Affinage

BAZ1B

Tyrosine-protein kinase BAZ1B · UniProt Q9UIG0

Length
1483 aa
Mass
170.9 kDa
Annotated
2026-06-09
40 papers in source corpus 20 papers cited in narrative 20 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 7/7 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

BAZ1B (WSTF) is a multifunctional chromatin regulator that serves as the indispensable, shared regulatory subunit of two distinct ATP-dependent remodeling complexes—the ISWI-type WICH (with SNF2H) and the SWI/SNF-type WINAC—coupling chromatin remodeling to replication, transcription, and the DNA damage response (PMID:19470456, PMID:16252006, PMID:11980720). Within WICH, BAZ1B binds PCNA and localizes to replication foci, where it maintains chromatin accessibility on newly replicated DNA and contributes to post-replication heterochromatin maturation, including transient association with the inactive X chromosome (PMID:15753658, PMID:23166813); it also assembles into the larger B-WICH complex with nuclear myosin 1 and other factors to promote RNA Pol I and Pol III transcription of rDNA and 5S/7SL genes (PMID:16514417, PMID:16603771). BAZ1B carries an atypical intrinsic tyrosine kinase activity—housed in a domain unrelated to canonical kinase folds—that phosphorylates H2A.X on Tyr142 to regulate the DNA damage response, and this mark, dynamically removed by EYA phosphatases and re-deposited by BAZ1B, governs transcription-coupled homologous recombination (PMID:19092802, PMID:31045206). Its bromodomain reads acetylated histones to dock WINAC on chromatin and direct nuclear-receptor-mediated transcription, including VDR-dependent regulation of CYP19A1 (PMID:16252006, PMID:23085504). BAZ1B occupies active loci alongside ASH2L and CBP to maintain H3K4me2 and histone acetylation and restrain Polycomb and Wnt/β-catenin signaling, and its haploinsufficiency dysregulates neurogenic and neural-crest transcriptional programs through aberrant Wnt activation (PMID:42258541, PMID:26755828, PMID:31840056). BAZ1B also acts at the mitotic chromosome scaffold to time chromosome condensation (PMID:30266865), interacts with ATAD5 to prevent premature de-ubiquitination of PCNA after oxidative damage (PMID:39627214), and during chronic inflammation is exported and degraded via nuclear ATG8 interaction, opening chromatin over NF-κB-driven inflammatory genes (PMID:40604282). BAZ1B activity is tuned by MOF-mediated K426 acetylation and SIRT1 deacetylation (PMID:32518374).

Mechanistic history

Synthesis pass · year-by-year structured walk · 15 steps
  1. 2002 High

    Established BAZ1B as the targeting subunit of a defined ISWI-family remodeling complex, answering what biochemical machine WSTF operates within.

    Evidence Biochemical purification of WICH from Xenopus extract, Co-IP with SNF2H, in vitro nucleosome spacing assay, and IF at pericentric heterochromatin

    PMID:11980720

    Open questions at the time
    • Did not define the in vivo essentiality of the complex
    • Did not connect remodeling to a specific physiological output
  2. 2005 Medium

    Connected WICH to DNA replication by showing BAZ1B binds PCNA and maintains open chromatin on nascent DNA, framing a role in epigenetic inheritance.

    Evidence Co-IP with PCNA, IF at replication foci, and WSTF depletion with chromatin accessibility readout

    PMID:15753658

    Open questions at the time
    • Mechanism of accessibility maintenance not resolved at nucleotide resolution
    • Did not test downstream heritability of marks directly
  3. 2005 High

    Assigned a transcriptional function to the BAZ1B bromodomain as an acetyl-histone reader required to recruit WINAC for nuclear-receptor signaling.

    Evidence In vitro chromatin template assays, bromodomain-deletion mutagenesis, and dominant-negative rescue at the CYP19A1/VDR axis

    PMID:16252006

    Open questions at the time
    • Acetyl-lysine specificity of the bromodomain not fully mapped
    • Composition of WINAC not exhaustively defined here
  4. 2006 High

    Extended BAZ1B function to RNA polymerase I and III transcription as part of the larger B-WICH assembly, broadening its role beyond replication.

