Affinage

ARID3A

AT-rich interactive domain-containing protein 3A · UniProt Q99856

Length
593 aa
Mass
62.9 kDa
Annotated
2026-04-28
100 papers in source corpus 20 papers cited in narrative 20 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

ARID3A is an ARID-domain transcription factor that binds AT-rich DNA motifs as a dimer to regulate cell fate decisions across multiple lineages, including B-lymphocyte differentiation, hematopoietic stem cell commitment, trophectoderm specification, and megakaryopoiesis. It activates immunoglobulin heavy-chain transcription through a ternary complex with TFII-I and Bruton's tyrosine kinase (Btk), where Btk-mediated phosphorylation of TFII-I is required for transcriptional activity (PMID:16738337, PMID:11594453), and it functions downstream of the Lin28b/Let-7 axis to specify fetal B-1 lymphopoiesis (PMID:25753579). ARID3A acts as both a transcriptional activator and repressor depending on context: it directly activates trophectoderm genes while repressing pluripotency genes through differential histone acetylation (PMID:25319825), cooperates with p53 to activate p21WAF1 after DNA damage (PMID:22172947), represses Mertk transcription in macrophages to limit efferocytosis (PMID:37659731), and represses PTEN to inhibit ferroptosis in cancer cells (PMID:38781729). Its expression is post-transcriptionally controlled by miR-125b and Let-7, and its nuclear import is regulated by NF-κB signaling; miR-125b-mediated repression of ARID3A synergizes with GATA1s mutations to drive acute megakaryoblastic leukemia (PMID:34570885, PMID:22469780, PMID:36215225).

Mechanistic history

Synthesis pass · year-by-year structured walk · 15 steps
  1. 2001 Medium

    Establishing that ARID3A/Bright is a sequence-specific transcription factor that activates immunoglobulin heavy-chain transcription in B cells, binds AT-rich DNA via the ARID domain, associates with nuclear matrix proteins, and requires Btk for DNA binding activity answered the foundational question of how IgH locus accessibility is regulated.

    Evidence Transcription reporter assays, DNA binding assays, Co-IP with sp100/LYSp100B, Btk dependence in B cells

    PMID:11594453

    Open questions at the time
    • Single-lab review of earlier data; individual experiments not independently detailed
    • Structural basis of ARID domain–DNA interaction unresolved
    • Mechanism by which Btk enables DNA binding not defined
  2. 2005 High

    Demonstrating that the Xenopus ARID3A ortholog is specifically required for TGF-β but not FGF-mediated mesoderm induction established ARID3A as a pathway-selective mediator of TGF-β/SMAD signaling during embryonic development.

    Evidence Morpholino knockdown, engrailed-Dril1 fusions, animal cap assays, and mRNA rescue in Xenopus tropicalis

    PMID:15680369

    Open questions at the time
    • Mammalian relevance of TGF-β selectivity not directly tested
    • Biochemical mechanism linking ARID3A to SMAD complexes not defined in this system
  3. 2006 High

    Identifying a three-component Bright/TFII-I/Btk complex and showing that Btk-dependent TFII-I phosphorylation is essential for Bright-driven IgH transcription resolved how ARID3A integrates signaling input with transcriptional activation at the IgH locus.

    Evidence Co-immunoprecipitation, domain mapping, IgH reporter assays, and siRNA knockdown in B-cell lines

    PMID:16738337

    Open questions at the time
    • Whether the ternary complex operates at endogenous chromatin genome-wide was untested
    • Stoichiometry and structural details of the complex unknown
  4. 2008 Medium

    Discovery that Id1 directly binds ARID3A/Dril1 and inhibits its DNA binding revealed a mechanism by which Id proteins suppress profibrotic gene activation downstream of TGF-β1.

    Evidence Protein interaction screen, Co-IP, co-localization, DNA binding assays, TGF-β1 target gene assays, Id1 KO mouse bleomycin model

    PMID:18583319

    Open questions at the time
    • Single-lab finding; reciprocal validation limited
    • Whether Id1 inhibition of ARID3A generalizes beyond fibrosis context unknown
  5. 2010 High

    Showing that ARID3A loss in somatic cells induced pluripotency gene expression and multilineage differentiation capacity fundamentally reframed ARID3A from an immunoglobulin-specific factor to a broad repressor of developmental plasticity.

    Evidence Knockout mouse models, siRNA knockdown, colony formation, multi-lineage differentiation, gene expression profiling

    PMID:20680960

    Open questions at the time
    • Epigenetic mechanism of pluripotency repression was not defined
    • Whether ARID3A loss achieves bona fide iPSC-equivalent reprogramming was unclear
  6. 2011 High

    Two discoveries in 2011 expanded ARID3A's mechanistic repertoire: cooperation with p53 to activate p21WAF1 at AT-rich promoter elements after DNA damage, and identification of ARID3C as a co-activating partner at IgH loci, revealed context-dependent transcriptional partnerships.

