ArticlePLoS genetics2010
Altering a histone H3K4 methylation pathway in glomerular podocytes promotes a chronic disease phenotype.
Article in PLoS genetics, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
42 citing papers in PubMed, 62 citations in OpenAlex.
- The response to kidney injury is epigenetically regulated through the activation of bivalent genes.American journal of physiology. Renal physiology · 2026Article
- Article
- Transcriptional Regulators YAP and TAZ Have Distinct Abilities to Compensate for One Another in Podocytes.Journal of the American Society of Nephrology : JASN · 2025Article
- Histone methylation modification and diabetic kidney disease: Potential molecular mechanisms and therapeutic approaches (Review).International journal of molecular medicine · 2024Review
- Morphogenesis-coupled DNA repair - in mammalian embryogenesis, morphogenesis and DNA double strand break (DSB) repair are carried out simultaneously to ensure normal development.Journal of radiation research · 2024Article
- Nucleic acid and protein methylation modification in renal diseases.Acta pharmacologica Sinica · 2024Review
- Epigenetic modification in diabetic kidney disease.Frontiers in endocrinology · 2023Review
- Histone modification in podocyte injury of diabetic nephropathy.Journal of molecular medicine (Berlin, Germany) · 2022Review
- The genomic stability regulator PTIP is required for proper chromosome segregation in mitosis.Cell division · 2022Article
- The Role of Histone H3 Methylation in Acute Kidney Injury.Drug design, development and therapy · 2022Review
- Whole Exome Sequencing in a Population With Severe Congenital Anomalies of Kidney and Urinary Tract.Frontiers in pediatrics · 2022Article
- H3K4 Methylation in Aging and Metabolism.Epigenomes · 2021Review
- DACH1 protects podocytes from experimental diabetic injury and modulates PTIP-H3K4Me3 activity.The Journal of clinical investigation · 2021Article
- Regeneration after acute kidney injury requires PTIP-mediated epigenetic modifications.JCI insight · 2020Article
- Dysregulated expression but redundant function of the long non-coding RNA HOTAIR in diabetic kidney disease.Diabetologia · 2019Article
- A KDM6A-KLF10 reinforcing feedback mechanism aggravates diabetic podocyte dysfunction.EMBO molecular medicine · 2019Article
- Article
- Shifts in podocyte histone H3K27me3 regulate mouse and human glomerular disease.The Journal of clinical investigation · 2018Article
- Epigenetic Modification Mechanisms Involved in Inflammation and Fibrosis in Renal Pathology.Mediators of inflammation · 2018Review
- Characterization of the early molecular changes in the glomeruli of Cd151Scientific reports · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
Methylation of specific lysine residues in core histone proteins is essential for embryonic development and can impart active and inactive epigenetic marks on chromatin domains. The ubiquitous nuclear protein PTIP is encoded by the Paxip1 gene and is an essential component of a histone H3 lysine 4 (H3K4) methyltransferase complex conserved in metazoans. In order to determine if PTIP and its associated complexes are necessary for maintaining stable gene expression patterns in a terminally differentiated, non-dividing cell, we conditionally deleted PTIP in glomerular podocytes in mice. Renal development and function were not impaired in young mice. However, older animals progressively exhibited proteinuria and podocyte ultra structural defects similar to chronic glomerular disease. Loss of PTIP resulted in subtle changes in gene expression patterns prior to the onset of a renal disease phenotype. Chromatin immunoprecipitation showed a loss of PTIP binding and lower H3K4 methylation at the Ntrk3 (neurotrophic tyrosine kinase receptor, type 3) locus, whose expression was significantly reduced and whose function may be essential for podocyte foot process patterning. These data demonstrate that alterations or mutations in an epigenetic regulatory pathway can alter the phenotypes of differentiated cells and lead to a chronic disease state.
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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.