    Evidence Biochemical fractionation, reciprocal Co-IP with NM1/Pol I and Pol III genes, ChIP, RNAi with transcript-level readouts, and in vitro chromatin transcription

    PMID:16514417 PMID:16603771

    Open questions at the time
    • Whether remodeling versus scaffolding drives transcriptional support is unresolved
    • Direct catalytic contribution of WSTF kinase to Pol I/III not tested
  5. 2008 High

    Revealed an unprecedented intrinsic tyrosine kinase activity in BAZ1B targeting H2A.X Tyr142, defining a direct enzymatic role in the DNA damage response.

    Evidence In vitro kinase assays, active-site characterization, mutagenesis, and MS identification of the Tyr142 phosphosite

    PMID:19092802

    Open questions at the time
    • Structural basis of the atypical kinase fold not solved
    • Full substrate repertoire beyond H2A.X not defined
  6. 2009 High

    Demonstrated in vivo that BAZ1B is the obligate shared subunit of both WINAC and WICH, separating its transcriptional and replication/repair functions genetically.

    Evidence WSTF knockout mouse with cardiovascular phenotype, complex-component overexpression rescue (epistasis), MEF assays, ChIP, and PCNA Co-IP

    PMID:19470456

    Open questions at the time
    • Tissue-specific division of the two complexes not mapped
    • Relative contribution of kinase activity to the knockout phenotype not isolated
  7. 2012 Medium

    Placed BAZ1B temporally at the replicating inactive X and at the CYP19A1 promoter, refining its roles in heterochromatin maturation and nuclear-receptor-regulated transcription.

    Evidence IF with cell-cycle staging on Xi; ChIP/Re-ChIP and siRNA with aromatase activity readouts at CYP19A1

    PMID:23085504 PMID:23166813

    Open questions at the time
    • Causal role of Xi association in silencing not established
    • How ligand triggers WSTF promoter dissociation is unknown
  8. 2016 High

    Linked BAZ1B dosage to developmental gene programs and oncogenic signaling, connecting chromatin function to neurogenesis and tumor phenotypes.

    Evidence ChIP-seq/RNA-seq in patient-derived neurons with Wnt-inhibitor rescue; overexpression/knockdown with PI3K/STAT3 inhibitor rescue and xenografts in lung cancer

    PMID:26755828 PMID:27449264

    Open questions at the time
    • Direct versus indirect control of Wnt target genes not fully separated
    • Whether oncogenic signaling depends on remodeling or kinase activity unclear
  9. 2018 Medium

    Identified a mitotic role for BAZ1B at the chromosome scaffold controlling condensation timing, distinct from its interphase chromatin functions.

    Evidence Quantitative proteomics of mitotic chromosome scaffold and CRISPR knockout with live-cell imaging in DT40 cells, aggravated by BAZ1A co-deletion

    PMID:30266865

    Open questions at the time
    • Molecular target on the axis not identified
    • Whether SNF2H is required for this role untested
  10. 2019 Medium

    Resolved how the H2AX-pTyr142 mark is dynamically regulated to switch between transcription and transcription-coupled homologous recombination at lesions.

    Evidence Co-IP of pTyr142-H2AX with RNAPII, ATM inhibition, EYA1/3 and WSTF knockdown, RAD51/RPA32 ChIP, and HR reporter assays; plus iPSC-NCSC functional dissection of neural-crest circuits

    PMID:31045206 PMID:31840056

    Open questions at the time
    • Direct demonstration of RNA template use during TC-HR incomplete
    • Kinetics of WSTF translocation to lesions not fully defined
  11. 2015 Medium

    Showed context dependence of BAZ1B function by demonstrating it is dispensable for H2AX Tyr142 phosphorylation in meiotic sex chromosome silencing despite its somatic kinase role.