    Evidence ChIP, in vitro binding, reporter assays, siRNA in p53-positive/null lines (p21 study); Co-IP, DNA binding, IgH reporters, SUMO assays (ARID3C study)

    PMID:21955986 PMID:22172947

    Open questions at the time
    • Genome-wide overlap of ARID3A and p53 co-regulation sites not mapped
    • ARID3C contribution relative to ARID3A at endogenous loci untested
  7. 2012 High

    Demonstrating that miR-125b directly targets ARID3A to block B-cell progenitor differentiation while conferring survival advantage established a post-transcriptional regulatory axis controlling ARID3A levels in hematopoiesis.

    Evidence 3′UTR luciferase reporter, miR-125b overexpression/inhibition, ARID3A siRNA, proliferation and apoptosis assays in murine and human leukemic B-cell lines

    PMID:22469780

    Open questions at the time
    • In vivo physiological relevance of miR-125b–ARID3A axis in normal B-cell development not directly shown here
  8. 2014 High

    Two parallel 2014 studies established ARID3A as a master regulator of early embryonic and hematopoietic lineage decisions: it drives trophectoderm specification upstream of Cdx2 via differential histone acetylation, and controls B-1 versus B-2 lineage allocation and chromatin accessibility at IgH enhancers.

    Evidence ARID3A KO mouse with placental defects, ES cell OE/KD, ChIP, histone acetylation assays (TE study); transgenic/KO mice, B cell subset flow cytometry, DNA binding assays (hematopoiesis study)

    PMID:24678314 PMID:25319825

    Open questions at the time
    • Direct ARID3A target genes in trophoblast beyond a few markers not comprehensively defined
    • Mechanism by which ARID3A opens chromatin at IgH enhancer molecularly unclear
  9. 2015 High

    Placing ARID3A downstream of the Lin28b/Let-7 axis and showing its sufficiency to reprogram adult pro-B cells toward B-1 fate resolved a key step in the fetal-to-adult B lymphopoiesis switch and explained how a single transcription factor coordinates developmental timing with lineage output.

    Evidence Retroviral transduction of ARID3A/Lin28b in adult BM progenitors, Let-7 modulation, ARID3A KD in fetal pro-B cells, transplantation, VH repertoire analysis

    PMID:25753579

    Open questions at the time
    • Direct transcriptional targets of ARID3A that enforce B-1 identity not identified
    • Whether ARID3A acts through chromatin remodeling or direct gene activation in this context unknown
  10. 2015 Medium

    Demonstrating that ARID3A knockdown in human cord blood HSCs shifted lineage output from B-lymphoid toward myeloid confirmed ARID3A as a conserved regulator of human multilineage hematopoietic decisions.

    Evidence Lentiviral KD and OE of ARID3A in cord blood CD34+ HSCs, in vitro differentiation, flow cytometry, transcription factor expression analysis

    PMID:26685208

    Open questions at the time
    • In vitro system only; in vivo human HSC repopulation not tested
    • Downstream transcriptional programs mediating lineage bias not comprehensively mapped
  11. 2016 Medium

    Identifying ARID3A+ B cells as IFN-α producers following TLR9 stimulation linked ARID3A to innate immune effector function and inflammatory amplification relevant to SLE pathogenesis.

    Evidence ARID3a+ B cell sorting, CpG stimulation, IFN-α ELISA, co-culture with plasmacytoid dendritic cells

    PMID:27522115

    Open questions at the time
    • Whether ARID3A directly regulates IFN-α gene transcription or acts indirectly is unknown
    • Causal role of ARID3A in SLE not established by genetic evidence
  12. 2019 Medium

    Validation that miR-574-5p directly targets ARID3A and modulates cardiac fibroblast-to-myofibroblast differentiation revealed a second miRNA axis regulating ARID3A levels in a non-hematopoietic, TGF-β-driven fibrotic context.

    Evidence 3′UTR luciferase reporter, miR-574-5p OE/silencing, ARID3A KD in human cardiac fibroblasts

    PMID:31672272

    Open questions at the time
    • Single-lab study; limited to in vitro cardiac fibroblast system
    • Whether ARID3A promotes or opposes fibrotic gene programs in this context appears opposite to the Id1 study — contradiction unresolved
  13. 2022 High

    Three 2022 studies expanded ARID3A's mechanism: (1) miR-125b repression of ARID3A cooperates with GATA1s to block megakaryocytic differentiation and drive AMKL, with ARID3A forming a complex with SMAD2/3; (2) ARID3A partners with CEP131 to activate KDM3A transcription, promoting cancer stemness via H3K9me2 demethylation; (3) ARID3A directly binds the let-7 gene cluster promoter to repress let-7 in macrophages, regulated by NF-κB-controlled nuclear import.

