Affinage

BAZ1A

Bromodomain adjacent to zinc finger domain protein 1A · UniProt Q9NRL2

Length
1556 aa
Mass
178.7 kDa
Annotated
2026-06-09
30 papers in source corpus 22 papers cited in narrative 22 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 5/5 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

BAZ1A (ACF1/hACF1) is the large non-catalytic subunit of ISWI-family chromatin remodeling complexes ACF and CHRAC, where it associates with the SNF2H/SMARCA5 (ISWI) ATPase and synergistically enhances ATP-dependent nucleosome assembly, sliding, and spacing roughly 10-fold relative to the ATPase alone (PMID:10385622, PMID:11447119). It contributes to remodeling through distinct modules: a WAC/DDT region that binds DNA and mediates the ISWI interaction, an acidic histone-contacting region, and C-terminal PHD fingers that engage core histone domains to anchor the nucleosome substrate (PMID:12192034, PMID:15457208), and it qualitatively reprograms the SNF2H remodeling strategy by changing DNA-overhang requirements and the accessibility profile of remodeled products (PMID:16877760); its PHD finger has a non-canonical DNA-binding activity while its bromodomain binds acetylated histones weakly (PMID:29021563). Through this activity BAZ1A organizes repressive and heterochromatic chromatin: it localizes to and is required for replication of pericentromeric heterochromatin, maintains nucleosome array periodicity, and supports transcriptional silencing (PMID:12434153, PMID:14752009). In the DNA damage response, BAZ1A and SNF2H rapidly accumulate at double-strand breaks and UV lesions, where BAZ1A directly interacts with KU70 to promote KU70/80 loading and both NHEJ and HR, supports the G2/M checkpoint, and is recruited to relaxed ADP-ribosylated chromatin via DNA binding independently of its ATPase partner (PMID:21172662, PMID:21745822, PMID:38170578); its recruitment to UV lesions proceeds through a DDB2-HBO1-MLL1-H3K4me axis that delivers BAZ1A for CPD removal in global genome NER (PMID:35940372). BAZ1A also acts in gene-specific transcriptional regulation, stabilizing the VDR-N-CoR corepressor complex at nuclear-receptor target promoters (PMID:17519354) and forming a BAZ1A-E2F1-SMARCA1/5 complex that opens E2F1 promoter chromatin to drive E2F1-dependent transcription and G1/S progression [PMID:bio_10.1101_2024.11.20.624462].

Mechanistic history

Synthesis pass · year-by-year structured walk · 17 steps
  1. 1999 High

    Established that the ISWI ATPase requires a partner subunit for full activity, identifying Acf1 as the defining accessory subunit that converts the bare motor into a functional chromatin assembly machine.

    Evidence Biochemical purification and reconstitution of recombinant two-subunit ACF with in vitro chromatin assembly assays in Drosophila

    PMID:10385622

    Open questions at the time
    • Did not map which Acf1 domains confer the added activity
    • Human ortholog not yet characterized
  2. 2001 High

    Showed Acf1 not only boosts but qualitatively reprograms the ISWI motor, defining CHRAC as a discrete four-subunit complex and explaining the ~10-fold enhancement of nucleosome sliding.

    Evidence Reconstitution and in vitro nucleosome sliding assays with mass spectrometry identification of CHRAC subunits

    PMID:11447119

    Open questions at the time
    • Mechanism by which Acf1 alters directionality not structurally resolved
    • Role of CHRAC-14/16 histone-fold proteins in the activity change unclear
  3. 2000 Medium

    Defined the human complex HuCHRAC, demonstrating that the ACF/CHRAC architecture including hACF1/BAZ1A and SNF2H is conserved in humans.

    Evidence Biochemical purification of HuCHRAC with co-IP and DNA-binding assays

    PMID:10880450

    Open questions at the time
    • Single-lab purification
    • Functional remodeling activity of human complex not yet quantified here
  4. 2002 High

    Dissected the modular architecture of Acf1, assigning DNA binding to the WAC motif, ISWI interaction to the DDT domain, and histone contact to an acidic region, showing all are needed for assembly.