    Evidence Conditional BAZ1B knockout in mouse spermatocytes with IF for pTyr142/γH2AX, fertility assays, and SMARCA5 localization

    PMID:25979708

    Open questions at the time
    • Identity of the compensating meiotic kinase unknown
    • Mechanism of the early-pachytene ectopic γH2AX phenotype unresolved
  12. 2020 Medium

    Defined an acetylation switch controlling BAZ1B activity, showing post-translational tuning of its kinase and transcriptional functions.

    Evidence MS site mapping of K426, in vitro/in vivo acetylation with MOF/SIRT1, MSL1v1-bridged Co-IP, K426R mutagenesis, and proliferation/invasion assays

    PMID:32518374

    Open questions at the time
    • How K426 acetylation mechanistically promotes Ser158 phosphorylation unclear
    • In vivo physiological context of the switch not established
  13. 2024 High

    Identified the BAZ1B–ATAD5 interaction as a mechanism protecting mono-ubiquitinated PCNA from premature de-ubiquitination after oxidative damage.

    Evidence Reciprocal Co-IP, domain mapping (overlap with UAF1-binding region), binding-deficient ATAD5 mutants, Ub-PCNA de-ubiquitination kinetics, and oxidative stress survival assays

    PMID:39627214

    Open questions at the time
    • Whether WICH remodeling is required for this protective role untested
    • Structural detail of the competition with UAF1 not resolved
  14. 2025 High

    Established a nuclear autophagy mechanism whereby ATG8-mediated degradation of BAZ1B opens inflammatory chromatin during chronic inflammation, with therapeutic implications.

    Evidence Co-IP with ATG8 family, nuclear fractionation, autophagy flux assays, KO/KD models, ATAC-seq, NF-κB reporter, MASH/osteoarthritis mouse models, and cell-penetrating peptide inhibitor rescue

    PMID:40604282

    Open questions at the time
    • Trigger that converts acute to chronic ATG8 engagement not defined
    • Whether kinase or remodeling activity of retained WSTF restrains inflammation untested
  15. 2026 Medium

    Mapped BAZ1B's co-activator partnership and active-mark maintenance at transcribed loci, explaining isoform switching and Wnt de-repression upon its loss.

    Evidence CUT&RUN, transcriptome and histone PTM profiling, and locus-specific ChIP at TCF7L2 in WSTF knockout HCT116 cells

    PMID:42258541

    Open questions at the time
    • Whether ASH2L/CBP recruitment is direct or via remodeling unresolved
    • Generality of isoform switching beyond profiled loci unclear

Open questions

Synthesis pass · forward-looking unresolved questions
  • How BAZ1B's distinct enzymatic (tyrosine kinase) and remodeling (WICH/WINAC) activities are coordinately deployed and selected across replication, transcription, repair, and inflammation contexts remains unresolved.
  • No structure of the atypical kinase domain
  • No unified model linking activity selection to upstream signals
  • Direct ubiquitin-ligase role toward P21 rests on single low-confidence evidence (idx 19)

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0140110 transcription regulator activity 3 GO:0140657 ATP-dependent activity 3 GO:0140096 catalytic activity, acting on a protein 2 GO:0016740 transferase activity 1 GO:0042393 histone binding 1
Localization
GO:0005634 nucleus 3 GO:0005694 chromosome 3 GO:0005730 nucleolus 2
Pathway
R-HSA-74160 Gene expression (Transcription) 4 R-HSA-4839726 Chromatin organization 3 R-HSA-73894 DNA Repair 3 R-HSA-1266738 Developmental Biology 2 R-HSA-69306 DNA Replication 2 R-HSA-1640170 Cell Cycle 1 R-HSA-168256 Immune System 1
Partners
ASH2LATAD5CBPMOFNM1PCNASIRT1SMARCA5
Complex memberships
B-WICHWICHWINAC

