ArticleNature communications2017
Non-canonical reader modules of BAZ1A promote recovery from DNA damage.
Article in Nature communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.
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Who cites it
21 citing papers in PubMed, 1 synthesis or guideline pooled it, 30 citations in OpenAlex.
- Genome-wide meta-analysis across East Asian and European populations provides insights into the molecular basis of lung cancer.Genome medicine · 2026Pooled it
- Whole-genome sequencing identifies genetic diversity and adaptive signatures of hypoxia and ultraviolet radiation in Chinese chickens.Journal of advanced research · 2026Article
- Comprehensive analysis of interactions between brain aging and late-onset psychoses using heuristic mapping models.Communications medicine · 2026Article
- WSTF-associated regulation of GLYCTK and metabolic adaptation in colorectal cancer.Frontiers in immunology · 2026Article
- Proteomic discovery of DEK and NUMA1 as new players in UV-induced DNA damage repair mechanisms.Cell death discovery · 2025Article
- SMARCA5 restricts chromatin accessibility to promote male meiosis and fertility in mammals.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- ATAD5-BAZ1B interaction modulates PCNA ubiquitination during DNA repair.Nature communications · 2024Article
- Two paralogous PHD finger proteins participate in natural genome editing in Paramecium tetraurelia.Journal of cell science · 2024Article
- Alternative splicing of BAZ1A in colorectal cancer disrupts the DNA damage response and increases chemosensitization.Cell death & disease · 2024Article
- ISWI chromatin remodeling complexes recruit NSD2 and H3K36me2 in pericentromeric heterochromatin.The Journal of cell biology · 2024Article
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- Non-histone binding functions of PHD fingers.Trends in biochemical sciences · 2023Review
- Somatic mutations in single human cardiomyocytes reveal age-associated DNA damage and widespread oxidative genotoxicity.Nature aging · 2022Article
- The emerging role of ISWI chromatin remodeling complexes in cancer.Journal of experimental & clinical cancer research : CR · 2021Review
- Cellular Reprogramming and Immortality: Expression Profiling Reveals Putative Genes Involved in Turritopsis dohrnii's Life Cycle Reversal.Genome biology and evolution · 2021Article
- Detection of genes positively selected in CubanEcology and evolution · 2021Article
- BAZ2B haploinsufficiency as a cause of developmental delay, intellectual disability, and autism spectrum disorder.Human mutation · 2020Article
- Bromodomains: a new target class for drug development.Nature reviews. Drug discovery · 2019Review
- Acetylation of CCAR2 Establishes a BET/BRD9 Acetyl Switch in Response to Combined Deacetylase and Bromodomain Inhibition.Cancer research · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Members of the ISWI family of chromatin remodelers mobilize nucleosomes to control DNA accessibility and, in some cases, are required for recovery from DNA damage. However, it remains poorly understood how the non-catalytic ISWI subunits BAZ1A and BAZ1B might contact chromatin to direct the ATPase SMARCA5. Here, we find that the plant homeodomain of BAZ1A, but not that of BAZ1B, has the unusual function of binding DNA. Furthermore, the BAZ1A bromodomain has a non-canonical gatekeeper residue and binds relatively weakly to acetylated histone peptides. Using CRISPR-Cas9-mediated genome editing we find that BAZ1A and BAZ1B each recruit SMARCA5 to sites of damaged chromatin and promote survival. Genetic engineering of structure-designed bromodomain and plant homeodomain mutants reveals that reader modules of BAZ1A and BAZ1B, even when non-standard, are critical for DNA damage recovery in part by regulating ISWI factors loading at DNA lesions and supporting transcriptional programs required for survival.ISWI chromatin remodelers regulate DNA accessibility and have been implicated in DNA damage repair. Here, the authors uncover functions, in response to DNA damage, for the bromodomain of the ISWI subunit BAZ1B and for the non-canonical PHD and bromodomain modules of the paralog BAZ1A.
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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.