    Evidence Systematic deletion/point mutagenesis with DNA-binding, chromatin assembly, and ATPase assays

    PMID:12192034

    Open questions at the time
    • PHD finger role not addressed in this study
    • Structural basis of DDT-ISWI interface not resolved
  5. 2002 High

    Linked ACF1 remodeling activity to a specific in vivo process by showing it is required for replication of condensed pericentromeric heterochromatin and timely late-S progression.

    Evidence RNAi depletion with BrdU localization, flow cytometry, and SNF2H-interaction mutant in human cells

    PMID:12434153

    Open questions at the time
    • How remodeling facilitates fork progression through heterochromatin not defined
    • No direct replication-factor interaction mapped
  6. 2004 High

    Identified the PHD fingers as a substrate-recognition module that contacts core histones and is required for efficient nucleosome mobilization.

    Evidence Domain deletion, zinc chelation, and in vitro nucleosome mobilization/binding assays

    PMID:15457208

    Open questions at the time
    • Histone surface contacted not pinpointed at residue level
    • Did not test DNA-binding function of PHD
  7. 2004 High

    Demonstrated in vivo that ACF/CHRAC promotes formation of repressive chromatin, regularizing nucleosome spacing and supporting heterochromatic and Polycomb silencing.

    Evidence Drosophila Acf1 null genetics, MNase nucleosome ladders, position-effect variegation, and nap1 epistasis

    PMID:14752009

    Open questions at the time
    • Direct targets of silencing not mapped genome-wide
    • Relationship to mammalian heterochromatin not established here
  8. 2006 High

    Showed human ACF1 changes the remodeling strategy of SNF2h, altering DNA-overhang requirements and product accessibility, providing the biochemical basis for spacing efficiency.

    Evidence Reconstituted hACF with defined-overhang nucleosome substrates and restriction-accessibility assays

    PMID:16877760

    Open questions at the time
    • Single-lab study
    • Structural mechanism of strategy switch unresolved
  9. 2007 Medium

    Extended BAZ1A function beyond remodeling to gene-specific repression by showing it stabilizes the VDR-N-CoR corepressor complex at hormone-responsive promoters.

    Evidence Yeast two-hybrid, ChIP, RNAi, and histone-modification analysis at IGFBP3/RANKL

    PMID:17519354

    Open questions at the time
    • Direct vs SNF2H-dependent recruitment not separated
    • Generality across nuclear receptors untested
  10. 2008 Medium

    Connected ACF1/ISWI to developmental signaling by showing they repress Wnt targets via TCF chromatin binding and antagonism of H4 acetylation.

    Evidence Drosophila RNAi, ChIP, reporter and histone-acetylation assays

    PMID:18786525

    Open questions at the time
    • Mammalian conservation of Wnt regulation untested
    • Mechanism linking remodeling to H4 acetylation unclear
  11. 2010 High

    Placed BAZ1A directly in DSB repair by identifying a direct KU70 interaction that drives KU70/80 loading and promotes both NHEJ and HR.

    Evidence Reciprocal co-IP, laser microirradiation live imaging, RNAi with NHEJ/HR reporters and clonogenic survival

    PMID:21172662

    Open questions at the time
    • How a single factor supports both NHEJ and HR not mechanistically resolved
    • Remodeling vs scaffolding contribution at breaks not separated
  12. 2011 Medium

    Showed BAZ1A is required for the G2/M checkpoint and genome stability under replication stress, linking its damage role to cell-cycle control.

    Evidence RNAi depletion with checkpoint, gammaH2AX/CHK2 phosphorylation, apoptosis, and chromosome-break readouts

    PMID:21745822

    Open questions at the time
    • Direct checkpoint-kinase connection not defined
    • Single-lab study
  13. 2017 High

    Provided structural basis for BAZ1A's non-canonical reader modules, showing its PHD binds DNA and its bromodomain binds acetyl-histones weakly, both required for ISWI loading at lesions.

