ArticleProceedings of the National Academy of Sciences of the United States of America2015
ATRX tolerates activity-dependent histone H3 methyl/phos switching to maintain repetitive element silencing in neurons.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 40 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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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
40 citing papers in PubMed, 61 citations in OpenAlex.
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- Structural requirements for activity of Mind bomb1 in Notch signaling.Structure (London, England : 1993) · 2024Article
- Context-specific functions of chromatin remodellers in development and disease.Nature reviews. Genetics · 2024Review
- c-Jun signaling during initial HSV-1 infection modulates latency to enhance later reactivation in addition to directly promoting the progression to full reactivation.Journal of virology · 2024Article
- Multiple Roles of dXNP and dADD1-International journal of molecular sciences · 2023Review
- c-Jun Signaling During Initial HSV-1 Infection Modulates Latency to Enhance Later Reactivation in addition to Directly Promoting the Progression to Full Reactivation.bioRxiv : the preprint server for biology · 2023Article
- The Intersection of Innate Immune Pathways with the Latent Herpes Simplex Virus Genome.Journal of virology · 2023Review
- PML-NB-dependent type I interferon memory results in a restricted form of HSV latency.EMBO reports · 2021Article
- Advances in Chromodomain Helicase DNA-Binding (CHD) Proteins Regulating Stem Cell Differentiation and Human Diseases.Frontiers in cell and developmental biology · 2021Review
- Progressive Phosphorylation Modulates the Self-Association of a Variably Modified Histone H3 Peptide.Frontiers in molecular biosciences · 2021Article
- Article
- Disruption of ATRX-RNA interactions uncovers roles in ATRX localization and PRC2 function.Nature communications · 2020Article
- Loss of the neural-specific BAF subunit ACTL6B relieves repression of early response genes and causes recessive autism.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Chromatin-enriched RNAs mark active and repressive cis-regulation: An analysis of nuclear RNA-seq.PLoS computational biology · 2020Article
- The Fate of Speckled Protein 100 (Sp100) During Herpesviruses Infection.Frontiers in cellular and infection microbiology · 2020Review
Corrections and comments
- Erratum issued
Authors and funding
9 authors at 5 institutions in 2 countries.
Funding
Abstract
ATRX (the alpha thalassemia/mental retardation syndrome X-linked protein) is a member of the switch2/sucrose nonfermentable2 (SWI2/SNF2) family of chromatin-remodeling proteins and primarily functions at heterochromatic loci via its recognition of "repressive" histone modifications [e.g., histone H3 lysine 9 tri-methylation (H3K9me3)]. Despite significant roles for ATRX during normal neural development, as well as its relationship to human disease, ATRX function in the central nervous system is not well understood. Here, we describe ATRX's ability to recognize an activity-dependent combinatorial histone modification, histone H3 lysine 9 tri-methylation/serine 10 phosphorylation (H3K9me3S10ph), in postmitotic neurons. In neurons, this "methyl/phos" switch occurs exclusively after periods of stimulation and is highly enriched at heterochromatic repeats associated with centromeres. Using a multifaceted approach, we reveal that H3K9me3S10ph-bound Atrx represses noncoding transcription of centromeric minor satellite sequences during instances of heightened activity. Our results indicate an essential interaction between ATRX and a previously uncharacterized histone modification in the central nervous system and suggest a potential role for abnormal repetitive element transcription in pathological states manifested by ATRX dysfunction.
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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.