Affinage

ARID3B

AT-rich interactive domain-containing protein 3B · UniProt Q8IVW6

Length
561 aa
Mass
60.6 kDa
Annotated
2026-04-28
37 papers in source corpus 19 papers cited in narrative 19 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

ARID3B is a nuclear AT-rich interaction domain (ARID) transcription factor that binds AT-rich sequence motifs at promoters and enhancers to activate diverse gene programs—including E2F cell cycle targets, p53 pro-apoptotic targets, stemness factors, and developmental regulators—thereby controlling cell survival, proliferation, and differentiation (PMID:26121572, PMID:33649863, PMID:26519881). ARID3B forms a triprotein complex with ARID3A and the histone demethylase KDM4C, reducing H3K9me3 to promote chromatin accessibility at target loci; this complex is regulated upstream by the LIN28/let-7 miRNA axis, and ARID3B nuclear confinement is governed by phosphorylation at Serine 89 (PMID:26776511, PMID:31415216, PMID:41972703). ARID3B undergoes liquid–liquid phase separation to recruit coactivators such as SMAD2/3 and establish enhancer activity, linking its biophysical properties to transcriptional activation during craniofacial development and nonsyndromic cleft lip/palate (PMID:41032419). Loss of ARID3B impairs B cell development, cardiac second heart field deployment, and apical ectodermal ridge morphogenesis, while its overexpression expands cancer stem cell populations, cooperates with MYCN in malignant transformation, and promotes chemoresistance (PMID:27537840, PMID:25336743, PMID:21307092, PMID:16951138, PMID:25327563).

Mechanistic history

Synthesis pass · year-by-year structured walk · 16 steps
  1. 1999 Medium

    Establishing ARID3B as a DNA-binding factor with links to cell differentiation: before this work, ARID3B had no known molecular function; Co-IP and DNA binding assays showed it binds hypophosphorylated pRb and the MAR element of the immunoglobulin heavy-chain locus, placing it at the intersection of chromatin architecture and differentiation gene regulation.

    Evidence Co-immunoprecipitation with pRb and MAR DNA binding assay in vitro

    PMID:10446990

    Open questions at the time
    • No reciprocal validation of the pRb interaction by independent groups
    • Functional consequence of pRb binding on transcription not tested
    • MAR binding specificity relative to other ARID family members unknown
  2. 2006 High

    Demonstrating oncogenic potential: it was unknown whether ARID3B had transforming activity; overexpression immortalized MEFs and cooperated with MYCN to induce tumors in vivo, establishing ARID3B as an oncogene with cooperative activity in malignant transformation.

    Evidence siRNA/antisense knockdown in neuroblastoma cells, MEF overexpression, and nude mouse xenograft

    PMID:16951138

    Open questions at the time
    • Mechanism of immortalization (bypass of senescence versus anti-apoptosis) not resolved
    • Identity of transcriptional targets mediating cooperation with MYCN unknown at this stage
  3. 2011 High

    Defining a developmental morphogenetic role: ARID3B's function in embryonic limb development was unexplored; loss-of-function in mouse and chick showed ARID3B is required for AER cell motility and actin cytoskeleton organization, without affecting proliferation or major signaling pathways.

    Evidence Loss-of-function constructs in mouse/chick embryos, DiI lineage tracing, phalloidin staining, motility assays

    PMID:21307092

    Open questions at the time
    • Direct transcriptional targets controlling motility in AER not identified
    • Whether ARID3B acts through the same ARID3A/KDM4C complex in this context unknown
  4. 2012 Medium

    Linking isoforms and subcellular localization to distinct functional outputs: the full-length nuclear isoform induces TNFα-mediated apoptosis by upregulating pro-apoptotic genes, whereas a short splice form lacking the C-terminal domain does not, establishing that ARID3B's nuclear transcriptional activity is required for its apoptotic function.

