ArticleNature communications2018
Phf8 histone demethylase deficiency causes cognitive impairments through the mTOR pathway.
Article in Nature communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 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
38 citing papers in PubMed, 63 citations in OpenAlex.
- Article
- Epigenetic regulation of serine biosynthesis by PHF8 during neurogenesis.EMBO reports · 2026Article
- Identification of shared gene signature between lung cancer and postoperative delirium by transcriptome data analysis.Medicine · 2026Article
- Article
- Homocysteine Metabolites, Endothelial Dysfunction, and Cardiovascular Disease.International journal of molecular sciences · 2025Review
- Discovery and structural studies of histone demethylases.Frontiers in epigenetics and epigenomics · 2025Review
- Histone Methylation, Energy Metabolism, and Alzheimer's Disease.Aging and disease · 2024Review
- The Molecular Bases of Anti-Oxidative and Anti-Inflammatory Properties of Paraoxonase 1.Antioxidants (Basel, Switzerland) · 2024Review
- PHF8 facilitates transcription recovery following DNA double-strand break repair.Nucleic acids research · 2024Article
- PHF8/KDM7B: A Versatile Histone Demethylase and Epigenetic Modifier in Nervous System Disease and Cancers.Epigenomes · 2024Review
- Homocysteine Thiolactone Detoxifying Enzymes and Alzheimer's Disease.International journal of molecular sciences · 2024Review
- Role of plant homeodomain finger protein 8 in P19 embryonic carcinoma cells revealed by genome editing and specific inhibitor.Biochemistry and biophysics reports · 2024Article
- PHF8-GLUL axis in lipid deposition and tumor growth of clear cell renal cell carcinoma.Science advances · 2023Article
- Loss of PHF8 induces a viral mimicry response by activating endogenous retrotransposons.Nature communications · 2023Article
- Cyclic peptides target the aromatic cage of a PHD-finger reader domain to modulate epigenetic protein function.Chemical science · 2023Article
- Review
- Proteomic Exploration of Paraoxonase 1 Function in Health and Disease.International journal of molecular sciences · 2023Review
- Article
- Article
- Deletion of the Homocysteine Thiolactone Detoxifying Enzyme Bleomycin Hydrolase, in Mice, Causes Memory and Neurological Deficits and Worsens Alzheimer's Disease-Related Behavioral and Biochemical Traits in the 5xFAD Model of Alzheimer's Disease.Journal of Alzheimer's disease : JAD · 2023Article
Corrections and comments
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Authors and funding
18 authors at 4 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Epigenomic abnormalities caused by genetic mutation in epigenetic regulators can result in neurodevelopmental disorders, deficiency in neural plasticity and mental retardation. As a histone demethylase, plant homeodomain finger protein 8 (Phf8) is a candidate gene for syndromal and non-specific forms of X-chromosome-linked intellectual disability (XLID). Here we report that Phf8 knockout mice displayed impaired learning and memory, and impaired hippocampal long-term potentiation (LTP) without gross morphological defects. We also show that mTOR signaling pathway is hyperactive in hippocampus in Phf8 knockout mouse. Mechanistically, we show that demethylation of H4K20me1 by Phf8 results in transcriptional suppression of RSK1 and homeostasis of mTOR signaling. Pharmacological suppression of mTOR signaling with rapamycin in Phf8 knockout mice recovers the weakened LTP and cognitive deficits. Together, our results indicate that loss of Phf8 in animals causes deficient learning and memory by epigenetic disruption of mTOR signaling, and provides a potential therapeutic drug target to treat XLID.
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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.