    Evidence Forward/reverse genetics and PDX rescue (AMKL); Co-IP, CUT&Tag, H3K9me2 ChIP (liver cancer); EMSA, ChIP, RIP, PRRSV infection models (macrophage/let-7)

    PMID:34570885 PMID:36008383 PMID:36215225

    Open questions at the time
    • SMAD2/3–ARID3A complex composition and DNA targets not genome-wide mapped
    • CEP131–ARID3A interaction awaits independent replication
    • NF-κB–ARID3A nuclear import mechanism molecularly undefined
  14. 2023 High

    Two 2023 findings revealed ARID3A as a direct transcriptional repressor of Mertk in macrophages limiting efferocytosis, and identified a non-coding enhancer variant (rs2238574) that modulates ARID3A expression to control myeloid differentiation, connecting genetic regulation of ARID3A levels to myeloid functional output.

    Evidence Myeloid-specific KO mouse, ChIP-seq, reporter assays, Mertk inhibitor rescue in vivo (Mertk study); CRISPR editing, allele-specific ChIP, luciferase, KD/OE in myeloid cells (enhancer study)

    PMID:36977669 PMID:37659731

    Open questions at the time
    • Additional direct ARID3A-repressed targets in macrophages beyond Mertk not mapped
    • rs2238574 functional impact on disease susceptibility in patient cohorts not established
  15. 2024 Medium

    Demonstrating that ARID3A directly represses PTEN transcription to sustain GPX4 and inhibit ferroptosis revealed a novel ARID3A–PTEN–ferroptosis axis mediating chemoresistance in pancreatic cancer.

    Evidence CUT&Tag, RNA-seq, ARID3A KD/OE, lipid peroxidation assays, GPX4/PTEN Western blots, in vivo tumor models, gemcitabine sensitivity assays

    PMID:38781729

    Open questions at the time
    • Single-lab study; PTEN repression mechanism (cofactors, chromatin changes) not detailed
    • Generalizability beyond pancreatic cancer untested

Open questions

Synthesis pass · forward-looking unresolved questions
  • Major unresolved questions include the structural basis of ARID3A dimerization and DNA recognition, the genome-wide chromatin landscape it occupies across cell types, the molecular mechanism by which NF-κB controls its nuclear import, and how its activating versus repressive functions are contextually switched.
  • No crystal or cryo-EM structure of ARID3A or its complexes
  • No unified genome-wide binding map across hematopoietic, trophoblast, and cancer contexts
  • Molecular basis for context-dependent activation versus repression unresolved

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0003677 DNA binding 8 GO:0140110 transcription regulator activity 7
Localization
GO:0005634 nucleus 4
Pathway
R-HSA-74160 Gene expression (Transcription) 7 R-HSA-1266738 Developmental Biology 3 R-HSA-162582 Signal Transduction 3 R-HSA-1643685 Disease 3 R-HSA-168256 Immune System 3
Partners
ARID3CBTKCEP131GTF2IID1SMAD2SMAD3TP53
Complex memberships
ARID3A/CEP131 complexARID3A/SMAD2/3 complexBright/TFII-I/Btk complex

