ArticleNature communications2023
Systemic and intrinsic functions of ATRX in glial cell fate and CNS myelination in male mice.
Article in Nature communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 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
9 citing papers in PubMed, 10 citations in OpenAlex.
- ATRX inactivation disrupts global chromatin state and topology to dysregulate neurodevelopmental pathways in glioma pathogenesis.Nucleic acids research · 2026Article
- Altered Brain Structure in an ATRX-Deficient Mouse Model of Autism Spectrum Disorder.Autism research : official journal of the International Society for Autism Research · 2026Article
- Differences in regional developmental origins of glioblastomas revealed by integrated molecular profiling.Journal of neuro-oncology · 2026Article
- ATRX safeguards cellular identity duringbioRxiv : the preprint server for biology · 2026Article
- ATRX: From Chromatin Remodeling to Disease.Genesis (New York, N.Y. : 2000) · 2025Review
- Microglial deficiency in the ATRX chromatin remodeler elicits a viral mimicry immune response that impacts neuronal function and behavior.PLoS biology · 2025Article
- Phase separated condensates of ATRX regulate neural progenitor identity.Nature communications · 2025Article
- ATRX ADD domain is a versatile module for recognizing macroH2A, H3, and beyond.Acta biochimica et biophysica Sinica · 2025Article
- The Involvement of CSRP1 in Neuroblastoma Differentiation and Apoptosis Impacting Tumor-Suppressive Therapeutic Responses.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
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
No grant is acknowledged in the PubMed record.
Abstract
Myelin, an extension of the oligodendrocyte plasma membrane, wraps around axons to facilitate nerve conduction. Myelination is compromised in ATR-X intellectual disability syndrome patients, but the causes are unknown. We show that loss of ATRX leads to myelination deficits in male mice that are partially rectified upon systemic thyroxine administration. Targeted ATRX inactivation in either neurons or oligodendrocyte progenitor cells (OPCs) reveals OPC-intrinsic effects on myelination. OPCs lacking ATRX fail to differentiate along the oligodendrocyte lineage and acquire a more plastic state that favors astrocytic differentiation in vitro and in vivo. ATRX chromatin occupancy in OPCs greatly overlaps with that of the chromatin remodelers CHD7 and CHD8 as well as H3K27Ac, a mark of active enhancers. Overall, our data indicate that ATRX regulates the onset of myelination systemically via thyroxine, and by promoting OPC differentiation and suppressing astrogliogenesis. These functions of ATRX identified in mice could explain white matter pathogenesis observed in ATR-X syndrome patients.
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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.