    Evidence Subcellular fractionation, isoform overexpression, gene expression and viability assays

    PMID:22860069

    Open questions at the time
    • Only overexpression used; endogenous isoform ratios and regulation not characterized
    • Direct DNA binding by the short isoform not tested
  5. 2012 Medium

    Connecting ARID3B to epigenetic reprogramming and stemness: ChIP demonstrated bivalent histone switching (H3K27me3 ↔ H3K4me3) at the Arid3b promoter during iPS reprogramming and neural crest differentiation, placing ARID3B within the epigenetic circuitry governing pluripotency and lineage commitment.

    Evidence ChIP for H3K27me3/H3K4me3 in mouse ES cells, iPS reprogramming, siRNA knockdown

    PMID:22751132

    Open questions at the time
    • Whether ARID3B is a cause or consequence of the histone mark switch unresolved
    • Downstream survival targets in ES cells not identified
  6. 2014 High

    Establishing a cardiac developmental requirement: conditional knockout revealed ARID3B is essential for second heart field progenitor addition and epithelial-to-mesenchymal transition in the atrioventricular canal, identifying Bhlhb2 and Lims2 as downstream targets.

    Evidence Conditional knockout mouse, DiI labeling of second heart field progenitors, RNA microarray, histology

    PMID:25336743

    Open questions at the time
    • Direct binding to Bhlhb2/Lims2 promoters not shown
    • Whether the ARID3A/KDM4C complex is involved in cardiac targets unknown
  7. 2014 High

    Demonstrating cancer stem cell expansion: ARID3B overexpression expanded CD133+ cells, upregulated stemness markers, and conferred paclitaxel resistance in vivo, linking its transcriptional activity to therapy-resistant cancer stem cell phenotypes.

    Evidence Intraperitoneal xenograft, flow cytometry for CD133+, gene expression profiling, drug resistance assay

    PMID:25327563

    Open questions at the time
    • Direct versus indirect regulation of stemness markers not distinguished
    • Whether ARID3B acts independently of ARID3A in this context not tested
  8. 2015 High

    Defining direct genomic targets and a DNA-binding motif: ChIP-chip identified genome-wide ARID3B binding at AT-rich motifs in promoters and enhancers (e.g., EGFR enhancer, WNT5A/FZD5 promoter), and functional assays showed ARID3B-driven FZD5 expression promotes cell–matrix adhesion.

    Evidence ChIP-chip, motif analysis, overexpression/knockdown, adhesion assays in ovarian cancer cells

    PMID:26121572

    Open questions at the time
    • Genome-wide binding map limited to one cell line
    • Co-factor requirements for binding specificity not addressed
  9. 2015 Medium

    Connecting ARID3B to p53-dependent apoptotic transcription: ARID3B directly binds ARID3 sites in p53 target gene promoters (PUMA, PIG3), and its silencing blocks pro-apoptotic transcription after DNA damage, revealing ARID3B as a required co-activator of p53 apoptotic targets.

    Evidence ChIP and EMSA for direct binding, siRNA knockdown, overexpression, apoptosis assays after DNA damage

    PMID:26519881

    Open questions at the time
    • Physical interaction with p53 protein not demonstrated
    • Whether ARID3B is needed at all p53 targets or a specific subset unclear
  10. 2016 High

    Elucidating the ARID3B–ARID3A–KDM4C complex and its upstream regulation by let-7: Co-IP identified a triprotein complex whose nuclear assembly depends on importin-9 (itself a let-7 target); the complex reduces H3K9me3 and activates stemness genes, and ARID3B is required for tumor initiation in let-7-depleted cells.

    Evidence Co-IP, ChIP for H3K9me3, luciferase miRNA reporter, nuclear import assay, tumor initiation assay

    PMID:26776511

    Open questions at the time
    • Stoichiometry and structure of the triprotein complex not determined
    • Whether KDM4C recruitment is direct or bridged through ARID3A unknown
  11. 2016 Medium

    Establishing a specific B-lineage requirement: conditional deletion in bone marrow depleted common lymphoid progenitors and downstream B cells without affecting T or myeloid lineages, defining a cell-autonomous role for ARID3B in B lymphopoiesis.

