ArticleThe Journal of biological chemistry2013
Alpha thalassemia/mental retardation syndrome X-linked gene product ATRX is required for proper replication restart and cellular resistance to replication stress.
Article in The Journal of biological chemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers, 1 of them a synthesis that pooled it.
What it found
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Who cites it
69 citing papers in PubMed, 1 synthesis or guideline pooled it, 116 citations in OpenAlex.
- ATR-X syndrome: genetics, clinical spectrum, and management.Human genetics · 2021Pooled it
- ATRX loss in sarcomas is associated with dysregulated gene and transposable element expression, loss of DNA methylation, and worse survival.ESMO rare cancers · 2026Article
- ATRX loss couples genome instability at a G-rich repeat to dysregulation of human alpha-globin expression.Nature communications · 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
- ATRX loss in sarcomas is associated with dysregulated gene and transposable element expression, loss of DNA methylation, and worse survival.medRxiv : the preprint server for health sciences · 2025Article
- Integrating Structural Bioinformatics and Functional Mechanisms of Sesquiterpene Synthases CARS and CADS inInternational journal of molecular sciences · 2025Article
- ATRX cooperates with TOP2B for replication fork stability and DNA damage response through G-quadruplex regulation.Nucleic acids research · 2025Article
- Alternative Lengthening of Telomeres: The Need forInternational journal of molecular sciences · 2025Article
- ATRX ADD domain is a versatile module for recognizing macroH2A, H3, and beyond.Acta biochimica et biophysica Sinica · 2025Article
- Genetic Analysis of Osteosarcoma Cells in a 9-year-old Boy: Genes Involved in Cell Cycle Control.Acta medica academica · 2025Article
- Elevated reactive oxygen species can drive the alternative lengthening of telomeres pathway in ATRX-null cancers.Nucleic acids research · 2025Article
- ATRX loss inhibits DDR to strengthen radio-sensitization in p53-deficent HCT116 cells.Scientific reports · 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
- Knockdown of ATRX enhances radiosensitivity in glioblastoma.Chinese neurosurgical journal · 2024Article
- Article
- Mutant ATRX: pathogenesis of ATRX syndrome and cancer.Frontiers in molecular biosciences · 2024Review
- Mitotic DNA Synthesis in Untransformed Human Cells Preserves Common Fragile Site Stability via a FANCD2-Driven Mechanism That Requires HELQ.Journal of molecular biology · 2023Article
- Inhibition of p53 and ATRX increases telomeric recombination in primary fibroblasts.FEBS open bio · 2023Article
- Induction of the alternative lengthening of telomeres pathway by trapping of proteins on DNA.Nucleic acids research · 2023Article
9 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 1 institution in 1 country.
Funding
Abstract
Alpha thalassemia/mental retardation syndrome X-linked (ATRX) is a member of the SWI/SNF protein family of DNA-dependent ATPases. It functions as a chromatin remodeler and is classified as an SNF2-like helicase. Here, we showed somatic knock-out of ATRX displayed perturbed S-phase progression as well as hypersensitivity to replication stress. ATRX is recruited to sites of DNA damage, required for efficient checkpoint activation and faithful replication restart. In addition, we identified ATRX as a binding partner of MRE11-RAD50-NBS1 (MRN) complex. Together, these results suggest a non-canonical function of ATRX in guarding genomic stability.
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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.