Evidence

Reading pass · 20 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2008 WSTF (BAZ1B) possesses intrinsic tyrosine kinase activity through a domain with no sequence homology to any known kinase fold, and directly phosphorylates H2A.X on Tyr142, regulating the DNA damage response. In vitro kinase assay, active-site characterization, mutagenesis, mass spectrometry identification of phosphorylation site Nature High 19092802
2002 WSTF forms a two-subunit chromatin remodeling complex (WICH) with the ISWI ATPase (SNF2H in mouse, ISWI in Xenopus), purified to homogeneity; the complex catalyzes assembly of regularly spaced nucleosomal arrays in vitro and localizes to pericentric heterochromatin coincident with its replication. Biochemical purification from Xenopus egg extract, Co-IP with SNF2H in mouse cells, in vitro nucleosome assembly assay, immunofluorescence The EMBO journal High 11980720
2005 The WSTF bromodomain binds acetylated histones and is required for WINAC complex association with chromatin and ligand-induced VDR-mediated transrepression of the 1α-hydroxylase (CYP19A1) gene; a bromodomain deletion mutant acts as a dominant-negative. In vitro chromatin template assays, domain-deletion mutagenesis, dominant-negative rescue experiments The EMBO journal High 16252006
2006 The WICH complex (WSTF-SNF2h) interacts with nuclear myosin 1 (NM1) and associates with RNA polymerase I and rDNA; RNAi knockdown of WSTF reduces pre-rRNA synthesis in vivo, and antibodies to WSTF inhibit Pol I transcription on chromatin but not naked DNA. Biochemical fractionation, co-immunoprecipitation, ChIP, RNAi knockdown, in vitro transcription on chromatin templates EMBO reports High 16514417
2006 WSTF-SNF2h (WICH) is part of a larger ~3 MDa assembly called B-WICH that also contains NM1, Sf3b155, RNA helicase II/Gualpha, Myb-binding protein 1a, CSB, and the proto-oncogene Dek; WSTF-SNF2h-NM1 is associated with RNA Pol III genes (5S rRNA, 7SL), and post-transcriptional silencing of WSTF reduces these Pol III transcripts. Biochemical fractionation, co-immunoprecipitation, ChIP, RNAi knockdown with transcript-level quantification The Journal of biological chemistry Medium 16603771
2009 WSTF is an indispensable shared subunit of both WINAC (SWI/SNF-type) and WICH (ISWI-type) complexes in vivo: WSTF knockout mice show neonatal lethality with cardiovascular defects linked to impaired WINAC-dependent transcription at the Gja5 promoter, and impaired WICH-dependent SNF2H recruitment to PCNA and reduced cell survival after DNA damage—each defect rescued by overexpression of the respective complex components. WSTF knockout mouse generation, genetic rescue by complex-component overexpression (epistasis), MEF cell assays, ChIP, co-IP with PCNA Proceedings of the National Academy of Sciences of the United States of America High 19470456
2005 WSTF (within WICH) binds PCNA and localizes to replication foci; depletion of WSTF results in decreased chromatin accessibility on newly replicated DNA and global heterochromatin formation, implicating WICH in epigenetic inheritance through post-replication nucleosome remodeling. Co-IP with PCNA, immunofluorescence at replication foci, WSTF depletion with chromatin accessibility assay Cell cycle (Georgetown, Tex.) Medium 15753658
2012 WSTF (WICH complex) transiently associates with the inactive X chromosome during late S-phase coincident with Xi DNA replication, and this elevated association precedes BRCA1 and γ-H2A.X recruitment, suggesting a distinct role in heterochromatin maturation post-replication. Immunofluorescence, cell-cycle staging, sequential localization analysis on Xi PloS one Medium 23166813
2019 WSTF-generated constitutive H2AX-pTyr142 associates with RNA polymerase II and active transcription; ATM-dependent EYA1/3 phosphatases remove this mark to silence transcription at DNA damage sites; subsequent re-phosphorylation by WSTF translocating to lesions facilitates transcription-coupled homologous recombination (TC-HR) in G1, using RNAPII-dependent RNA as donor templates. Co-IP of pTyr142-H2AX with RNAPII, ATM inhibition, EYA1/3 knockdown, WSTF knockdown, RAD51/RPA32 ChIP, HR reporter assays Nucleic acids research Medium 31045206
2020 WSTF is acetylated at Lys426 by MOF acetyltransferase and deacetylated by SIRT1; MSL1v1 bridges WSTF and MOF for this acetylation. K426 acetylation promotes WSTF Ser158 phosphorylation and enhances both kinase and transcriptional regulatory activities of WSTF. Mass spectrometry identification of acetylation site, in vitro and in vivo acetylation assays with MOF/SIRT1, co-IP, mutagenesis (K426R), functional proliferation/invasion assays Oncogene Medium 32518374