    Evidence Conditional knockout mouse, flow cytometry of bone marrow populations

    PMID:27537840

    Open questions at the time
    • Target genes mediating B cell specification not identified
    • Functional redundancy with ARID3A in B lineage not tested
  12. 2016 High

    Revealing a role in viral DNA replication: ARID3B binds AT-rich elements in the KSHV lytic origin of replication in a lytic cycle-dependent manner and inhibits lytic reactivation, demonstrating that its DNA-binding activity is co-opted during herpesvirus infection.

    Evidence SILAC proteomics, ChIP for oriLyt, DNA affinity assay, bidirectional perturbation (siRNA/overexpression), immunofluorescence

    PMID:27512077

    Open questions at the time
    • Mechanism by which ARID3B inhibits lytic reactivation not resolved
    • Whether the ARID3A/KDM4C complex participates in viral replication control unknown
  13. 2019 High

    Validating the triprotein complex in a non-cancer developmental context: in trophoblast cells, ARID3B knockout disrupted the ARID3A/ARID3B/KDM4C complex and decreased expression of HMGA1, c-MYC, VEGF-A, and WNT1, confirming the complex as a broadly utilized transcriptional activation module under LIN28/let-7 control.

    Evidence Co-IP, ChIP, CRISPR knockout, LIN28 double KO/KI lines, qRT-PCR in trophoblast cells

    PMID:31415216

    Open questions at the time
    • Whether ARID3B is limiting for complex assembly or acts catalytically not established
    • Global chromatin accessibility changes upon ARID3B KO not assessed
  14. 2021 High

    Establishing ARID3B as a direct co-activator of E2F target genes: ChIP and mutational reporter assays showed ARID3B binds ARID3 sites in E2F target promoters (Cdc2, cyclin E1, p107) and cooperates with E2F1 to activate transcription; its knockdown arrests cell cycle progression.

    Evidence ChIP, luciferase reporter with ARID3-BS mutations, siRNA knockdown, overexpression, cell cycle analysis

    PMID:33649863

    Open questions at the time
    • Physical interaction between ARID3B and E2F1 not shown
    • Whether the ARID3B–E2F cooperation requires KDM4C unknown
  15. 2025 Medium

    Discovering liquid–liquid phase separation as a mechanism for enhancer activation: ARID3B forms LLPS granules that recruit SMAD2/3 coactivators to establish enhancer activity required for craniofacial gene expression; disruption of LLPS rescues developmental defects in zebrafish, linking phase separation to nonsyndromic cleft lip/palate.

    Evidence In vitro and in vivo LLPS assays, Co-IP for SMAD2/3, ChIP for enhancer marks, zebrafish loss-of-function model

    PMID:41032419

    Open questions at the time
    • Structural determinants of ARID3B phase separation not mapped
    • Whether LLPS is required at all ARID3B-bound enhancers or context-specific unknown
    • Confirmation in mammalian craniofacial models pending
  16. 2026 High

    Identifying Ser89 phosphorylation as a regulatory switch for nuclear confinement: phospho-Ser89 confines ARID3B to the nucleus, while dephosphorylation permits cytoplasmic and membrane localization; phospho-mimetic S89D recapitulates wild-type transcriptional activity and chromatin binding, establishing post-translational control of ARID3B localization and function.

    Evidence Site-directed mutagenesis (S89A/S89D), phospho-specific antibody, subcellular fractionation, ChIP, transcriptional assays in multiple cell lines

    PMID:41972703

    Open questions at the time
    • Identity of the kinase(s) phosphorylating Ser89 unknown
    • Whether phosphorylation affects LLPS or complex formation with ARID3A/KDM4C not tested

Open questions

Synthesis pass · forward-looking unresolved questions
  • Key unresolved questions include the identity of the kinase controlling Ser89 phosphorylation, the structural basis of the ARID3A/ARID3B/KDM4C complex, whether LLPS-mediated enhancer activation is a general or tissue-specific mechanism, and the full extent of functional redundancy versus specialization between ARID3A and ARID3B across developmental and oncogenic contexts.
  • Ser89 kinase identity unknown
  • No structural model of the triprotein complex
  • LLPS contribution to non-craniofacial gene programs untested
  • Systematic comparison of ARID3A vs ARID3B genome-wide binding and function lacking

