ArticleThe FEBS journal2019
E2F1 activates MFN2 expression by binding to the promoter and decreases mitochondrial fission and mitophagy in HeLa cells.
Article in The FEBS journal, 2019. 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, 26 citations in OpenAlex.
- Transcriptional and epigenetic regulation of autophagy: mechanisms, disease relevance and therapeutic opportunities.Signal transduction and targeted therapy · 2026Review
- Predicting Which Mitophagy Proteins Are Dysregulated in Spinocerebellar Ataxia Type 3 (SCA3) Using the Auto-p2docking Pipeline.International journal of molecular sciences · 2025Article
- Molecular mechanisms and Biological Functions of Autophagy in Endometrial Diseases.International journal of medical sciences · 2025Review
- Astragaloside IV Protects Against Podocyte Injury by Upregulating Mitophagy via Mfn2/Pink1/Parkin Axis.Current molecular medicine · 2025Article
- β-arrestin1 protects intestinal tight junction through promoting mitofusin 2 transcription to drive parkin-dependent mitophagy in colitis.Gastroenterology report · 2024Article
- Transcriptional regulation of autophagy and its implications in human disease.Cell death and differentiation · 2023Review
- Sp1 promotes tumour progression by remodelling the mitochondrial network in cervical cancer.Journal of translational medicine · 2023Article
- Mitophagy and immune infiltration in vitiligo: evidence from bioinformatics analysis.Frontiers in immunology · 2023Article
- Heterogenous circulating miRNA changes in ME/CFS converge on a unified cluster of target genes: A computational analysis.PloS one · 2023Article
- LARS2 Regulates Apoptosis via ROS-Mediated Mitochondrial Dysfunction and Endoplasmic Reticulum Stress in Ovarian Granulosa Cells.Oxidative medicine and cellular longevity · 2022Article
- E2F1 sumoylation as a protective cellular mechanism in oxidative stress response.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- New relationship of E2F1 and BNIP3 with caveolin-1 in lung cancer-associated fibroblasts.Thoracic cancer · 2020Article
- Inhibition of Kv10.1 Channels Sensitizes Mitochondria of Cancer Cells to Antimetabolic Agents.Cancers · 2020Article
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3 authors at 1 institution in 1 country.
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Abstract
Mitofusin-2 (MFN2) is primarily involved in mitochondrial fusion and participates in diverse biological processes. Several reports show that MFN2 is a target of different miRNAs; however, the transcriptional regulation of MFN2 has not been extensively studied. To gain insight into the transcriptional regulation of MFN2, we expressed E2F transcription factor 1 (E2F1) exogenously and observed that it increased the endogenous expression of MFN2 by binding to its putative promoter region. Although the levels of E2F1 were shown to vary during the cell cycle, the expression of MFN2 and its regulator SP1 did not change throughout the different phases, suggesting that E2F1 regulates MFN2 in a cell-cycle-independent manner. In the cell-cycle phases, where the expression of E2F1 was reduced, SP1 might act in its place to regulate the expression of MFN2. We showed that E2F1 and SP1 are present as a complex on the promoter of MFN2 during the S-phase as well as in E2F1 overexpressing cells, suggesting that they may regulate the expression of MFN2 synergistically. Furthermore, we found that E2F1 modulated mitochondrial fusion and mitophagy, likely through regulation of MFN2. Bioinformatic analysis revealed that several potential targets of E2F1 are localized in mitochondria and associated with autophagy. Collectively, these data identify the E2F1-MFN2 axis as a regulator of mitochondrial morphology and mitophagy, suggesting a potential therapeutic target for the treatment of mitochondrial disorders.
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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.