Evidence

Reading pass · 20 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2006 ARID3A (Bright) directly interacts with TFII-I through amino acids in Bright's protein interaction domain, and specific tyrosine residues of TFII-I (phosphorylated by Bruton's tyrosine kinase, Btk) are essential for Bright-induced immunoglobulin heavy-chain reporter gene activity. Inhibition of TFII-I in B cells decreased heavy-chain transcript levels, identifying a three-component complex (Bright/TFII-I/Btk) required for immunoglobulin transcription. Co-immunoprecipitation, domain-mapping interaction assays, immunoglobulin reporter gene assays, siRNA inhibition of TFII-I in B-cell lines Molecular and cellular biology High 16738337
2010 Loss of Bright/ARID3a function (via knockout mouse models or direct siRNA knockdown of human Bright) promotes developmental plasticity: Bright-deficient somatic cells expressed pluripotency-associated gene products, expanded indefinitely, and spontaneously differentiated into cells of multiple lineages, indicating Bright normally represses pluripotency. Knockout mouse models, siRNA knockdown, colony formation assays, multi-lineage differentiation assays, gene expression profiling Stem cells (Dayton, Ohio) High 20680960
2011 ARID3A cooperates with p53 to transcriptionally activate p21WAF1 in response to DNA damage. ARID3A binds directly to AT-rich sites in the p21WAF1 promoter in vitro and in vivo (ChIP), and its knockdown suppressed p21WAF1 transcription after DNA damage without affecting NOXA or PUMA. Additionally, p53 and ARID3A show interdependence: p53 knockdown decreased ARID3A transcription, and ARID3A overexpression/knockdown increased/decreased p53 stability. ChIP, in vitro DNA binding, reporter gene assays, siRNA knockdown, co-expression studies in p53-positive and p53-null cell lines Biochemical and biophysical research communications High 22172947
2011 A third ARID3 family member, Brightlike/ARID3C, physically associates with ARID3A (Bright) in solution and at common DNA binding sites in vitro, and co-activates Bright-dependent IgH transcription. Brightlike undergoes nuclear-cytoplasmic shuttling dependent on the REKLES domain and localizes to lipid rafts after BCR stimulation. Sumoylation of Brightlike reduces its co-activation capacity. Co-immunoprecipitation, in vitro DNA binding, IgH reporter gene assays, nuclear-cytoplasmic fractionation, lipid raft fractionation, SUMO modification assays Molecular immunology Medium 21955986
2012 miR-125b directly targets and represses ARID3A/Bright in B-cell progenitors, and this repression blocks differentiation while conferring a survival advantage. Forced Bright/ARID3A repression in pre-BI cells mimicked miR-125b-induced differentiation blockade, increased proliferation, and inhibited apoptosis via caspase pathway inhibition independent of p53 and BAK1. miR-125b overexpression/inhibition in murine and human leukemic B-cell lines, 3'UTR luciferase reporter assays, siRNA knockdown of ARID3A, proliferation/differentiation/apoptosis assays Leukemia High 22469780
2014 Upregulation and nuclear entry of Arid3a drives trophectoderm (TE)-like transcriptional programs in ES cells, maintains trophoblast stem cell self-renewal, and promotes trophoblastic differentiation upstream and independent of Cdx2. Arid3a directly activates TE-specific genes while repressing pluripotency genes via differential regulation of histone acetylation/deacetylation. Arid3a-/- mice show severely impaired post-implantation placental development. Arid3a knockout mouse, ES cell overexpression/knockdown, ChIP for Arid3a at target promoters, histone acetylation assays, transcriptomic analysis, trophoblast stem cell self-renewal assays Genes & development High 25319825
2014 ARID3a/Bright is expressed in hematopoietic stem/progenitor cells and regulates hematopoietic lineage decisions. In mice, over-expression skewed mature B cell subsets and altered follicular B cell gene expression, while loss of function eliminated B1 lineage B cells and caused hematopoietic defects. The protein interacts with DNA as a dimer through its ARID domain and requires association with other proteins to increase transcription of immunoglobulin heavy chain and chromatin accessibility at the heavy chain enhancer. Transgenic and knockout mouse models, gene expression profiling, B cell subset analysis by flow cytometry, DNA binding assays Frontiers in immunology Medium 24678314
2015 ARID3a is a key target of the miRNA Let-7 (regulated by Lin28b) in fetal B-cell progenitors. Ectopic ARID3a expression in adult pro-B cells is sufficient to induce B-1 development, while ARID3a knockdown blocks B-1 development in fetal pro-B cells, placing ARID3a downstream of Lin28b/Let-7 as a critical regulator of the fetal B-1 versus adult B-2 lymphopoiesis switch. Intact BCR signaling is also required for Lin28b-induced B1a cell generation. Retroviral transduction of Lin28b or ARID3a in adult bone marrow progenitors, Let-7 modulation, ARID3a knockdown in fetal pro-B cells, transplantation into immunodeficient recipients, VH repertoire analysis The Journal of experimental medicine High 25753579
2015 ARID3a is important for human hematopoiesis: inhibition of ARID3a in cord blood hematopoietic stem/progenitor cells decreased B lineage cell production and increased cells with myeloid markers, while ARID3a overexpression inhibited both myeloid and erythroid differentiation. ARID3a knockdown also altered expression of lineage-determining transcription factors. Lentiviral siRNA knockdown and overexpression of ARID3a in cord blood CD34+ HSCs, in vitro differentiation assays, flow cytometry for lineage markers, transcription factor expression analysis Journal of immunology Medium 26685208
2016 ARID3a+ human B lymphocytes produce interferon alpha (IFNa). TLR9 agonist (CpG) stimulation induced both ARID3a expression and IFNa production in healthy control B cells. IFNa secreted from ARID3a+ B cells stimulated increased IFNa production in plasmacytoid dendritic cells, identifying ARID3a+ B cells as a novel effector B cell type linking ARID3a to IFN-associated inflammatory responses in SLE. Flow cytometry for ARID3a+ B cell sorting, CpG stimulation, ELISA for IFNa, co-culture with plasmacytoid dendritic cells, gene expression profiling for IFN signature genes Journal of autoimmunity Medium 27522115
