ArticleThe Journal of biological chemistry2012
Nuclear factor erythroid-derived 2 (Nfe2) regulates JunD DNA-binding activity via acetylation: a novel mechanism regulating trophoblast differentiation.
Article in The Journal of biological chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 20 citations in OpenAlex.
- Gcm1 Orchestrates Lef1 Expression in Folate Deficiency-Induced Neural Tube Defects.Molecular neurobiology · 2025Article
- Associations Between Prenatal Vitamin D and Placental Gene Expression.bioRxiv : the preprint server for biology · 2024Article
- Procoagulant Extracellular Vesicles Alter Trophoblast Differentiation in Mice by a Thrombo-Inflammatory Mechanism.International journal of molecular sciences · 2021Article
- Current State of Preeclampsia Mouse Models: Approaches, Relevance, and Standardization.Frontiers in physiology · 2021Review
- Discovery of cell-type specific DNA motif grammar in cis-regulatory elements using random Forest.BMC genomics · 2018Article
- Farnesoid X Receptor Agonism Protects against Diabetic Tubulopathy: Potential Add-On Therapy for Diabetic Nephropathy.Journal of the American Society of Nephrology : JASN · 2017Article
- Activated Protein C Ameliorates Renal Ischemia-Reperfusion Injury by Restricting Y-Box Binding Protein-1 Ubiquitination.Journal of the American Society of Nephrology : JASN · 2015Article
- Dynamic Regulation of AP-1 Transcriptional Complexes Directs Trophoblast Differentiation.Molecular and cellular biology · 2015Article
- Regulation and function of the NFE2 transcription factor in hematopoietic and non-hematopoietic cells.Cellular and molecular life sciences : CMLS · 2015Review
- Defective podocyte insulin signalling through p85-XBP1 promotes ATF6-dependent maladaptive ER-stress response in diabetic nephropathy.Nature communications · 2015Article
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Authors and funding
13 authors at 5 institutions in 3 countries.
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No grant is acknowledged in the PubMed record.
Abstract
We recently demonstrated that the bZip transcription factor nuclear factor erythroid-derived 2 (Nfe2) represses protein acetylation and expression of the transcription factor glial cell missing 1 (Gcm1) in trophoblast cells, preventing excess syncytiotrophoblast formation and permitting normal placental vascularization and embryonic growth. However, the Gcm1 promoter lacks a Nfe2-binding site and hence the mechanisms linking Nfe2 and Gcm1 expression remained unknown. Here we show that Nfe2 represses JunD DNA-binding activity to the Gcm1 promoter during syncytiotrophoblast differentiation. Interventional studies using knockdown and knockin approaches show that enhanced JunD DNA-binding activity is required for increased expression of Gcm1 and syncytiotrophoblast formation as well as impaired placental vascularization and reduced growth of Nfe2(-/-) embryos. Induction of Gcm1 expression requires binding of JunD to the -1441 site within the Gcm1 promoter, which is distinct from the -1314 site previously shown to induce Gcm1 expression by other bZip transcription factors. Nfe2 modulates JunD binding to the Gcm1 promoter via acetylation, as reducing JunD acetylation using the histone acetyltransferase inhibitor curcumin reverses the increased JunD DNA-binding activity observed in the absence of Nfe2. This identifies a novel mechanism through which bZip transcription factors interact. Within the placenta this interaction regulates Gcm1 expression, syncytiotrophoblast formation, placental vascularization, and embryonic growth.
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