ArticleOncogene2011
A mitotic function for the high-mobility group protein HMG20b regulated by its interaction with the BRC repeats of the BRCA2 tumor suppressor.
Article in Oncogene, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 32 citations in OpenAlex.
- CPSF4-mediated regulation of alternative splicing of HMG20B facilitates the progression of triple-negative breast cancer.Journal of translational medicine · 2024Article
- Generation of Schwann cell derived melanocytes from hPSCs identifies pro-metastatic factors in melanoma.bioRxiv : the preprint server for biology · 2023Article
- Evaluation of Personalized Skincare Through in-silico Gene Interactive Networks and Cellular Responses to UVR and Oxidative Stress.Clinical, cosmetic and investigational dermatology · 2022Article
- Review
- Pharmacological inhibition of HDAC1/3-interacting proteins induced morphological changes, and hindered the cell proliferation and migration of hepatocellular carcinoma cells.Environmental science and pollution research international · 2021Article
- Guardians of the Genome: BRCA2 and Its Partners.Genes · 2021Review
- The phospho-dependent role of BRCA2 on the maintenance of chromosome integrity.Cell cycle (Georgetown, Tex.) · 2021Review
- Identification and Biochemical Characterization of High Mobility Group Protein 20A as a Novel CaBiomolecules · 2021Article
- How do mutations affecting the breast cancer genes BRCA1 and BRCA2 cause cancer susceptibility?DNA repair · 2019Review
- Emerging Roles of the TRIM E3 Ubiquitin Ligases MID1 and MID2 in Cytokinesis.Frontiers in physiology · 2019Review
- Genotypic and Phenotypic Variables Affect Meiotic Cell Cycle Progression, Tumor Ploidy, and Cancer-Associated Mortality in aJournal of oncology · 2019Article
- Single-molecule localization microscopy reveals molecular transactions during RAD51 filament assembly at cellular DNA damage sites.Nucleic acids research · 2018Article
- A comprehensive analysis of BRCA2 gene: focus on mechanistic aspects of its functions, spectrum of deleterious mutations, and therapeutic strategies targeting BRCA2-deficient tumors.Medical oncology (Northwood, London, England) · 2018Review
- Molding BRCA2 function through its interacting partners.Cell cycle (Georgetown, Tex.) · 2015Review
- High levels of BRC4 induced by a Tet-On 3G system suppress DNA repair and impair cell proliferation in vertebrate cells.DNA repair · 2014Article
- Tumour suppressor mechanisms in the control of chromosome stability: insights from BRCA2.Molecules and cells · 2014Review
- A cancer-associated mutation inactivates a region of the high-mobility group protein HMG20b essential for cytokinesis.Cell cycle (Georgetown, Tex.) · 2014Article
- RAS promotes tumorigenesis through genomic instability induced by imbalanced expression of Aurora-A and BRCA2 in midbody during cytokinesis.International journal of cancer · 2013Article
- BRCA2 localization to the midbody by filamin A regulates cep55 signaling and completion of cytokinesis.Developmental cell · 2012Article
- DNA double strand breaks but not interstrand crosslinks prevent progress through meiosis in fully grown mouse oocytes.PloS one · 2012Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
Abstract
The inactivation of BRCA2, a suppressor of breast, ovarian and other epithelial cancers, triggers instability in chromosome structure and number, which are thought to arise from defects in DNA recombination and mitotic cell division, respectively. Human BRCA2 controls DNA recombination via eight BRC repeats, evolutionarily conserved motifs of ∼35 residues, that interact directly with the recombinase RAD51. How BRCA2 controls mitotic cell division is debated. Several studies by different groups report that BRCA2 deficiency affects cytokinesis. Moreover, its interaction with HMG20b, a protein of uncertain function containing a promiscuous DNA-binding domain and kinesin-like coiled coils, has been implicated in the G2-M transition. We show here that HMG20b depletion by RNA interference disturbs the completion of cell division, suggesting a novel function for HMG20b. In vitro, HMG20b binds directly to the BRC repeats of BRCA2, and exhibits the highest affinity for BRC5, a motif that binds poorly to RAD51. Conversely, the BRC4 repeat binds strongly to RAD51, but not to HMG20b. In vivo, BRC5 overexpression inhibits the BRCA2-HMG20b interaction, recapitulating defects in the completion of cell division provoked by HMG20b depletion. In contrast, BRC4 inhibits the BRCA2-RAD51 interaction and the assembly of RAD51 at sites of DNA damage, but not the completion of cell division. Our findings suggest that a novel function for HMG20b in cytokinesis is regulated by its interaction with the BRC repeats of BRCA2, and separate this unexpected function for the BRC repeats from their known activity in DNA recombination. We propose that divergent tumor-suppressive pathways regulating chromosome segregation as well as chromosome structure may be governed by the conserved BRC motifs in BRCA2.
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Registered trials
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