2008 ARID3A (Dril1) was identified as a novel binding partner for Id1 by protein interaction screening. Dril1 enhanced activation of TGF-β1 target genes in fibroblasts, while Id1 decreased their expression. Id1 inhibited DNA binding by Dril1, and the two proteins co-localized in vitro and in vivo, providing a mechanism by which Id1 suppresses fibrosis through inhibition of profibrotic Dril1 activity. Protein interaction screening, co-immunoprecipitation, co-localization (in vitro and in vivo), DNA binding assays, TGF-β1 target gene activation assays, Id1 knockout mouse bleomycin model The American journal of pathology Medium 18583319
2005 The Xenopus ortholog of ARID3A (Dril1) is required for TGF-β signaling during mesoderm induction. Morpholino depletion of dril1 inhibited gastrulation, blocked induction of mesodermal markers (Xbra, chordin, noggin, Xlim1), and prevented both smad2-mediated dorsal/endodermal induction and smad1-mediated ventral mesoderm induction in animal caps, while FGF-mediated mesoderm induction was unaffected, indicating pathway-specific regulation of TGF-β signaling. Morpholino knockdown, engrailed repressor-dril1 fusion constructs, animal cap assays, secondary axis induction assays, mRNA rescue experiments in Xenopus tropicalis Developmental biology High 15680369
2022 ARID3A promotes megakaryocytic differentiation in concert with GATA1 and mediates TGF-β-induced apoptosis and cell cycle arrest in complex with SMAD2/3. miR-125b (encoded on chromosome 21) post-transcriptionally represses ARID3A, synergizing with GATA1s mutations to block megakaryocytic/erythroid differentiation and drive acute megakaryoblastic leukemia (AMKL). Restoring ARID3A expression in AMKL patient-derived xenografts relieved the differentiation block. Forward and reverse genetics, miR-125b overexpression/knockdown, ARID3A knockdown/restoration, Co-IP for SMAD2/3 complex, patient-derived xenograft model, flow cytometry for differentiation markers Blood High 34570885
2022 ARID3A interacts with CEP131 and together they transcriptionally activate KDM3A by co-occupying its promoter, which in turn upregulates embryonic stem cell signature genes via demethylation of H3K9me2, promoting liver cancer stemness and metastasis. Co-immunoprecipitation of ARID3A-CEP131 complex, CUT&Tag chromatin profiling, RNA-seq, ChIP for H3K9me2, in vitro and in vivo functional assays (viability, metastasis) Cell death & disease Medium 36008383
2023 Arid3a negatively regulates Mertk transcription by directly binding to the Mertk promoter (demonstrated by ChIP-seq and luciferase reporter assay) in macrophages. Myeloid-specific Arid3a knockout enhanced Mertk-mediated efferocytosis of apoptotic cholangiocytes, alleviating cholestatic liver injury. In vivo Mertk inhibition reversed the protective phenotype of Arid3a deficiency. Myeloid-specific Arid3a knockout mouse, ChIP-seq, luciferase reporter assay, efferocytosis assays, in vivo Mertk inhibitor (UNC2025), flow cytometry, RNA-seq Journal of hepatology High 37659731
2024 ARID3A transcriptionally represses PTEN expression (demonstrated by CUT&Tag profiling), leading to GPX4 upregulation and resistance to ferroptosis. ARID3A knockdown in pancreatic cancer cells alleviates PTEN transcriptional inhibition, resulting in GPX4 depletion, increased lipid peroxidation, and activated ferroptosis, thereby reducing gemcitabine chemoresistance in vitro and in vivo. CUT&Tag chromatin profiling, RNA-seq, ARID3A knockdown (siRNA/shRNA), overexpression, lipid peroxidation assays, GPX4 and PTEN Western blotting, in vivo tumor models, gemcitabine sensitivity assays Redox biology Medium 38781729
2019 miR-574-5p directly targets ARID3A (validated by luciferase reporter assay), and decreased ARID3A levels promote fibroblast-to-myofibroblast differentiation of human cardiac fibroblasts (HCFs) in TGF-β-induced conditions. Silencing miR-574-5p increased ARID3A and suppressed myofibroblast differentiation markers. Luciferase 3'UTR reporter assay, miR-574-5p overexpression/silencing in HCFs, ARID3A knockdown, fibrosis gene expression assays, wound healing and transwell migration assays Biochemical and biophysical research communications Medium 31672272
2022 ARID3A expression in macrophages is regulated by NEAT1 acting as a ceRNA to sponge miR-147a, preventing degradation of ARID3A mRNA. ARID3A binds to the promoter region of the let-7a/let-7f/let-7d gene cluster (confirmed by EMSA and ChIP) and inhibits let-7 family expression; NF-κB signaling inhibits let-7 expression by affecting nuclear import of ARID3A. The NEAT1/ARID3A/let-7 axis regulates macrophage polarization and PRRSV replication. EMSA, ChIP, luciferase reporter assay, RNA immunoprecipitation, miRNA sequencing, in vitro and in vivo PRRSV infection models PLoS pathogens Medium 36215225
2001 Bright/ARID3a increases immunoglobulin heavy chain transcription three- to sevenfold in antigen-activated B cells. It interacts with DNA through the ARID (A/T-rich interaction domain) and associates with nuclear matrix proteins sp100 and LYSp100B, suggesting it may affect chromatin configuration and nuclear sublocalization. Bruton's tyrosine kinase (Btk) is required for Bright DNA binding activity. Transcription reporter assays, ARID domain DNA-binding assays, co-immunoprecipitation with sp100/LYSp100B, Btk requirement for DNA binding activity Immunologic research Medium 11594453
2023 A non-coding intronic variant in ARID3A (rs2238574) acts as an allele-specific enhancer in myeloid cells to regulate ARID3A expression. Luciferase reporter assay and allele-specific ChIP prioritized rs2238574 as causal; genome editing confirmed its regulatory effect. ARID3A knockdown inhibited myeloid differentiation and activation pathways, while overexpression had the opposite effect, functionally linking ARID3A levels to myeloid cell behavior. Luciferase reporter assay, allele-specific ChIP, CRISPR genome editing, ARID3A knockdown/overexpression in myeloid cells, myeloid differentiation assays Nature communications Medium 36977669