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0003677 DNA binding 5 GO:0140110 transcription regulator activity 5
Localization
GO:0005634 nucleus 3 GO:0005829 cytosol 2 GO:0005886 plasma membrane 2
Pathway
R-HSA-74160 Gene expression (Transcription) 5 R-HSA-1266738 Developmental Biology 3 R-HSA-4839726 Chromatin organization 3 R-HSA-5357801 Programmed Cell Death 2 R-HSA-1640170 Cell Cycle 1
Partners
ARID3AE2F1IPO9KDM4CRB1SMAD2SMAD3
Complex memberships
ARID3A/ARID3B/KDM4C complex

Evidence

Reading pass · 19 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1999 ARID3B (Bdp) binds to the COOH-terminal region of hypophosphorylated retinoblastoma protein (pRb) through its conserved region, and also binds to the matrix attachment region (MAR) of the immunoglobulin heavy-chain locus, implicating it in transcriptional regulation of differentiation and tissue-specific genes. Co-immunoprecipitation, DNA binding assay (MAR binding) Cancer research Medium 10446990
2006 ARID3B is required for survival of neural crest during embryogenesis, can immortalize mouse embryonic fibroblasts (MEFs) on its own, and confers malignancy to MEFs when co-expressed with MYCN, demonstrating oncogenic activity and a cooperative role with MYCN in malignant transformation. siRNA knockdown in neuroblastoma cell lines, antisense inhibition, transfection/overexpression, in vivo tumor growth assay in nude mice Cancer research High 16951138
2011 Arid3b is expressed in the apical ectodermal ridge (AER) and regulates cell motility and actin cytoskeleton distribution; interference with Arid3b activity causes aberrant AER development due to defective cell movements without changes in cell number or major signaling pathway gene expression. Loss-of-function in mouse and chick embryos (interference constructs), in vitro motility assay, actin cytoskeleton staining (phalloidin), DiI labeling of progenitor cells in vivo Development (Cambridge, England) High 21307092
2012 ARID3B full-length isoform (Fl) is predominantly nuclear but also present at the plasma membrane and cytosol; a novel splice form (Sh) lacking C-terminal exons 5-9 accumulates in cytosol and membrane when overexpressed. ARID3B Fl overexpression induces TNFα-mediated apoptosis by upregulating pro-apoptotic genes (BIM, TNFα, TRAIL, TRADD, TNF-R2, Caspase 10, Caspase 7), while ARID3B Sh does not induce apoptosis. Subcellular fractionation, overexpression of isoforms, gene expression analysis, cell viability assays PloS one Medium 22860069
2012 ARID3B is a direct target of miR-125b; restoration of miR-125b in MCF7 breast cancer cells decreases ARID3B expression and reduces cell motility and migration. Transient silencing of ARID3B phenocopies miR-125b's effect on cell migration. miRNA overexpression, siRNA knockdown of ARID3B, wound closure and transwell migration assays, phalloidin staining Cell structure and function Medium 22307404
2012 In mouse ES cells, Arid3b promotes cell survival (avoiding cell death) while MYCN drives cell cycle progression; epigenetic switching from H3K27me3 to H3K4me3 at the Arid3b and Mycn promoters occurs during somatic reprogramming to iPS cells, and the reverse switch occurs during neural crest differentiation. Gene expression analysis in ES cells, siRNA knockdown, ChIP for histone marks (H3K27me3, H3K4me3), reprogramming assay Oncogene Medium 22751132
2014 ARID3B increases ovarian tumor burden in vivo, promotes expression of cancer stem cell markers (CD44, LGR5, CD133/PROM1, Notch2), expands the CD133+ cell population, and enhances paclitaxel resistance. Intraperitoneal xenograft in nude mice, flow cytometry for CD133+, gene expression profiling of ascites cells, drug resistance assay Oncotarget High 25327563
2014 Arid3b is expressed in the myocardium and second heart field progenitors; Arid3b-deficient embryos show cardiac pole shortening, absence of myocardial differentiation, and failed epithelial-to-mesenchymal transition in the atrioventricular canal, with defective second heart field progenitor cell addition to the heart. Downstream targets identified include Bhlhb2 and Lims2. Conditional knockout mouse model, DiI labeling of second heart field progenitors, RNA microarray, histological and immunofluorescence analysis Development (Cambridge, England) High 25336743
2015 ARID3B directly binds to a defined AT-rich sequence motif at target gene promoters/enhancers (including EGFR enhancer and WNT5A/FZD5 promoter) and induces their expression. ARID3B-driven FZD5 upregulation increases ovarian cancer cell adhesion to extracellular matrix components (collagen IV, fibronectin, vitronectin), with adhesion to collagens II and IV requiring FZD5. ChIP followed by microarray (ChIP-chip), quantitative RT-PCR, motif-finding analysis, overexpression and knockdown, adhesion assays PloS one High 26121572