    Evidence Crystal structures, CRISPR-engineered mutants, in vitro binding, and cell survival assays

    PMID:29021563

    Open questions at the time
    • Endogenous chromatin marks read at lesions not defined
    • Relative contributions of PHD-DNA vs bromodomain not quantified in vivo
  14. 2022 Medium

    Defined the recruitment pathway for BAZ1A at UV lesions, placing it downstream of a DDB2-HBO1-MLL1-H3K4me axis required for CPD removal in global genome NER.

    Evidence ChIP, immunofluorescence at UV sites, RNAi epistasis, and CPD removal assay

    PMID:35940372

    Open questions at the time
    • Direct H3K4me-BAZ1A reading not shown biochemically
    • Step at which BAZ1A acts in NER unresolved
  15. 2024 Medium

    Showed BAZ1A and SMARCA5 are recruited to breaks independently of each other via DNA binding at relaxed ADP-ribosylated chromatin, decoupling BAZ1A recruitment from its ATPase partner.

    Evidence Live-cell imaging, laser microirradiation, ADP-ribosylation inhibitors, FRAP, and domain mutants

    PMID:38170578

    Open questions at the time
    • Whether independent recruitment produces functional complexes at breaks unclear
    • Single-lab study
  16. 2024 Medium

    Identified a transcription-activating role for BAZ1A in a BAZ1A-E2F1-SMARCA1/5 complex that opens E2F1 promoter chromatin to drive E2F1-dependent transcription and cell-cycle progression.

    Evidence Co-IP, ChIP-ReChIP co-occupancy, DNaseI sensitivity, RNAi, RNA-seq, and orthotopic xenograft (preprint)

    PMID:bio_10.1101_2024.11.20.624462

    Open questions at the time
    • Preprint, not peer-reviewed
    • How a repressive remodeler activates here mechanistically unclear
  17. 2025 Medium

    Identified USP10 as a deubiquitinase that stabilizes BAZ1A, which complexes with SOX2 to drive enhancer-promoter looping and BRD4 recruitment in cancer stem cells.

    Evidence Co-IP, ubiquitination assay, and ChIP in head and neck squamous cell carcinoma

    PMID:40204721

    Open questions at the time
    • Direct vs indirect SOX2/BRD4 association not fully separated
    • Single-lab, disease-specific context

Open questions

Synthesis pass · forward-looking unresolved questions
  • How BAZ1A switches between its core repressive/heterochromatin-organizing remodeling role and its context-specific transcription-activating and germline/metabolic functions, and what selects between its many partners, remains unresolved.
  • No unifying model integrating remodeling, DDR, and gene-specific roles
  • Post-translational control (lactylation, deubiquitination) of partner choice uncharacterized
  • Mammalian heterochromatin/germline functions lack mechanistic depth

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0098772 molecular function regulator activity 3 GO:0003677 DNA binding 2 GO:0140110 transcription regulator activity 2 GO:0042393 histone binding 1 GO:0060090 molecular adaptor activity 1
Localization
GO:0000228 nuclear chromosome 2 GO:0005634 nucleus 2 GO:0005694 chromosome 2
Pathway
R-HSA-4839726 Chromatin organization 4 R-HSA-73894 DNA Repair 3 R-HSA-1640170 Cell Cycle 2 R-HSA-74160 Gene expression (Transcription) 2 R-HSA-69306 DNA Replication 1
Partners
E2F1KU70NCOR1SMARCA1SMARCA5SOX2USP10
Complex memberships
ACFCHRAC