Source papers

Stage 0 corpus · 100 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2020 ROS in cancer therapy: the bright side of the moon. Experimental & molecular medicine 1485 32060354
1982 Heritable true fitness and bright birds: a role for parasites? Science (New York, N.Y.) 1370 7123238
2013 A bright monomeric green fluorescent protein derived from Branchiostoma lanceolatum. Nature methods 1004 23524392
2016 mScarlet: a bright monomeric red fluorescent protein for cellular imaging. Nature methods 852 27869816
2007 Bright monomeric red fluorescent protein with an extended fluorescence lifetime. Nature methods 482 17572680
2012 Rational design of true monomeric and bright photoactivatable fluorescent proteins. Nature methods 367 22581370
2019 Bright and photostable chemigenetic indicators for extended in vivo voltage imaging. Science (New York, N.Y.) 340 31371562
2020 CAR T Cell Therapy for Solid Tumors: Bright Future or Dark Reality? Molecular therapy : the journal of the American Society of Gene Therapy 286 32979309
2020 Extracellular vesicles: A bright star of nanomedicine. Biomaterials 271 33189359
2019 Visualizing RNA dynamics in live cells with bright and stable fluorescent RNAs. Nature biotechnology 270 31548726
2016 Bright monomeric near-infrared fluorescent proteins as tags and biosensors for multiscale imaging. Nature communications 231 27539380
1999 Reporter gene technology: the future looks bright. Biochemical pharmacology 223 10449183
2022 A highly photostable and bright green fluorescent protein. Nature biotechnology 198 35468954
2013 Immunosurveillance of senescent cells: the bright side of the senescence program. Biogerontology 174 24114507
2014 Bright and fast multicoloured voltage reporters via electrochromic FRET. Nature communications 149 25118186
2019 Electrochemical Sensors, a Bright Future in the Fabrication of Portable Kits in Analytical Systems. Chemical record (New York, N.Y.) 141 31845511
2020 Novel NanoLuc substrates enable bright two-population bioluminescence imaging in animals. Nature methods 139 32661427
2019 NanoBRET: The Bright Future of Proximity-Based Assays. Frontiers in bioengineering and biotechnology 131 30972335
2005 Anthocyans from fruits and vegetables--does bright colour signal cancer chemopreventive activity? European journal of cancer (Oxford, England : 1990) 124 16084717
2021 The bright side of fibroblasts: molecular signature and regenerative cues in major organs. NPJ Regenerative medicine 120 34376677
2018 Imaging organoids: a bright future ahead. Nature methods 110 29298292
1994 TOTO and YOYO: new very bright fluorochromes for DNA content analyses by flow cytometry. Cytometry 109 7513274
2015 Lin28b promotes fetal B lymphopoiesis through the transcription factor Arid3a. The Journal of experimental medicine 107 25753579
2014 Pheomelanin-induced oxidative stress: bright and dark chemistry bridging red hair phenotype and melanoma. Pigment cell & melanoma research 106 24814217
2010 DNA Encapsulation of Ten Silver Atoms Produces a Bright, Modulatable, Near Infrared-Emitting Cluster. The journal of physical chemistry letters 103 21116486
2016 PMEL Amyloid Fibril Formation: The Bright Steps of Pigmentation. International journal of molecular sciences 93 27589732
2014 TIGAR, TIGAR, burning bright. Cancer & metabolism 90 24383451
2014 18F-Labeled Peptides: The Future Is Bright. Molecules (Basel, Switzerland) 90 25493636
1994 Thioredoxin: a multifunctional regulatory protein with a bright future in technology and medicine. Archives of biochemistry and biophysics 90 7979362
2012 The bright and the dark sides of activin in wound healing and cancer. Journal of cell science 89 22991378
2008 Bright molecules with sense, logic, numeracy and utility. Organic & biomolecular chemistry 87 18600265
2007 Quantum dots and peptides: a bright future together. Biopolymers 80 17167795
2017 Cancer secretome and inflammation: The bright and the dark sides of NF-κB. Seminars in cell & developmental biology 75 28779979
2018 A bright future: optogenetics to dissect the spatiotemporal control of cell behavior. Current opinion in chemical biology 71 30529586
2022 Exosomal lncRNA HMMR-AS1 mediates macrophage polarization through miR-147a/ARID3A axis under hypoxia and affects the progression of hepatocellular carcinoma. Environmental toxicology 65 35179300