2016 WSTF overexpression activates PI3K/Akt and IL-6/STAT3 oncogenic signaling pathways to promote EMT (upregulation of fibronectin, N-cadherin, Snail, Slug, Twist; downregulation of E-cadherin) and increases lung cancer cell proliferation and invasion; these effects are reversed by PI3K or STAT3 inhibitors. cDNA overexpression, shRNA knockdown, cDNA microarray, qRT-PCR, western blot for EMT markers, pharmacological inhibition, xenograft models Cellular signalling Medium 27449264
2016 BAZ1B haploinsufficiency causes transcriptional dysregulation enriched for neurogenesis and neuron differentiation genes (identified by ChIP-seq); BAZ1B loss activates Wnt signaling and impairs neurogenic commitment in neural progenitor cells, and this differentiation defect is rescued by inhibiting over-active Wnt signaling. ChIP-seq of BAZ1B targets in iPSC-derived neurons, RNA-seq of WS patient-derived neurons, BAZ1B haploinsufficiency models, Wnt inhibitor rescue Human molecular genetics High 26755828
2018 BAZ1B localizes to the mitotic chromosome axis (scaffold) and knockout of BAZ1B in chicken DT40 cells causes prophase delay due to altered chromosome condensation timing and mitosis progression errors; simultaneous knockout of BAZ1A aggravates this phenotype. Quantitative proteomics of mitotic chromosome scaffold, CRISPR/Cas9 knockout, live-cell imaging, microscopy of condensation timing Molecular & cellular proteomics : MCP Medium 30266865
2024 BAZ1B (as part of the WICH complex) interacts with ATAD5, and the BAZ1B-binding region on ATAD5 overlaps the UAF1-binding domain; BAZ1B binding to ATAD5 prevents premature de-ubiquitination of mono-ubiquitinated PCNA after oxidative DNA damage, and disruption of this interaction increases cellular sensitivity to oxidative stress. Co-IP of BAZ1B with ATAD5, domain mapping, WSTF binding-deficient ATAD5 mutants, Ub-PCNA de-ubiquitination kinetics assay, oxidative stress survival assay Nature communications High 39627214
2019 BAZ1B is a key regulator of neural crest stem cell (NCSC) induction and migration in vitro, and controls NC-specific transcriptional circuits and distal regulatory elements, as established by functional dissection in patient-derived iPSC-NCSCs from WS and atypical 7q11.23 CNV patients. iPSC differentiation to NCSC, migration assays, ChIP/ATAC-seq, transcriptome analysis in BAZ1B haploinsufficiency and overexpression patient-derived cells Science advances Medium 31840056
2025 During chronic (but not acute) inflammation, WSTF interacts with the ATG8 autophagy protein family in the nucleus, leading to WSTF nuclear export and degradation by autophagosomes/lysosomes; loss of WSTF opens chromatin over inflammatory genes and amplifies NF-κB-driven inflammation; cell-penetrating peptides blocking WSTF-ATG8 interaction suppress chronic inflammation in MASH and osteoarthritis mouse models. Co-IP of WSTF with ATG8 family members, nuclear fractionation, autophagy flux assays, WSTF knockout/knockdown, ATAC-seq, NF-κB reporter, in vivo mouse models (MASH, osteoarthritis), cell-penetrating peptide inhibitor Nature High 40604282
2015 BAZ1B (WSTF) is dispensable for H2AX Tyr142 phosphorylation on sex chromosomes during meiosis and for male fertility; conditional BAZ1B deletion in spermatocytes causes ectopic γH2AX on synapsed autosomes at early pachytene but does not affect sex chromosome silencing or SNF2H localization during meiosis—demonstrating context-dependent roles distinct from somatic cells. Conditional BAZ1B knockout in mouse spermatocytes, immunofluorescence for pTyr142/γH2AX, fertility assays, SMARCA5 localization Biology open Medium 25979708
2012 WSTF acts as a comodulator bound to the CYP19A1 (aromatase) promoter and is required for its transcriptional activity; treatment with vitamin D analog EB1089 causes WSTF dissociation from the promoter (detected by ChIP/Re-ChIP), and WSTF gene silencing reduces CYP19A1 expression and aromatase activity. ChIP, Re-ChIP, siRNA-mediated WSTF silencing, qRT-PCR, aromatase activity assay Biochimica et biophysica acta Medium 23085504
2026 WSTF localizes to promoters and gene bodies of actively transcribed loci together with co-activators ASH2L and CBP; WSTF loss depletes ASH2L/CBP at these loci, causes loss of H3K4me2 and multiple acetylation marks, gain of Polycomb components, widespread isoform switching, and activates Wnt/β-catenin signaling—with TCF7L2 showing locus-specific isoform switching due to gene-body loss of active marks. CUT&RUN chromatin profiling, transcriptome profiling, histone PTM analysis, microscopy in WSTF knockout HCT116 cells; locus-specific ChIP validation at TCF7L2 Nucleic acids research Medium 42258541
2026 BAZ1B mediates ubiquitination-dependent degradation of P21 (CDKN1A); BAZ1B knockdown suppresses this degradation, leading to P21 accumulation, cellular senescence, and trophoblast dysfunction in a 6PPD-exposure model; supplementation with Baz1b or P21 downregulation rescues placental senescence in vivo. BAZ1B knockdown/overexpression in trophoblast cells, ubiquitination assays, western blot for P21, mouse 6PPD exposure model with Baz1b rescue EBioMedicine Low 42224779

