ArticleHuman molecular genetics2011
The ATRX-ADD domain binds to H3 tail peptides and reads the combined methylation state of K4 and K9.
Article in Human molecular genetics, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 93 papers, 1 of them a synthesis that pooled it.
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Who cites it
93 citing papers in PubMed, 1 synthesis or guideline pooled it, 160 citations in OpenAlex.
- ATR-X syndrome: genetics, clinical spectrum, and management.Human genetics · 2021Pooled it
- ATRX: From Chromatin Remodeling to Disease.Genesis (New York, N.Y. : 2000) · 2025Review
- Interferon dependent immune memory during HSV-1 neuronal latency via increased H3K9me3 and restriction by ATRX.Nature communications · 2025Article
- Daxx and HIRA go viral - How chromatin remodeling complexes affect DNA virus infection.Tumour virus research · 2025Review
- ATRX ADD domain is a versatile module for recognizing macroH2A, H3, and beyond.Acta biochimica et biophysica Sinica · 2025Article
- ATRX silences Cartpt expression in osteoblastic cells during skeletal development.The Journal of clinical investigation · 2025Article
- Phosphorylation of 'SDT-like' motifs in ATRX mediates its interaction with the MRN complex and is important for ALT pathway suppression.Open biology · 2024Article
- DAXX promotes centromeric stability independently of ATRX by preventing the accumulation of R-loop-induced DNA double-stranded breaks.Nucleic acids research · 2024Article
- HIRA vs. DAXX: the two axes shaping the histone H3.3 landscape.Experimental & molecular medicine · 2024Review
- A novel variant ofSAGE open medical case reports · 2024Article
- Mutant ATRX: pathogenesis of ATRX syndrome and cancer.Frontiers in molecular biosciences · 2024Review
- Multiple Roles of dXNP and dADD1-International journal of molecular sciences · 2023Review
- Article
- DAXX adds a de novo H3.3K9me3 deposition pathway to the histone chaperone network.Molecular cell · 2023Article
- Histone Readers and Their Roles in Cancer.Cancer treatment and research · 2023Article
- Studying Chromatin Epigenetics with Fluorescence Microscopy.International journal of molecular sciences · 2022Review
- Domain Structure of the Dnmt1, Dnmt3a, and Dnmt3b DNA Methyltransferases.Advances in experimental medicine and biology · 2022Article
- Impact of Chromatin Dynamics and DNA Repair on Genomic Stability and Treatment Resistance in Pediatric High-Grade Gliomas.Cancers · 2021Review
- ATRX proximal protein associations boast roles beyond histone deposition.PLoS genetics · 2021Article
- Deletion of the XIST promoter from the human inactive X chromosome compromises polycomb heterochromatin maintenance.Chromosoma · 2021Article
33 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
8 authors at 2 institutions in 2 countries.
Funding
Abstract
Mutations in the ATRX protein are associated with the alpha-thalassemia and mental retardation X-linked syndrome (ATR-X). Almost half of the disease-causing mutations occur in its ATRX-Dnmt3-Dnmt3L (ADD) domain. By employing peptide arrays, chromatin pull-down and peptide binding assays, we show specific binding of the ADD domain to H3 histone tail peptides containing H3K9me3. Peptide binding was disrupted by the presence of the H3K4me3 and H3K4me2 modification marks indicating that the ATRX-ADD domain has a combined readout of these two important marks (absence of H3K4me2 and H3K4me3 and presence of H3K9me3). Disease-causing mutations reduced ATRX-ADD binding to H3 tail peptides. ATRX variants, which fail in the H3K9me3 interaction, show a loss of heterochromatic localization in cells, which indicates the chromatin targeting function of the ADD domain of ATRX. Disruption of H3K9me3 binding may be a general pathogenicity pathway of ATRX mutations in the ADD domain which may explain the clustering of disease mutations in this part of the ATRX protein.
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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.