2015 ARID3B and ARID3A bind to putative ARID3-binding sites in p53 target genes (PUMA, PIG3, p53) in vitro and in vivo; ARID3B silencing blocks transcriptional activation of pro-apoptotic p53 target genes and blocks apoptosis following DNA damage, while ARID3B (but not ARID3A) overexpression induces apoptosis. ChIP (in vivo binding), EMSA (in vitro binding), siRNA knockdown, overexpression, apoptosis assays after DNA damage Biochemical and biophysical research communications Medium 26519881
2016 Let-7 miRNA directly represses ARID3B, ARID3A, and importin-9 expression. In the absence of let-7, importin-9 facilitates nuclear import of ARID3A, which forms a complex with ARID3B; the nuclear ARID3B complex recruits histone demethylase KDM4C to reduce H3K9me3 and promotes transcription of stemness factors. ARID3B expression is critical for tumor initiation in let-7-depleted cancer cells. Luciferase reporter assay for miRNA targeting, Co-immunoprecipitation of ARID3A/ARID3B/KDM4C complex, ChIP for H3K9me3, nuclear import assay, tumor initiation assay Cell reports High 26776511
2016 Conditional deletion of Arid3b in mouse bone marrow decreases common lymphoid progenitors and downstream B cell populations while leaving T cell and myeloid lineages intact, and HSC populations are unperturbed, establishing a specific, cell-autonomous role for Arid3b in B cell development. Conditional knockout mouse model, flow cytometry of bone marrow populations PloS one Medium 27537840
2016 KSHV lytic switch protein RTA upregulates ARID3B expression; ARID3B relocalizes to viral replication compartments upon lytic reactivation and directly binds A/T-rich elements in the KSHV lytic origin of replication (oriLyt) in a lytic cycle-dependent manner. ARID3B knockdown enhances and overexpression inhibits lytic reactivation. SILAC-based quantitative proteomics, siRNA knockdown, overexpression, DNA affinity assay, ChIP for oriLyt binding, immunofluorescence for relocalization Journal of virology High 27512077
2019 In human trophoblast cells, ARID3A, ARID3B, and KDM4C form a triprotein complex (ARID3B-complex) that binds to promoter regions of HMGA1, c-MYC, VEGF-A, and WNT1. ARID3B knockout disrupts this complex and decreases expression of these target genes. LIN28/let-7 axis regulates this complex upstream. Co-immunoprecipitation, ChIP, CRISPR knockout of ARID3B, LIN28 double knockout and double knockin cell lines, qRT-PCR FASEB journal High 31415216
2020 ARID3A and ARID3B regulate nearly identical gene sets in ovarian cancer cells, including stemness/cancer genes (Twist, MYCN, MMP2, GLI2, TIMP3, WNT5B); each induces expression of the other, providing evidence of cooperativity. High-level ARID3B (but not ARID3A) induces cell death. Lentiviral transduction with ARID3A-GFP and ARID3B-RFP, RNA-sequencing, expression analysis Gene Medium 32061921
2021 ARID3B directly binds to ARID3-binding sites in the promoters of E2F target genes (Cdc2, cyclin E1, p107) in living cells; ARID3B knockdown blocks transcription of these genes and attenuates cell cycle progression. ARID3B overexpression activates cyclin E1 transcription cooperatively with E2F1 and induces cell death. ChIP for direct binding, luciferase reporter assays with ARID3-BS mutations, siRNA knockdown, overexpression, cell cycle analysis International journal of oncology High 33649863
2023 ARID3B overexpression increases the expression of lncRNAs MALAT1 and NORAD in NSCLC cells, placing ARID3B upstream of these lncRNAs in the pRB-E2F and p53 regulatory pathways. Overexpression of ARID3A and ARID3B, qRT-PCR/expression analysis of lncRNAs Pathology, research and practice Low 37977034
2025 ARID3B undergoes liquid-liquid phase separation (LLPS) to form granules both in vivo and in vitro; this ARID3B-mediated LLPS recruits coactivators SMAD2/3 and establishes enhancer activity necessary for initiating gene expression related to nonsyndromic cleft lip/palate (nsCL/P). Disruption of LLPS rescues migration, apoptosis, and phenotype deficits in zebrafish models. LLPS assays in vitro and in vivo, Co-IP for SMAD2/3 interaction, ChIP for enhancer activity, zebrafish loss-of-function model Cell reports Medium 41032419
2026 Phosphorylation of ARID3B at Serine 89 controls its subcellular localization: phosphorylated ARID3B is confined to the nucleus, while unphosphorylated ARID3B can localize to the nucleus, cytoplasm, and membrane. Phospho-mimetic S89D mirrors wild-type ARID3B in transcriptional regulation and chromatin binding, while phospho-dead S89A shows divergent regulation consistent with altered localization. Site-directed mutagenesis (S89A, S89D phospho-dead/mimetic constructs), phospho-specific antibody generation, subcellular fractionation, ChIP, functional transcriptional assays in ovarian cancer and glioblastoma cells Cells High 41972703