2014 Bright fluorescent Streptococcus pneumoniae for live-cell imaging of host-pathogen interactions. Journal of bacteriology 61 25512311
2024 Bright and stable monomeric green fluorescent protein derived from StayGold. Nature methods 60 38409224
2001 Green fluorescent protein--a bright idea for the study of bacterial protein localization. FEMS microbiology letters 60 11682170
2020 The bright and the dark sides of L-carnitine supplementation: a systematic review. Journal of the International Society of Sports Nutrition 57 32958033
2021 Ultra-bright Raman dots for multiplexed optical imaging. Nature communications 55 33637723
2006 Induction of immunoglobulin heavy-chain transcription through the transcription factor Bright requires TFII-I. Molecular and cellular biology 52 16738337
2012 B-cell regulator of immunoglobulin heavy-chain transcription (Bright)/ARID3a is a direct target of the oncomir microRNA-125b in progenitor B-cells. Leukemia 50 22469780
2019 Isomeric Tuning Yields Bright and Targetable Red Ca2+ Indicators. Journal of the American Chemical Society 48 31430138
2020 Novel Genetically Encoded Bright Positive Calcium Indicator NCaMP7 Based on the mNeonGreen Fluorescent Protein. International journal of molecular sciences 47 32121243
2015 Dark dyes-bright complexes: fluorogenic protein labeling. Current opinion in chemical biology 47 26056741
2010 Loss of Bright/ARID3a function promotes developmental plasticity. Stem cells (Dayton, Ohio) 46 20680960
2012 Dipolar 3-methoxychromones as bright and highly solvatochromic fluorescent dyes. Physical chemistry chemical physics : PCCP 45 22237699
2022 CD39 - A bright target for cancer immunotherapy. Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie 43 35550530
2014 Arid3a is essential to execution of the first cell fate decision via direct embryonic and extraembryonic transcriptional regulation. Genes & development 43 25319825
2022 CAR T-cell therapies in China: rapid evolution and a bright future. The Lancet. Haematology 42 36455608
2017 Bright Polymer Dots Tracking Stem Cell Engraftment and Migration to Injured Mouse Liver. Theranostics 42 28638470
2020 A Bright and Colorful Future for G-Protein Coupled Receptor Sensors. Frontiers in cellular neuroscience 41 32265667
2023 Avidity-based bright and photostable light-up aptamers for single-molecule mRNA imaging. Nature chemical biology 38 36658339
2023 Protein dynamics: The future is bright and complicated! Structural dynamics (Melville, N.Y.) 38 36865927
2018 Sulfonylurea and neuroprotection: The bright side of the moon. Journal of advanced pharmaceutical technology & research 38 30637228
2024 Imaging the dynamics of messenger RNA with a bright and stable green fluorescent RNA. Nature chemical biology 36 38783134
2020 Can nanoparticles and nano‒protein interactions bring a bright future for insulin delivery? Acta pharmaceutica Sinica. B 35 33777673
2011 In vivo confocal microscopy of conjunctival roundish bright objects: young, older, and Sjögren subjects. Investigative ophthalmology & visual science 35 21508113
2023 Bright future or blind alley? CAR-T cell therapy for solid tumors. Frontiers in immunology 34 36761757
2018 Pentacyclic adenine: a versatile and exceptionally bright fluorescent DNA base analogue. Chemical science 33 29780479
2023 A+T rich interaction domain protein 3a (Arid3a) impairs Mertk-mediated efferocytosis in cholestasis. Journal of hepatology 31 37659731
2022 The megakaryocytic transcription factor ARID3A suppresses leukemia pathogenesis. Blood 31 34570885
2020 Stealth and Bright Monomolecular Fluorescent Organic Nanoparticles Based on Folded Amphiphilic Polymer. ACS nano 30 33022173
2022 Directed Evolution of a Bright Variant of mCherry: Suppression of Nonradiative Decay by Fluorescence Lifetime Selections. The journal of physical chemistry. B 29 35709514
2024 The role of CD56bright NK cells in neurodegenerative disorders. Journal of neuroinflammation 28 38350967
2024 Personalized neoantigen cancer vaccines: current progression, challenges and a bright future. Clinical and experimental medicine 28 39325256
2022 miRNA let-7 family regulated by NEAT1 and ARID3A/NF-κB inhibits PRRSV-2 replication in vitro and in vivo. PLoS pathogens 28 36215225
2014 The Bright Side of Hematopoiesis: Regulatory Roles of ARID3a/Bright in Human and Mouse Hematopoiesis. Frontiers in immunology 28 24678314