Evidence

Reading pass · 22 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1999 ACF consists of two subunits, Acf1 (Drosophila ortholog of BAZ1A) and ISWI, that function synergistically in ATP-dependent chromatin assembly; ISWI alone has ~3% of ACF activity, indicating Acf1 confers additional functionality to the ISWI motor. Acf1 contains two PHD fingers, one bromodomain, and WAC/DDT conserved regions. Biochemical purification, reconstitution of recombinant two-subunit complex, in vitro chromatin assembly assay Genes & development High 10385622
2001 Acf1 (Drosophila BAZ1A ortholog) is the p175 subunit of CHRAC; its interaction with ISWI enhances nucleosome sliding efficiency ~10-fold and qualitatively modulates ISWI by altering directionality of nucleosome movements and histone tail requirements. CHRAC is molecularly defined as ISWI, Acf1, CHRAC-14, and CHRAC-16. Biochemical purification, reconstitution, in vitro nucleosome sliding assay, mass spectrometry identification The EMBO journal High 11447119
2002 ACF1-SNF2H (ISWI) complex specifically localizes to replicating pericentromeric heterochromatin; RNAi depletion of ACF1 specifically impairs replication of pericentromeric heterochromatin and delays cell-cycle progression through late S phase. An ACF1 mutant unable to interact with SNF2H also interferes with condensed chromatin replication. RNAi depletion, BrdU incorporation/immunofluorescence localization, flow cytometry cell-cycle analysis, domain mutant expression Nature genetics High 12434153
2002 Acf1 (Drosophila BAZ1A ortholog) binds DNA through a WAC motif in its N-terminus; interacts with ISWI through a DDT domain; an acidic region likely contacts histones during deposition. All three regions are required for full chromatin assembly activity of ACF. Systematic deletion/point mutagenesis of Acf1 domains, DNA-binding assays, in vitro chromatin assembly assay, ATPase assay Molecular and cellular biology High 12192034
2000 Human ACF1 (hACF1/BAZ1A) is a subunit of human CHRAC (HuCHRAC), which also contains SNF2H (ISWI isoform) and two histone-fold proteins (human orthologs of CHRAC-14/16). The two small histone-fold proteins form a stable sub-complex that binds naked DNA but not nucleosomes. Biochemical purification of HuCHRAC, co-purification/co-immunoprecipitation, DNA binding assay The EMBO journal Medium 10880450
2004 Deletion of the C-terminal PHD finger modules of ACF1 (Drosophila BAZ1A ortholog), or their disruption by zinc chelation, profoundly reduces nucleosome mobilization by associated ISWI. PHD fingers of ACF1 interact with core histone central domains, contributing to ACF nucleosome substrate binding. Domain deletion mutagenesis, in vitro nucleosome mobilization assay, zinc chelation, nucleosome binding assay The EMBO journal High 15457208
2004 Loss of Acf1 (Drosophila BAZ1A ortholog) in vivo decreases periodicity and repeat length of nucleosome arrays in bulk chromatin, compromises transcriptional silencing in pericentric heterochromatin and Polycomb-dependent repression, and accelerates S-phase progression. ACF/CHRAC promotes formation (not disruption) of repressive chromatin in vivo. Genetic interaction with nap1 (NAP-1 histone chaperone) confirmed. Drosophila Acf1 null genetics, micrococcal nuclease nucleosome ladder analysis, position effect variegation assay, flow cytometry, genetic epistasis with nap1 Genes & development High 14752009
