ArticleOncogene2013
BRCA1 targets G2/M cell cycle proteins for ubiquitination and proteasomal degradation.
Article in Oncogene, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers, 1 of them a synthesis that pooled it.
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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.
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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
48 citing papers in PubMed, 1 synthesis or guideline pooled it, 71 citations in OpenAlex.
- Expression of tripartite motif-containing 44 and its prognostic and clinicopathological value in human malignancies:a meta-analysis.BMC cancer · 2020Pooled it
- Functional assays for BRCA1 and BRCA2 variant analysis: new tools and their applications.NPJ breast cancer · 2026Review
- BRCA1 and BRCA2 gene expression: p53- and cell cycle-dependent repression requires RB and DREAM.Cell death and differentiation · 2026Article
- Aberrant accumulation of phosphorylated BRCA1 in brainstem-type and cortical-type Lewy bodies in Lewy body disease.Journal of neuropathology and experimental neurology · 2025Article
- Ubiquitin-Proteasome-Mediated Protein Degradation and Disorders of the Central Nervous System.International journal of molecular sciences · 2025Review
- BRCA1 and BRCA2: from cancer susceptibility to synthetic lethality.Genes & development · 2025Review
- Developing a prognostic signature and characterizing the tumor microenvironment based on centrosome-related genes in lung adenocarcinoma.Oncology research · 2025Article
- Cellular mechanisms mediating the anti-cancer effects of carnosol on gingiva carcinoma.Scientific reports · 2024Article
- ReCorDE: a framework for identifying drug classes targeting shared vulnerabilities with applications to synergistic drug discovery.Frontiers in oncology · 2024Article
- Bioinformatic Analyses and Integrated Machine Learning to Predict prognosis and therapeutic response Based on E3 Ligase-Related Genes in colon cancer.Journal of Cancer · 2024Article
- Arsenite Impairs BRCA1-Dependent DNA Double-Strand Break Repair, a Mechanism Potentially Contributing to Genomic Instability.International journal of molecular sciences · 2023Article
- Identification of the c.829_832delAATA Deletion Variants in theJournal of genomics · 2022Article
- A Novel Copper(II) Indenoisoquinoline Complex Inhibits Topoisomerase I, Induces G2 Phase Arrest, and Autophagy in Three Adenocarcinomas.Frontiers in oncology · 2022Article
- Effects of Silver Nanoparticles and Silver Nitrate on mRNA and microRNA Expression in Human Hepatocellular Carcinoma Cells (HepG2).Journal of nanoscience and nanotechnology · 2021Article
- The BRCA1/BARD1 ubiquitin ligase and its substrates.The Biochemical journal · 2021Review
- Article
- Functional characterization of full-length BARD1 strengthens its role as a tumor suppressor in neuroblastoma.Journal of Cancer · 2020Article
- Regulatory Mechanisms of Cell Polyploidy in Insects.Frontiers in cell and developmental biology · 2020Review
- Article
- A Multidimensional Characterization of E3 Ubiquitin Ligase and Substrate Interaction Network.iScience · 2019Article
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 2 countries.
Funding
Abstract
The BRCA1 tumor suppressor protein heterodimerizes with its partner protein, BARD1, via the RING domain present in both proteins. The heterodimer contains an E3 ubiquitin ligase activity and participates in multiple cellular functions such as cell cycle control, DNA repair and regulation of gene transcription, collectively aimed at maintaining genomic stability and tumor suppression. Yet, the precise role of BRCA1 E3 ligase in these cellular functions is poorly understood. We present data showing that BRCA1 ubiquitinates G2/M cell cycle proteins, cyclin B and Cdc25C, leading to their accelerated degradation via a mechanism that is independent of APC/C. BRCA1-dependent degradation of cyclin B and Cdc25C is reversed by proteasome inhibitors and is enhanced following DNA damage, which may represent a possible mechanism to prevent cyclin B and Cdc25C accumulation, a requirement for mitotic entry. Our data provide mechanistic insight into how BRCA1 E3 ligase activity regulates the G2/M cell cycle checkpoint and, thus, contributes to maintenance of genomic stability.
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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.