ArticleThe Journal of cell biology2015
Histone demethylase KDM4B regulates otic vesicle invagination via epigenetic control of Dlx3 expression.
Article in The Journal of cell biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
16 citing papers in PubMed, 25 citations in OpenAlex.
- Transcriptome analysis reveals an Atoh1b-dependent gene set downstream of Dlx3b/4b during early inner ear development in zebrafish.Biology open · 2023Article
- Inhibition of histone methyltransferase PRMT5 attenuates cisplatin-induced hearing loss through the PI3K/Akt-mediated mitochondrial apoptotic pathway.Journal of pharmaceutical analysis · 2023Article
- KMT2D deficiency disturbs the proliferation and cell cycle activity of dental epithelial cell line (LS8) partially via Wnt signaling.Bioscience reports · 2021Article
- The KDM4B-CCAR1-MED1 axis is a critical regulator of osteoclast differentiation and bone homeostasis.Bone research · 2021Article
- The Diverse Roles of Histone Demethylase KDM4B in Normal and Cancer Development and Progression.Frontiers in cell and developmental biology · 2021Review
- Inhibition of Protein arginine methyltransferase 6 reduces reactive oxygen species production and attenuates aminoglycoside- and cisplatin-induced hair cell death.Theranostics · 2020Article
- Epigenetics in neuronal regeneration.Seminars in cell & developmental biology · 2020Review
- TBX1 is required for normal stria vascularis and semicircular canal development.Developmental biology · 2020Article
- Bromodomain Protein BRD4 Is Essential for Hair Cell Function and Survival.Frontiers in cell and developmental biology · 2020Article
- KDM4B: A Nail for Every Hammer?Genes · 2019Review
- CTCF Regulates Otic Neurogenesis via Histone Modification in theMolecules and cells · 2018Article
- Lsd1 interacts with cMyb to demethylate repressive histone marks and maintain inner ear progenitor identity.Development (Cambridge, England) · 2018Article
- Insights into inner ear-specific gene regulation: Epigenetics and non-coding RNAs in inner ear development and regeneration.Seminars in cell & developmental biology · 2017Review
- Spatiotemporal expression of Ezh2 in the developing mouse cochlear sensory epithelium.Frontiers of medicine · 2016Article
- The role of post-translational modifications in hearing and deafness.Cellular and molecular life sciences : CMLS · 2016Review
- The molecular basis of craniofacial placode development.Wiley interdisciplinary reviews. Developmental biologyReview
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
Abstract
In vertebrates, the inner ear arises from the otic placode, a thickened swathe of ectoderm that invaginates to form the otic vesicle. We report that histone demethylase KDM4B is dynamically expressed during early stages of chick inner ear formation. A loss of KDM4B results in defective invagination and striking morphological changes in the otic epithelium, characterized by abnormal localization of adhesion and cytoskeletal molecules and reduced expression of several inner ear markers, including Dlx3. In vivo chromatin immunoprecipitation reveals direct and dynamic occupancy of KDM4B and its target, H3K9me3, at regulatory regions of the Dlx3 locus. Accordingly, coelectroporations of DLX3 or KDM4B encoding constructs, but not a catalytically dead mutant of KDM4B, rescue the ear invagination phenotype caused by KDM4B knockdown. Moreover, a loss of DLX3 phenocopies a loss of KDM4B. Collectively, our findings suggest that KDM4B play a critical role during inner ear invagination via modulating histone methylation of the direct target Dlx3.
Indexed as
Identifiers
What OpenQuestion holds
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.