2006 Human ACF1 (hACF1/BAZ1A) alters the remodeling strategy of SNF2h: it changes the DNA overhang requirement for nucleosome remodeling and alters the DNA accessibility profile of remodeled products, likely contributing to nucleosome spacing efficiency. Reconstitution of hACF complex, in vitro nucleosome remodeling assay with defined DNA overhang substrates, restriction enzyme accessibility assay The Journal of biological chemistry High 16877760
2007 Human Acf1 (BAZ1A) interacts with nuclear receptor corepressor N-CoR (identified by yeast two-hybrid); hAcf1 is required for stabilizing the VDR-N-CoR repression complex at target gene promoters (IGFBP3, RANKL). Hormone (vitamin D3) treatment releases hAcf1 from target promoters, and hAcf1 depletion alters histone modification profiles (H3/H4) and histone occupancy at these genes. Yeast two-hybrid, ChIP, RNAi knockdown, histone modification analysis Molecular endocrinology Medium 17519354
2008 ACF1 (Drosophila BAZ1A ortholog) and ISWI are required for basal repression of Wingless/Wnt target genes in Drosophila; ISWI localizes to Wg target gene chromatin at TCF binding sites while ACF1 distributes more broadly in a manner dependent on ISWI; they are required for TCF binding to chromatin and repress targets by antagonizing histone H4 acetylation. Wingless signaling reduces ACF1 binding to Wg target loci. Drosophila genetics (RNAi), ChIP, reporter assays, histone acetylation analysis Developmental biology Medium 18786525
2010 ACF1 (BAZ1A) and SNF2H rapidly accumulate at DNA double-strand breaks (DSBs) and are required for DSB repair in human cells. ACF1 directly interacts with KU70 and is required for KU70/80 accumulation at DSBs. The CHRAC complex (ACF1, SNF2H, CHRAC15, CHRAC17) becomes more associated with chromatin after DSB-inducing treatments. Depletion of either ACF1 or SNF2H significantly reduces both NHEJ and HR frequencies. Co-immunoprecipitation, laser microirradiation with live-cell imaging, RNAi knockdown, NHEJ/HR reporter assays, clonogenic survival Molecular cell High 21172662
2011 hACF1 (BAZ1A) and SNF2H accumulate at laser-induced DNA damage sites; depletion of hACF1 compromises the G2/M checkpoint activated by UV and X-rays, reduces γH2AX and CHK2 phosphorylation signals, increases apoptosis, and causes cells to enter mitosis despite unresolved replication stress lesions (aphidicolin model), resulting in metaphase chromosome breaks. RNAi depletion, laser microirradiation/immunofluorescence, flow cytometry (cell cycle), γH2AX/CHK2ph immunofluorescence, clonogenic survival Nucleic acids research Medium 21745822
2017 The PHD domain of BAZ1A (but not BAZ1B) has the non-canonical function of binding DNA. The BAZ1A bromodomain has a non-canonical gatekeeper residue and binds acetylated histone peptides relatively weakly. Both BAZ1A and BAZ1B recruit SMARCA5 to sites of DNA damage; structure-designed bromodomain and PHD mutants impair DNA damage recovery by disrupting ISWI factor loading at lesions. CRISPR-Cas9 genome editing, crystal structure determination, in vitro binding assays (DNA and acetyl-histone peptide), cell survival assays, structure-based mutagenesis Nature communications High 29021563
2016 ACF1 expression is under strict developmental control in Drosophila, persisting at high levels in undifferentiated cells (germ cell precursors, larval neuroblasts); constitutive expression is lethal. Cell-specific ectopic ACF1 expression perturbs chromatin organization. ACF1-containing factors are involved in the initial establishment of heterochromatin structures during development. Immunostaining, transgenic expression, developmental staging, chromatin organization analysis Development Medium 20843858