Source papers

Stage 0 corpus · 37 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2013 GFAP-BDP as an acute diagnostic marker in traumatic brain injury: results from the prospective transforming research and clinical knowledge in traumatic brain injury study. Journal of neurotrauma 166 23489259
2015 Measurement of the glial fibrillary acidic protein and its breakdown products GFAP-BDP biomarker for the detection of traumatic brain injury compared to computed tomography and magnetic resonance imaging. Journal of neurotrauma 96 25264814
2020 The Role of LIN28-let-7-ARID3B Pathway in Placental Development. International journal of molecular sciences 50 32455665
2016 let-7 Modulates Chromatin Configuration and Target Gene Repression through Regulation of the ARID3B Complex. Cell reports 42 26776511
2012 miR-125b targets ARID3B in breast cancer cells. Cell structure and function 40 22307404
1999 Bdp, a new member of a family of DNA-binding proteins, associates with the retinoblastoma gene product. Cancer research 39 10446990
2006 ARID3B induces malignant transformation of mouse embryonic fibroblasts and is strongly associated with malignant neuroblastoma. Cancer research 37 16951138
2012 Epigenetic regulation of the neuroblastoma genes, Arid3b and Mycn. Oncogene 31 22751132
2011 Apical ectodermal ridge morphogenesis in limb development is controlled by Arid3b-mediated regulation of cell movements. Development (Cambridge, England) 31 21307092
2015 ARID3B Directly Regulates Ovarian Cancer Promoting Genes. PloS one 29 26121572
2020 ARID3A and ARID3B induce stem promoting pathways in ovarian cancer cells. Gene 26 32061921
2014 ARID3B increases ovarian tumor burden and is associated with a cancer stem cell gene signature. Oncotarget 22 25327563
2014 Differential expression of ARID3B in normal adult tissue and carcinomas. Gene 19 24704276
2019 LIN28-let-7 axis regulates genes in immortalized human trophoblast cells by targeting the ARID3B-complex. FASEB journal : official publication of the Federation of American Societies for Experimental Biology 16 31415216
2012 ARID3B induces tumor necrosis factor alpha mediated apoptosis while a novel ARID3B splice form does not induce cell death. PloS one 16 22860069
2017 A novel chalcone-based molecule, BDP inhibits MDA‑MB‑231 triple-negative breast cancer cell growth by suppressing Hsp90 function. Oncology reports 14 28849241
2014 Arid3b is essential for second heart field cell deployment and heart patterning. Development (Cambridge, England) 13 25336743
2021 Distinct and overlapping roles of ARID3A and ARID3B in regulating E2F‑dependent transcription via direct binding to E2F target genes. International journal of oncology 12 33649863
2015 BDP-30, a systemic resistance inducer from Boerhaavia diffusa L., suppresses TMV infection, and displays homology with ribosome-inactivating proteins. Journal of biosciences 11 25740147
2016 Arid3b Is Critical for B Lymphocyte Development. PloS one 10 27537840
2003 Assessment of inhaled BDP-dose dependency of exhaled nitric oxide and local and serum eosinophilic markers in steroids-naive nonatopic asthmatics. Allergy 10 14510719