Source papers

Stage 0 corpus · 40 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2008 WSTF regulates the H2A.X DNA damage response via a novel tyrosine kinase activity. Nature 324 19092802
2002 WSTF-ISWI chromatin remodeling complex targets heterochromatic replication foci. The EMBO journal 195 11980720
2006 The chromatin remodelling complex WSTF-SNF2h interacts with nuclear myosin 1 and has a role in RNA polymerase I transcription. EMBO reports 130 16514417
2006 The WSTF-SNF2h chromatin remodeling complex interacts with several nuclear proteins in transcription. The Journal of biological chemistry 126 16603771
1998 A novel human gene, WSTF, is deleted in Williams syndrome. Genomics 93 9828126
2005 Ligand-induced transrepression by VDR through association of WSTF with acetylated histones. The EMBO journal 80 16252006
2019 Dosage analysis of the 7q11.23 Williams region identifies BAZ1B as a major human gene patterning the modern human face and underlying self-domestication. Science advances 61 31840056
2016 WSTF promotes proliferation and invasion of lung cancer cells by inducing EMT via PI3K/Akt and IL-6/STAT3 signaling pathways. Cellular signalling 51 27449264
2011 WSTF does it all: a multifunctional protein in transcription, repair, and replication. Biochemistry and cell biology = Biochimie et biologie cellulaire 49 21326359
2016 Haploinsufficiency of BAZ1B contributes to Williams syndrome through transcriptional dysregulation of neurodevelopmental pathways. Human molecular genetics 48 26755828
2009 Distinct function of 2 chromatin remodeling complexes that share a common subunit, Williams syndrome transcription factor (WSTF). Proceedings of the National Academy of Sciences of the United States of America 45 19470456
1998 Identification of the WBSCR9 gene, encoding a novel transcriptional regulator, in the Williams-Beuren syndrome deletion at 7q11.23. Cytogenetics and cell genetics 45 9858827
2005 Chromatin remodeling by WSTF-ISWI at the replication site: opening a window of opportunity for epigenetic inheritance? Cell cycle (Georgetown, Tex.) 35 15753658
2019 De novo phosphorylation of H2AX by WSTF regulates transcription-coupled homologous recombination repair. Nucleic acids research 22 31045206
2012 Vitamin D analog EB1089 inhibits aromatase expression by dissociation of comodulator WSTF from the CYP19A1 promoter-a new regulatory pathway for aromatase. Biochimica et biophysica acta 22 23085504
2022 Combinatorial targeting of a chromatin complex comprising Dot1L, menin and the tyrosine kinase BAZ1B reveals a new therapeutic vulnerability of endocrine therapy-resistant breast cancer. Breast cancer research : BCR 19 35850772
2020 WSTF acetylation by MOF promotes WSTF activities and oncogenic functions. Oncogene 18 32518374
2018 Quantitative Proteomics of the Mitotic Chromosome Scaffold Reveals the Association of BAZ1B with Chromosomal Axes. Molecular & cellular proteomics : MCP 17 30266865
2006 Cloning and developmental expression of WSTF during Xenopus laevis embryogenesis. Gene expression patterns : GEP 16 16448863