2022 BAZ1A/ACF1 is recruited to UV-damaged chromatin in an MLL1-dependent manner: HBO1 interacts with DDB2 at UV lesions, maintains phosphorylated MLL1 at those sites, and MLL1 catalyzes H3K4 methylation that recruits BAZ1A. Depletion of MLL1 suppresses BAZ1A accumulation at UV-irradiated sites and inhibits CPD removal, placing BAZ1A downstream of the DDB2-HBO1-MLL1 axis in global genome NER. ChIP, immunofluorescence at UV-irradiated sites, RNAi depletion, CPD removal assay Biochimica et biophysica acta. Molecular cell research Medium 35940372
2024 ACF1 (BAZ1A) and SMARCA5 each accumulate at DNA breaks independently of each other in an ADP-ribosylation-dependent manner; their recruitment is not due to direct binding to ADP-ribose moieties but is facilitated by DNA binding at relaxed (ADP-ribosylated) chromatin. Live-cell imaging, laser microirradiation, ADP-ribosylation inhibitors, FRAP, domain mutant analysis Molecular biology of the cell Medium 38170578
2019 BAZ1A knockdown induces cellular senescence phenotypes; mechanistically, BAZ1A depletion upregulates SMAD3, which in turn activates transcription of the p21-encoding gene CDKN1A, causing senescence-associated phenotypes in human cancer cells. shRNA knockdown, SA-β-Gal staining, EdU incorporation, CCK-8 assay, gene expression analysis Life sciences Low 31085244
2025 USP10 physically interacts with BAZ1A, deubiquitinates it, and stabilizes BAZ1A protein levels. BAZ1A complexes with SOX2 to drive enhancer-promoter interactions and recruit BRD4, thereby activating cancer stem cell-related gene expression programs in head and neck squamous cell carcinoma. Co-immunoprecipitation, ubiquitination assay, chromatin immunoprecipitation (ChIP), gene expression analysis Cell death & disease Medium 40204721
2024 BAZ1A interacts with E2F1; BAZ1A, E2F1, and SMARCA1/5 form a complex that binds the E2F1 promoter. BAZ1A depletion reduces DNaseI sensitivity at E2F1 binding regions of the E2F1 promoter and reduces E2F1-dependent transcription, leading to G1-phase arrest. ChIP-ReChIP confirmed co-occupancy of BAZ1A-bound chromatin by E2F1 at specific E2F1 promoter sites. Co-immunoprecipitation, ChIP, ChIP-ReChIP, DNaseI sensitivity assay, RNAi knockdown, RNA-seq, orthotopic xenograft bioRxivpreprint Medium bio_10.1101_2024.11.20.624462
2022 BAZ1A localizes to heterochromatin during spermatogenesis and interacts with DICER and major satellite repeat (MSR) chromatin in mouse testes, suggesting a role in heterochromatin regulation in the male germline. Immunofluorescence, co-immunoprecipitation, ChIP in mouse testis Reproduction Low 36194437
2026 NAA20 interacts with ACF1 (BAZ1A), promotes its lactylation (enhanced by lactate), and this modification drives nuclear translocation of ACF1. Lactylated ACF1 increases H3K27ac and H3K4me3 at the GCLM promoter, recruiting Myc and activating GCLM-dependent glutathione synthesis in neuroblastoma. Co-immunoprecipitation, chromatin immunoprecipitation (ChIP), luciferase assay, immunofluorescence, RNAi knockdown, xenograft models Cell biology and toxicology Low 41644856
2025 In yeast, the WAC-downWAC module (N-terminal region of Itc1, the BAZ1A ortholog) forms a conserved structural module predicted to interact with DNA; deletion of this module abolishes ISW2 complex function at target genes (nucleosome positioning at +1 positions) without affecting global nucleosome organization, functionally equivalent to a null allele. Yeast genetics, genome-wide nucleosome mapping (MNase-seq), structural prediction, growth assays bioRxivpreprint Medium bio_10.1101_2025.04.27.650761