2016 ARID3B: a Novel Regulator of the Kaposi's Sarcoma-Associated Herpesvirus Lytic Cycle. Journal of virology 8 27512077
2015 Critical role of ARID3B in the expression of pro-apoptotic p53-target genes and apoptosis. Biochemical and biophysical research communications 8 26519881
2005 Effect of beclomethasone dipropionate (BDP) as extrafine aerosol on bronchoalveolar lavage (BAL) lymphocytes in chronic sarcoidosis. Sarcoidosis, vasculitis, and diffuse lung diseases : official journal of WASOG 6 16315785
2014 ARID3B expression in primary breast cancers and breast cancer-derived cell lines. Cellular oncology (Dordrecht, Netherlands) 4 25120063
2007 [A multicenter, open-label, randomized comparison of suppressive effects on asthmatic inflammation of lower airways and improved effects on health-related QOL between HFA-BDP and fluticasone propionate]. Arerugi = [Allergy] 3 17615501
1997 Inhaled beclomethasone dipropionate (BDP) prevents seasonal changes in atopic asthmatics. Monaldi archives for chest disease = Archivio Monaldi per le malattie del torace 3 9203805
2023 ARID3A and ARID3B exert direct regulatory control over the long non-coding RNAs (lncRNAs) MALAT1 and NORAD within the context of non-small cell lung cancer (NSCLC). Pathology, research and practice 2 37977034
2005 [The small airway inflammation of asthmatic patients who have used dry powder type inhaled steroid for moderate-long term evaluated by induced sputum and the efficacy of HFA-BDP (QVAR) inhalation]. Arerugi = [Allergy] 2 15841673
1996 [A comparison of the pharmacological actions between DSCG (disodium cromoglycate) and BDP (beclomethasone dipropionate) in the treatment of bronchial asthma]. Nihon rinsho. Japanese journal of clinical medicine 2 8950946
2026 LvID-BDP: A Conotoxin-Based Fluorescent Probe for Visualizing α7 nAChR Expression in Intestinal Inflammation. Journal of medicinal chemistry 0 41731686
2026 Serine 89 Phosphorylation Controls Nuclear Localization and Transcriptional Activity of ARID3B. Cells 0 41972703
2025 Genetic regulation of ARID3B confers cleft lip with/without cleft palate susceptibility through LLPS-mediated transcriptional program. Cell reports 0 41032419
2025 mmu_circ_0000684/hsa_circ_0067098 mediates renal tubular epithelial cells apoptosis to ischemia-reperfusion-induced acute kidney injury by targeting the mmu_miR_671-5p/ARID3B axis. Archives of biochemistry and biophysics 0 41320129
2001 [The effects of BDP on the inflammatory cells in nasal secretions of the patients with allergic rhinitis]. Lin chuang er bi yan hou ke za zhi = Journal of clinical otorhinolaryngology 0 12541826
2000 [Immunohistochemical analysis of bronchial mucosa in severe asthmatics treated with long-term, high-dose inhaled BDP]. Nihon Kokyuki Gakkai zasshi = the journal of the Japanese Respiratory Society 0 10774164
1998 [The effects of BDP on eosinophils in nasal secretions of the patient with allergic rhinilis]. Lin chuang er bi yan hou ke za zhi = Journal of clinical otorhinolaryngology 0 11189187