Affinage

CBFA2T3

Transcriptional corepressor CBFA2T3 · UniProt O75081

Length
653 aa
Mass
71.2 kDa
Annotated
2026-06-09
89 papers in source corpus 36 papers cited in narrative 36 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 6/6 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

CBFA2T3 (ETO2/MTG16) is a nuclear transcriptional corepressor that operates as a dimerizing scaffold within hematopoietic and epithelial transcription factor complexes to set the timing and direction of lineage gene expression programs (PMID:10022820, PMID:16407974, PMID:32553763). It is recruited into the SCL/TAL1 master regulatory complex through E proteins (E2A/HEB) and the TAL1 bHLH domain, and assembles tripartite corepressor modules with Gfi-1b and GATA1; in erythroid and megakaryocytic progenitors it represses target genes such as Gfi-1b, p21Cip, Pf4, and the globin genes (HBB, HBA, ALAS2), and a stoichiometric decline in ETO2 within the complex during differentiation de-represses these terminal genes (PMID:16287841, PMID:16407974, PMID:18625887, PMID:23127762). Repression is executed in part by recruiting the NuRD complex via the ETO2 hydrophobic heptad/NHR domains—NHR4 engages multivalent polyproline-leucine motifs in GATAD2A, with NHR3 oligomerization enhancing affinity—to control histone acetylation and nucleosome occupancy at the β-globin LCR and γ/ζ-globin genes, governing globin switching (PMID:32960220, PMID:40421803, PMID:39757769). ETO2 also binds N-CoR through its MYND domain and partners with sequence-specific factors ZNF652/ZNF651, Kaiso (ZBTB33), and the Notch/CSL axis to direct context-specific repression of targets including HEB and MMP-7 (PMID:15231665, PMID:18456661, PMID:23251453, PMID:20123979). In vivo it controls hematopoietic progenitor expansion and stress responses (downstream of c-Myc), T- and B-lymphopoiesis and dendritic cell subset balance through E protein and Notch-dependent repression of targets such as Id2, and intestinal/colonic stem cell niche exit and differentiation by repressing stem-cell and secretory-lineage genes—where the separation-of-function point mutations P209T (E protein binding) and F210A (NHR1/E protein) define E protein repression as a core mechanism (PMID:18710942, PMID:21536648, PMID:24980046, PMID:32553763, PMID:35503250, PMID:40316246). Beyond corepression, CBFA2T3 acts in oncogenic contexts: it potentiates RUNX1 transcriptional activity in BCP-ALL and is required for PRDM14-driven T-ALL, and as the CBFA2T3-GLIS2/ETO2-GLIS2 fusion it drives pediatric acute megakaryoblastic leukemia through NHR2-dependent oligomerization, co-occupation of enhancers with ERG, and aberrant activation of transcription factor networks (PMID:31015254, PMID:33743795, PMID:28292442, PMID:39384814).

Mechanistic history

Synthesis pass · year-by-year structured walk · 31 steps
  1. 1999 Medium

    Established that CBFA2T3 is a nuclear protein capable of homo- and hetero-dimerization with other ETO family members, defining the dimerization architecture that underlies its later scaffolding function.

    Evidence Nuclear localization studies and dimerization mapping by domain deletion in transfected cells

    PMID:10022820

    Open questions at the time
    • Did not identify physiological transcriptional partners
    • No functional consequence of dimerization established
  2. 2002 Medium

    Demonstrated that CBFA2T3 is an intrinsic transcriptional repressor with tumor-suppressor-like activity, the first functional assignment.

    Evidence GAL4-fusion reporter assay plus colony formation/soft agar rescue in breast cancer lines

    PMID:12183414

    Open questions at the time
    • No direct target genes identified
    • Mechanism of repression not defined
  3. 2004 Medium

    Identified N-CoR as a corepressor partner via the MYND domain and showed AML1-ETO competes for this site, linking CBFA2T3 to myeloid differentiation control.

    Evidence Co-IP and MYND-domain competition with overexpression rescue in 32Dcl3 and CD34+ cells

    PMID:15231665

    Open questions at the time
    • Direct chromatin targets not mapped
    • Quantitative competition with endogenous proteins unclear
  4. 2005 High

    Placed CBFA2T3 inside the SCL/TAL1 transcription factor complex with Gfi-1b, establishing it as a corepressor of erythroid/megakaryocytic master regulators whose complex is dissolved during differentiation.

