ArticleDevelopment (Cambridge, England)2015
Histone deacetylase 1 and 2 regulate Wnt and p53 pathways in the ureteric bud epithelium.
Article in Development (Cambridge, England), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
33 citing papers in PubMed, 1 synthesis or guideline pooled it, 47 citations in OpenAlex.
- Fluid-electrolyte homeostasis requires histone deacetylase function.JCI insight · 2020Pooled it
- Epigenetic regulation of kidney development.Nature reviews. Nephrology · 2026Review
- Bridging Kidney Organoid Innovation and Regenerative Medicine: Current Advances and Future Directions.Cell proliferation · 2026Review
- Renal dysplasia development and chronic kidney disease.Pediatric research · 2025Review
- Histone deacetylases and their inhibitors in kidney diseases.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Review
- Hdac1 and Hdac2 regulate the quiescent state and survival of hair-follicle mesenchymal niche.Nature communications · 2023Article
- Nuclear SPHK2/S1P induces oxidative stress and NLRP3 inflammasome activation via promoting p53 acetylation in lipopolysaccharide-induced acute lung injury.Cell death discovery · 2023Article
- MicroRNA-495 suppresses pre-eclampsia via activation of p53/PUMA axis.Cell death discovery · 2022Article
- Kidney cell type-specific changes in the chromatin and transcriptome landscapes following epithelialPhysiological genomics · 2022Article
- 6-Shogaol Inhibits Oxidative Stress-Induced Rat Vascular Smooth Muscle Cell Apoptosis by Regulating OXR1-p53 Axis.Frontiers in molecular biosciences · 2022Article
- Targeted disruption of the histone lysine 79 methyltransferase Dot1L in nephron progenitors causes congenital renal dysplasia.Epigenetics · 2021Article
- Postnatal prolongation of mammalian nephrogenesis by excess fetal GDNF.Development (Cambridge, England) · 2021Article
- Effects of Environmental Conditions on Nephron Number: Modeling Maternal Disease and Epigenetic Regulation in Renal Development.International journal of molecular sciences · 2021Article
- MicroRNA-874-3p promotes testosterone-induced granulosa cell apoptosis by suppressing HDAC1-mediated p53 deacetylation.Experimental and therapeutic medicine · 2021Article
- The roles of histone deacetylases in kidney development and disease.Clinical and experimental nephrology · 2021Review
- Post-translational modifications of EZH2 in cancer.Cell & bioscience · 2020Review
- HDAC1-mediated deacetylation of LSD1 regulates vascular calcification by promoting autophagy in chronic renal failure.Journal of cellular and molecular medicine · 2020Article
- Epigenetic regulation of kidney progenitor cells.Stem cells translational medicine · 2020Review
- Histone Deacetylases in Kidney Physiology and Acute Kidney Injury.Seminars in nephrology · 2020Review
- Structurally Diverse Histone Deacetylase Photoreactive Probes: Design, Synthesis, and Photolabeling Studies in Live Cells and Tissue.ChemMedChem · 2019Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
Histone deacetylases (HDACs) regulate a broad range of biological processes through removal of acetyl groups from histones as well as non-histone proteins. Our previous studies showed that Hdac1 and Hdac2 are bound to promoters of key renal developmental regulators and that HDAC activity is required for embryonic kidney gene expression. However, the existence of many HDAC isoforms in embryonic kidneys raises questions concerning the possible specificity or redundancy of their functions. We report here that targeted deletion of both the Hdac1 and Hdac2 genes from the ureteric bud (UB) cell lineage of mice causes bilateral renal hypodysplasia. One copy of either Hdac1 or Hdac2 is sufficient to sustain normal renal development. In addition to defective cell proliferation and survival, genome-wide transcriptional profiling revealed that the canonical Wnt signaling pathway is specifically impaired in UB(Hdac1,2-/-) kidneys. Our results also demonstrate that loss of Hdac1 and Hdac2 in the UB epithelium leads to marked hyperacetylation of the tumor suppressor protein p53 on lysine 370, 379 and 383; these post-translational modifications are known to boost p53 stability and transcriptional activity. Genetic deletion of p53 partially rescues the development of UB(Hdac1,2-/-) kidneys. Together, these data indicate that Hdac1 and Hdac2 are crucial for kidney development. They perform redundant, yet essential, cell lineage-autonomous functions via p53-dependent and -independent pathways.
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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.