing papers in PubMed, 55 citations in OpenAlex.
- PHIP suppresses NuRD to enable the growth of SWI/SNF-mutant cancers.Nature communications · 2026Article
- RepID promotes metastatic potential in osteosarcoma through regulation of the PRC1-GATA6 axis.Animal cells and systems · 2026Article
- Telomeric repeat-containing RNA increases in aged human cells.Nucleic acids research · 2025Article
- Neuroendocrinology and the Genetics of Obesity.Endocrinology · 2025Review
- 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
- Pathogenic PHIP Variants are Variably Associated With CAKUT.Kidney international reports · 2024Article
- Article
- Where and when to start: Regulating DNA replication origin activity in eukaryotic genomes.Nucleus (Austin, Tex.) · 2023Review
- The CUL4B-based E3 ubiquitin ligase regulates mitosis and brain development by recruiting phospho-specific DCAFs.The EMBO journal · 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
- DNA replication initiation factor RECQ4 possesses a role in antagonizing DNA replication initiation.Nature communications · 2023Article
- Unscheduled DNA replication in G1 causes genome instability and damage signatures indicative of replication collisions.Nature communications · 2022Article
- Italian Precision Medicine in Pediatric Oncology: Moving beyond Actionable Alterations.International journal of molecular sciences · 2022Article
- USP7 substrates identified by proteomics analysis reveal the specificity of USP7.Genes & development · 2022Article
- PHIP variants associated with Chung-Jansen syndrome disrupt replication fork stability and genome integrity.Cold Spring Harbor molecular case studies · 2022Article
- Preventing excess replication origin activation to ensure genome stability.Trends in genetics : TIG · 2022Review
- A trivalent nucleosome interaction by PHIP/BRWD2 is disrupted in neurodevelopmental disorders and cancer.Genes & development · 2021Article
- Molecular double clips within RepID WD40 domain control chromatin binding and CRL4-substrate assembly.Biochemical and biophysical research communications · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 1 institution in 1 country.
Funding
Abstract
Cell cycle progression in mammals is modulated by two ubiquitin ligase complexes, CRL4 and SCF, which facilitate degradation of chromatin substrates involved in the regulation of DNA replication. One member of the CRL4 complex, the WD-40 containing protein RepID (DCAF14/PHIP), selectively binds and activates a group of replication origins. Here we show that RepID recruits the CRL4 complex to chromatin prior to DNA synthesis, thus playing a crucial architectural role in the proper licensing of chromosomes for replication. In the absence of RepID, cells rely on the alternative ubiquitin ligase, SKP2-containing SCF, to progress through the cell cycle. RepID depletion markedly increases cellular sensitivity to SKP2 inhibitors, which triggered massive genome re-replication. Both RepID and SKP2 interact with distinct, non-overlapping groups of replication origins, suggesting that selective interactions of replication origins with specific CRL components execute the DNA replication program and maintain genomic stability by preventing re-initiation of DNA replication.
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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.