ArticleOncotarget2016
miR-29 regulates Tet1 expression and contributes to early differentiation of mouse ESCs.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
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Who cites it
19 citing papers in PubMed, 30 citations in OpenAlex.
- miRNA-29 regulates epidermal and mesenchymal functions in skin repair.FEBS letters · 2025Article
- Potential role of miR-29b from mesenchymal stromal cell-derived extracellular vesicles in leukemic cell progression.PloS one · 2025Article
- Multi-omics data integration for the identification of biomarkers for bull fertility.PloS one · 2024Article
- Involvement of Small Non-Coding RNA and Cell Antigens in Pathogenesis of Extramedullary Multiple Myeloma.International journal of molecular sciences · 2022Article
- Epigenetics as "conductor" in "orchestra" of pluripotent states.Cell and tissue research · 2022Review
- Epigenetic and metabolic regulation of epidermal homeostasis.Experimental dermatology · 2021Review
- MicroRNAs and Stem-like Properties: The Complex Regulation Underlying Stemness Maintenance and Cancer Development.Biomolecules · 2021Review
- Epigenetic Contribution and Genomic Imprinting Dlk1-Dio3 miRNAs in Systemic Lupus Erythematosus.Genes · 2021Review
- Overview of host miRNA properties and their association with epigenetics, long non-coding RNAs, and Xeno-infectious factors.Cell & bioscience · 2021Review
- miR‑29 promotes the proliferation of cultured rat neural stem/progenitor cells via the PTEN/AKT signaling pathway.Molecular medicine reports · 2019Article
- A Systematic Review of miR-29 in Cancer.Molecular therapy oncolytics · 2019Review
- miR-29a contributes to breast cancer cells epithelial-mesenchymal transition, migration, and invasion via down-regulating histone H4K20 trimethylation through directly targeting SUV420H2.Cell death & disease · 2019Article
- Overexpression of MicroRNA-10a in Germ Cells Causes Male Infertility by Targeting Rad51 in Mouse and Human.Frontiers in physiology · 2019Article
- Tet Enzymes, Variants, and Differential Effects on Function.Frontiers in cell and developmental biology · 2018Review
- MiR-29b/TET1/ZEB2 signaling axis regulates metastatic properties and epithelial-mesenchymal transition in breast cancer cells.Oncotarget · 2017Article
- Involment of RAS/ERK1/2 signaling and MEF2C in miR-155-3p inhibition-triggered cardiomyocyte differentiation of embryonic stem cell.Oncotarget · 2017Article
- Tiny But Mighty: Promising Roles of MicroRNAs in the Diagnosis and Treatment of Parkinson's Disease.Neuroscience bulletin · 2017Review
- MicroRNA-29: A Crucial Player in Fibrotic Disease.Molecular diagnosis & therapy · 2017Review
- miR-29a regulates the proliferation and differentiation of retinal progenitors by targeting Rbm8a.Oncotarget · 2017Article
Corrections and comments
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Authors and funding
5 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The ten-eleven translocation-1 (Tet1), which converts 5-methylcytosine (5mC) to 5-hydroxymethycytosine (5hmC), plays important roles in many important biological processes, such as mouse embryonic stem cells (ESCs) maintenance. However, the mechanisms for Tet-1 regulation remain largely unknown. Here we showed that miR-29 family (miR-29a, miR-29b and miR-29c) can directly repress Tet1 expression. We found that Tet1 was highly expressed and 5hmC was presented at relatively high levels in mouse ESCs, but the levels of both Tet1 and 5hmC were reduced during the early differentiation of ESCs. On the contrary, miR-29 level was increased in this process. ESCs stably transfecting with miR-29 precursors showed lower levels of Tet1 protein and 5hmC. Furthermore, we demonstrated that miR-29 overexpression selectively affected cell lineage markers and skewed ESC differentiation, which was similar in Tet1 knockdown ESCs. Our results indicate that miR-29 is a direct regulator of Tet1 in mouse ESCs.
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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.