Source papers

Stage 0 corpus · 30 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
1999 ACF consists of two subunits, Acf1 and ISWI, that function cooperatively in the ATP-dependent catalysis of chromatin assembly. Genes & development 277 10385622
2002 An ACF1-ISWI chromatin-remodeling complex is required for DNA replication through heterochromatin. Nature genetics 250 12434153
2000 HuCHRAC, a human ISWI chromatin remodelling complex contains hACF1 and two novel histone-fold proteins. The EMBO journal 184 10880450
2010 The ACF1 complex is required for DNA double-strand break repair in human cells. Molecular cell 171 21172662
2004 Acf1 confers unique activities to ACF/CHRAC and promotes the formation rather than disruption of chromatin in vivo. Genes & development 146 14752009
2001 Acf1, the largest subunit of CHRAC, regulates ISWI-induced nucleosome remodelling. The EMBO journal 121 11447119
2004 ACF1 improves the effectiveness of nucleosome mobilization by ISWI through PHD-histone contacts. The EMBO journal 91 15457208
2011 Role for hACF1 in the G2/M damage checkpoint. Nucleic acids research 60 21745822
2006 Human ACF1 alters the remodeling strategy of SNF2h. The Journal of biological chemistry 57 16877760
2002 Binding of Acf1 to DNA involves a WAC motif and is important for ACF-mediated chromatin assembly. Molecular and cellular biology 52 12192034
2016 A Role for the Chromatin-Remodeling Factor BAZ1A in Neurodevelopment. Human mutation 33 27328812
2008 The chromatin remodelers ISWI and ACF1 directly repress Wingless transcriptional targets. Developmental biology 31 18786525
2017 Non-canonical reader modules of BAZ1A promote recovery from DNA damage. Nature communications 24 29021563
2007 Novel regulatory role for human Acf1 in transcriptional repression of vitamin D3 receptor-regulated genes. Molecular endocrinology (Baltimore, Md.) 21 17519354
2023 African American Prostate Cancer Displays Quantitatively Distinct Vitamin D Receptor Cistrome-transcriptome Relationships Regulated by BAZ1A. Cancer research communications 19 37082578
2010 Developmental role for ACF1-containing nucleosome remodellers in chromatin organisation. Development (Cambridge, England) 19 20843858
2018 Exome sequencing in syndromic brain malformations identifies novel mutations in ACTB, and SLC9A6, and suggests BAZ1A as a new candidate gene. Birth defects research 18 29388391
2019 Chromatin remodeling factor BAZ1A regulates cellular senescence in both cancer and normal cells. Life sciences 17 31085244
2016 A role for tuned levels of nucleosome remodeler subunit ACF1 during Drosophila oogenesis. Developmental biology 11 26851213
2022 Chromatin-remodeling factor BAZ1A/ACF1 targets UV damage sites in an MLL1-dependent manner to facilitate nucleotide excision repair. Biochimica et biophysica acta. Molecular cell research 10 35940372
2010 Adjuvant properties of AcF1, an immunostimulant fraction of Alchornea cordifolia extract. Immunological investigations 7 20136620
1979 Linkage of the locus for conversion of albumin (Acf-1) in the house mouse, Mus musculus. Biochemical genetics 7 454356
2025 USP10 stabilizes BAZ1A to drive tumor stemness via an epigenetic mechanism in head and neck squamous cell carcinoma. Cell death & disease 6 40204721
2020 Discovery of BAZ1A bromodomain inhibitors with the aid of virtual screening and activity evaluation. Bioorganic & medicinal chemistry letters 6 33333161
2024 The recruitment of ACF1 and SMARCA5 to DNA lesions relies on ADP-ribosylation dependent chromatin unfolding. Molecular biology of the cell 4 38170578
2024 Alternative splicing of BAZ1A in colorectal cancer disrupts the DNA damage response and increases chemosensitization. Cell death & disease 4 39112459
2022 Chromatin remodelers HELLS, WDHD1 and BAZ1A are dynamically expressed during mouse spermatogenesis. Reproduction (Cambridge, England) 4 36194437
2015 Backbone and side-chain NMR assignments for the bromodomain of mouse BAZ1A (ACF1). Biomolecular NMR assignments 1 26542424
2026 NAA20-mediated ACF1 lactylation drives neuroblastoma progression through enhancing GCLM-dependent glutathione synthesis. Cell biology and toxicology 0 41644856
2026 A regulatory role of novel long non-coding RNA, BAZ1A-AS1, in vascular smooth muscle cell functions during neointima formation in human saphenous veins. bioRxiv : the preprint server for biology 0 41676513

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