ArticleCell cycle (Georgetown, Tex.)2013
The multi zinc-finger protein Trps1 acts as a regulator of histone deacetylation during mitosis.
Article in Cell cycle (Georgetown, Tex.), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 25 citations in OpenAlex.
- Clinical significance and biological function of transcriptional repressor GATA binding 1 in gastric cancer: a study based on data mining, RT-qPCR, immunochemistry, and vitro experiment.Cell cycle (Georgetown, Tex.) · 2020Article
- The Role of HDACs and HDACi in Cartilage and Osteoarthritis.Frontiers in cell and developmental biology · 2020Review
- Polygenic risk score for disability and insights into disability-related molecular mechanisms.GeroScience · 2019Article
- Atypical GATA protein TRPS1 plays indispensable roles in mouse two-cell embryo.Cell cycle (Georgetown, Tex.) · 2019Article
- TRPS1 Is a Lineage-Specific Transcriptional Dependency in Breast Cancer.Cell reports · 2018Article
- TRPS1 Suppresses Breast Cancer Epithelial-mesenchymal Transition Program as a Negative Regulator of SUZ12.Translational oncology · 2018Article
- Identification of Novel Potentially Pleiotropic Variants Associated With Osteoporosis and Obesity Using the cFDR Method.The Journal of clinical endocrinology and metabolism · 2018Article
- Zinc as a Gatekeeper of Immune Function.Nutrients · 2017Review
- Histone Deacetylases in Bone Development and Skeletal Disorders.Physiological reviews · 2015Review
- Nuclear cathepsin D enhances TRPS1 transcriptional repressor function to regulate cell cycle progression and transformation in human breast cancer cells.Oncotarget · 2015Article
- Article
- Review
- A novel TRPS1 gene mutation causing trichorhinophalangeal syndrome with growth hormone responsive short stature: a case report and review of the literature.International journal of pediatric endocrinology · 2014Article
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7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
TRPS1, the gene mutated in human "Tricho-Rhino-Phalangeal syndrome," encodes a multi zinc-finger nuclear regulator of chondrocyte proliferation and differentiation. Here, we have identified a new function of Trps1 in controlling mitotic progression in chondrocytes. Loss of Trps1 in mice leads to an increased proportion of cells arrested in mitosis and, subsequently, to chromosome segregation defects. Searching for the molecular basis of the defect, we found that Trps1 acts as regulator of histone deacetylation. Trps1 interacts with two histone deacetylases, Hdac1 and Hdac4, thereby increasing their activity. Loss of Trps1 results in histone H3 hyperacetylation, which is maintained during mitosis. Consequently, chromatin condensation and binding of HP1 is impaired, and Trps1-deficient chondrocytes accumulate in prometaphase. Overexpression of Hdac4 rescues the mitotic defect of Trps1-deficient chondrocytes, identifying Trps1 as an important regulator of chromatin deacetylation during mitosis in chondrocytes. Our data provide the first evidence that the control of mitosis can be linked to the regulation of chondrocyte differentiation by epigenetic consequences of altered Hdac activity.
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