2013 Bright ion channels and lipid bilayers. Accounts of chemical research 28 23597020
2010 The bright and the dark sides of DNA repair in stem cells. Journal of biomedicine & biotechnology 28 20396397
2019 Trophoblast-derived CXCL12 promotes CD56bright CD82- CD29+ NK cell enrichment in the decidua. American journal of reproductive immunology (New York, N.Y. : 1989) 27 31650642
2024 ARID3A enhances chemoresistance of pancreatic cancer via inhibiting PTEN-induced ferroptosis. Redox biology 26 38781729
2019 Carotenoid Nuclear Reorganization and Interplay of Bright and Dark Excited States. The journal of physical chemistry. B 26 31553605
2016 Human effector B lymphocytes express ARID3a and secrete interferon alpha. Journal of autoimmunity 26 27522115
2019 Vaccine vectors: the bright side of cytomegalovirus. Medical microbiology and immunology 24 30900089
2018 Building on Success: A Bright Future for Peptide Therapeutics. Protein and peptide letters 24 30430932
2021 Amplified Fluorescence in Situ Hybridization by Small and Bright Dye-Loaded Polymeric Nanoparticles. ACS nano 23 34928570
2019 Haem Biology in Metazoan Parasites - 'The Bright Side of Haem'. Trends in parasitology 23 30686614
2017 Bright fluorescent silica-nanoparticle probes for high-resolution STED and confocal microscopy. Beilstein journal of nanotechnology 22 28690964
2016 The bright side of plasmonic gold nanoparticles; activation of Nrf2, the cellular protective pathway. Nanoscale 22 27224746
2015 The Transcription Factor ARID3a Is Important for In Vitro Differentiation of Human Hematopoietic Progenitors. Journal of immunology (Baltimore, Md. : 1950) 22 26685208
2011 Characterization of a new ARID family transcription factor (Brightlike/ARID3C) that co-activates Bright/ARID3A-mediated immunoglobulin gene transcription. Molecular immunology 22 21955986
2008 Cross talk between Id1 and its interactive protein Dril1 mediate fibroblast responses to transforming growth factor-beta in pulmonary fibrosis. The American journal of pathology 22 18583319
2021 Extracting quantitative biological information from bright-field cell images using deep learning. Biophysics reviews 21 38505631
2022 Hepatic ARID3A facilitates liver cancer malignancy by cooperating with CEP131 to regulate an embryonic stem cell-like gene signature. Cell death & disease 20 36008383
2019 The Bright and Dark Side of DNA Methylation: A Matter of Balance. Cells 20 31614870
2019 MiR-574-5p promotes the differentiation of human cardiac fibroblasts via regulating ARID3A. Biochemical and biophysical research communications 20 31672272
2017 Flow cytometry in Spermatology: A bright future ahead. Reproduction in domestic animals = Zuchthygiene 20 28815751
2015 Highly surface functionalized carbon nano-onions for bright light bioimaging. Methods and applications in fluorescence 20 29148503
2023 Spotlight on P2X7 Receptor PET Imaging: A Bright Target or a Failing Star? International journal of molecular sciences 19 36674884
2011 Cooperation between ARID3A and p53 in the transcriptional activation of p21WAF1 in response to DNA damage. Biochemical and biophysical research communications 19 22172947
2005 The ARID domain protein dril1 is necessary for TGF(beta) signaling in Xenopus embryos. Developmental biology 17 15680369
2023 Diversified Mammalian Visuasl Adaptations to Bright- or Dim-Light Environments. Molecular biology and evolution 16 36929909
2022 Engineering Bright and Mechanosensitive Alkaline-Earth Rare-Earth Upconverting Nanoparticles. The journal of physical chemistry letters 16 35133831
2021 Novel Strategy in Breast Cancer Therapy: Revealing The Bright Side of Ginsenosides. Current molecular pharmacology 16 33494691
2024 2X-Rhodamine: A Bright and Fluorogenic Scaffold for Developing Near-Infrared Chemigenetic Indicators. Journal of the American Chemical Society 15 38605649
2001 The transcription factor, Bright, and immunoglobulin heavy chain expression. Immunologic research 15 11594453
1981 Photobiology and photomedicine: the future is bright. The Journal of investigative dermatology 15 7252254
2023 A regulatory variant at 19p13.3 is associated with primary biliary cholangitis risk and ARID3A expression. Nature communications 14 36977669
2019 New Frontiers: ARID3a in SLE. Cells 14 31554207