ArticleBMC molecular biology2010
Deficiency of the dual ubiquitin/SUMO ligase Topors results in genetic instability and an increased rate of malignancy in mice.
Article in BMC molecular biology, 2010. 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, 27 citations in OpenAlex.
- Article
- The fission yeast SUMO-targeted ubiquitin ligase Slx8 functionally associates with clustered centromeres and the silent mating-type region at the nuclear periphery.Biology open · 2024Article
- TOPORS E3 ligase mediates resistance to hypomethylating agent cytotoxicity in acute myeloid leukemia cells.Nature communications · 2024Article
- Inhibition of TOPORS ubiquitin ligase augments the efficacy of DNA hypomethylating agents through DNMT1 stabilization.Nature communications · 2024Article
- miR-198 targetsFrontiers in oncology · 2024Article
- TOPORS as a novel causal gene for Joubert syndrome.American journal of medical genetics. Part A · 2023Article
- RING finger protein TOPORS modulates the expression of tumor suppressor SMAR1 in colorectal cancer via the TLR4-TRIF pathway.Molecular oncology · 2022Article
- TOPORS-mediated RAD51 SUMOylation facilitates homologous recombination repair.Nucleic acids research · 2022Article
- Regulation of p53 by E3s.Cancers · 2021Review
- Chromosome Instability; Implications in Cancer Development, Progression, and Clinical Outcomes.Cancers · 2020Review
- Regulation of the p53 Family Proteins by the Ubiquitin Proteasomal Pathway.International journal of molecular sciences · 2019Review
- Functional Genomics of the Retina to Elucidate its Construction and Deconstruction.International journal of molecular sciences · 2019Review
- Genetic Aberration Analysis in Thai Colorectal Adenoma and Early-Stage Adenocarcinoma Patients by Whole-Exome Sequencing.Cancers · 2019Article
- Prognostic cancer gene signatures share common regulatory motifs.Scientific reports · 2017Article
- Control of Meiotic Crossovers: From Double-Strand Break Formation to Designation.Annual review of genetics · 2016Review
- Article
- Limiting the power of p53 through the ubiquitin proteasome pathway.Genes & development · 2014Review
- Protein sumoylation in brain development, neuronal morphology and spinogenesis.Neuromolecular medicine · 2013Review
- SUMO: a multifaceted modifier of chromatin structure and function.Developmental cell · 2013Review
- Nuclear structure and chromosome segregation in Drosophila male meiosis depend on the ubiquitin ligase dTopors.Genetics · 2011Article
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundTopors is a nuclear protein that co-localizes with promyelocytic leukemia bodies and has both ubiquitin and SUMO E3 ligase activity. Expression studies implicated Topors as a tumor suppressor in various malignancies. To gain insight into the function of Topors, we generated a Topors-deficient mouse strain.
resultsMice homozygous for a mutant Topors allele exhibited a high rate of perinatal mortality and decreased lifespan. In addition, heterozygotes were found to have an increased incidence of malignancy, involving a variety of tissues. Consistent with this finding, primary embryonic fibroblasts lacking Topors exhibited an increased rate of malignant transformation, associated with aneuploidy and defective chromosomal segregation. While loss of Topors did not alter sensitivity to DNA-damaging or microtubule-targeting agents, cells lacking Topors exhibited altered pericentric heterochromatin, manifested by mislocalization of HP1alpha and an increase in transcription from pericentric major satellite DNA. Topors-deficient cells exhibited a transcriptional profile similar to that of cells treated with histone deacetylase inhibitors, and were resistant to the anti-proliferative effects of the histone deacetylase inhibitor trichostatin A.
conclusionThese results indicate a unique role for Topors in the maintenance of genomic stability and pericentric heterochromatin, as well as in cellular sensitivity to histone deacetylase inhibitors.
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