2022 baz1b loss-of-function in zebrafish produces phenotypic alterations consistent with the domestication syndrome. iScience 15 36582821
2015 BAZ1B is dispensable for H2AX phosphorylation on Tyrosine 142 during spermatogenesis. Biology open 15 25979708
2025 WSTF nuclear autophagy regulates chronic but not acute inflammation. Nature 13 40604282
2019 K-ras-ERK1/2 down-regulates H2A.XY142ph through WSTF to promote the progress of gastric cancer. BMC cancer 13 31151422
2021 BAZ1B the Protean Protein. Genes 12 34680936
2017 Williams syndrome transcription factor (WSTF) acts as an activator of estrogen receptor signaling in breast cancer cells and the effect can be abrogated by 1α,25-dihydroxyvitamin D3. The Journal of steroid biochemistry and molecular biology 12 28610873
2012 The WSTF-ISWI chromatin remodeling complex transiently associates with the human inactive X chromosome during late S-phase prior to BRCA1 and γ-H2AX. PloS one 11 23166813
2022 Triptolide Shows High Sensitivity and Low Toxicity Against Acute Myeloid Leukemia Cell Lines Through Inhibiting WSTF-RNAPII Complex. Frontiers in oncology 10 35251980
2020 BAZ1B is a candidate gene responsible for hypothyroidism in Williams syndrome. European journal of medical genetics 10 32081709
2016 KRASG12 mutant induces the release of the WSTF/NRG3 complex, and contributes to an oncogenic paracrine signaling pathway. Oncotarget 9 27449290
2024 ATAD5-BAZ1B interaction modulates PCNA ubiquitination during DNA repair. Nature communications 7 39627214
2023 Loss of Baz1b in mice causes perinatal lethality, growth failure, and variable multi-system outcomes. Developmental biology 3 37827362
2021 Downregulation of Williams syndrome transcription factor (WSTF) suppresses glioblastoma cell growth and invasion by inhibiting PI3K/AKT signal pathway. European journal of histochemistry : EJH 3 34784707
2022 Baz1b Dosage Influences Cardiovascular Function, Predisposing to Dilated Cardiomyopathy. FASEB journal : official publication of the Federation of American Societies for Experimental Biology 2 35723872
2022 Evidence supporting the oncogenic role of BAZ1B in colorectal cancer. American journal of cancer research 2 36381331
2025 MOF promotes cisplatin resistance in lung cancer cells by enhancing WSTF acetylation. In vitro cellular & developmental biology. Animal 1 41252101
2026 WSTF-associated regulation of GLYCTK and metabolic adaptation in colorectal cancer. Frontiers in immunology 0 42112339
2026 Exposure to high doses of tyre antioxidant 6PPD causes senescence to induce unexplained miscarriage by suppressing BAZ1B-mediated ubiquitination degradation of P21. EBioMedicine 0 42224779
2026 WSTF deficiency reprograms regulatory networks by linking locus-specific chromatin remodeling to altered isoform expression and misdirected signaling. Nucleic acids research 0 42258541
2025 Targeting WSTF degradation to resolve chronic inflammation. Trends in immunology 0 40738769
2015 WITHDRAWN: WSTF Phosphorylation Specifically Links H3K9ac with H4K16ac through PCAF/WSTF/MOF Complex. The Journal of biological chemistry 0 25837249

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