ArticleNature communications2016
Yap is required for ependymal integrity and is suppressed in LPA-induced hydrocephalus.
Article in Nature communications, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 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.
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Who cites it
65 citing papers in PubMed, 122 citations in OpenAlex.
- Hippo-YAP/TAZ signalling at the crossroads of brain ageing and neurological disorders: mechanisms, crosstalk, and therapeutic prospects.Biogerontology · 2026Review
- Molecular signatures and lineage diversification of neurogenic and gliogenic radial glia in the gyrencephalic ferret cortex.Communications biology · 2026Article
- Yap1 regulates motility and vertebral development and prevents kyphoscoliosis in zebrafish.PLoS genetics · 2026Article
- Integrated ERK-PKA-YAP/TAZ-SHH Signaling Orchestrates Cortical Radial Glia Identity and Lineage Diversification.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Molecular signatures and lineage diversification of neurogenic and gliogenic radial glia in the gyrencephalic ferret cortex.Research square · 2025Article
- Article
- Galectin-3 induces neurodevelopmental apical-basal polarity and regulates gyrification.Science advances · 2025Article
- TEAD switches interacting partners along neural progenitor lineage progression to execute distinct functions.Genes & development · 2025Article
- IFN-γ signaling links ventriculomegaly to choroid plexus and ependyma dysfunction following maternal immune activation.Journal of neuroinflammation · 2025Article
- The Hippo effector TEAD1 regulates postnatal murine cerebellar development.Brain structure & function · 2025Article
- YAP Signaling in Glia: Pivotal Roles in Neurological Development, Regeneration and Diseases.Neuroscience bulletin · 2025Review
- RGS22 maintains the physiological function of ependymal cells to prevent hydrocephalus.Science China. Life sciences · 2025Article
- YAP/TAZ-associated cell signaling - at the crossroads of cancer and neurodevelopmental disorders.Frontiers in cell and developmental biology · 2025Review
- Review
- Multiciliated ependymal cells: an update on biology and pathology in the adult brain.Acta neuropathologica · 2024Review
- Cerebral furin deficiency causes hydrocephalus in mice.Genes & diseases · 2024Article
- LIPH contributes to glycolytic phenotype in pancreatic ductal adenocarcinoma by activating LPA/LPAR axis and maintaining ALDOA stability.Journal of translational medicine · 2023Article
- The transcriptional co-activator Yap1 promotes adult hippocampal neural stem cell activation.The EMBO journal · 2023Article
- Single-nucleus multiregion transcriptomic analysis of brain vasculature in Alzheimer's disease.Nature neuroscience · 2023Article
- Outcomes of the 2019 hydrocephalus association workshop, "Driving common pathways: extending insights from posthemorrhagic hydrocephalus".Fluids and barriers of the CNS · 2023Review
5 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Timely generation and normal maturation of ependymal cells along the aqueduct are critical for preventing physical blockage between the third and fourth ventricles and the development of fetal non-communicating hydrocephalus. Our study identifies Yap, the downstream effector of the evolutionarily conserved Hippo pathway, as a central regulator for generating developmentally controlled ependymal cells along the ventricular lining of the aqueduct. Yap function is necessary for proper proliferation of progenitors and apical attachment of ependymal precursor cells. Importantly, an injury signal initiated by lysophosphatidic acid (LPA), an upstream regulator of Yap that can cause fetal haemorrhagic hydrocephalus, deregulates Yap in the developing aqueduct. LPA exposure leads to the loss of N-cadherin concentrations at the apical endfeet, which can be partially restored by forced Yap expression and more efficiently by phosphomimetic Yap. These results reveal a novel function of Yap in retaining tissue junctions during normal development and after fetal brain injury.
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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.