    Evidence Proteomics and reciprocal endogenous co-IP in primary erythroid/megakaryocytic cells with knockdown

    PMID:16287841

    Open questions at the time
    • Direct DNA occupancy at target loci not yet shown
    • Trigger for complex dissolution undefined
  5. 2006 High

    Defined the recruitment mechanism (via E2A/HEB) and the stoichiometric-switch model in which falling ETO2 levels de-repress erythroid genes, explaining how a repressor governs differentiation timing.

    Evidence Proteomics of TAL-1 complexes plus siRNA knockdown and overexpression with expression profiling

    PMID:16407974

    Open questions at the time
    • Mechanism controlling ETO2 protein decline not identified
    • Direct vs indirect target distinction limited
  6. 2006 Medium

    Showed CBFA2T3 repression is antagonized by the ErbB-4 s80 intracellular domain, linking receptor signaling to corepressor output.

    Evidence Co-IP, colocalization, reporter assay, kinase-dead mutant analysis

    PMID:16815842

    Open questions at the time
    • Physiological context of ErbB-4/ETO2 crosstalk untested
    • Endogenous target genes not identified
  7. 2008 High

    Mapped a specific ZNF652/ZNF651 corepressor partnership (NHR3/NHR4 binding a proline-rich motif) and demonstrated direct promoter occupancy and repression of HEB, providing a sequence-specific recruitment route.

    Evidence Yeast two-hybrid, domain mapping, ChIP, and reporter assays

    PMID:16966434 PMID:18456661 PMID:20116376

    Open questions at the time
    • Genome-wide ZNF652/ETO2 target repertoire incomplete
    • ZNF651 partnership only reporter/co-IP validated
  8. 2008 High

    Established in vivo roles in hematopoiesis: Mtg16 controls myeloid-vs-MEP lineage allocation and stress progenitor expansion via a c-Myc-dependent mechanism.

    Evidence Mtg16 knockout mice with progenitor phenotyping and c-Myc/Bcl2 complementation

    PMID:18710942

    Open questions at the time
    • Direct ETO2 targets driving the c-Myc effect not defined
    • Cell-intrinsic vs niche contributions not fully separated
  9. 2008 High

    Demonstrated direct GATA1 partnership and promoter occupancy at megakaryocyte genes (Pf4), with knockdown promoting terminal differentiation, integrating ETO2 into the GATA1/SCL pentameric complex.

    Evidence Biotinylated GATA1 pull-down proteomics, co-IP, ChIP, knockdown, reporter assay

    PMID:18625887

    Open questions at the time
    • Full GATA1-target genome occupancy not mapped
    • Switch controlling repression release at differentiation unclear
  10. 2009 High

    Resolved the cooperative assembly of ETO2 and Mtgr1 on TAL1 (via TAF110/bHLH domains) and showed chromatin occupancy declines with ETO2 protein during differentiation at direct targets like P4.2.

    Evidence TAP/LC-MS, co-IP, GAL4 domain mapping, GST pulldown, ChIP in MEL cells

    PMID:19799863

    Open questions at the time
    • Quantitative stoichiometry in vivo not measured
    • How Mtgr1 mutually enhances Tal1 binding unresolved
  11. 2009 Medium

    Extended CBFA2T3 function to the nucleolus as an rRNA transcription repressor that counteracts MYC, broadening its role beyond Pol II target genes.

    Evidence RNAi knockdown, nucleolar localization, rRNA transcription and 3D acinar assays

    PMID:19961547

    Open questions at the time
    • Molecular mechanism of rDNA repression undefined
    • Relationship to its Pol II corepressor activity unclear
  12. 2010 High

    Linked CBFA2T3 to Notch signaling via CSL/Notch ICD binding and showed this interaction is required for Notch-dependent hematopoietic fate, integrating it into a major developmental pathway.

    Evidence Co-IP, Mtg16 KO progenitor fate assays, domain-specific rescue

    PMID:20123979

    Open questions at the time
    • Direct CSL-target genes regulated by MTG16 not enumerated
    • Notch ICD displacement kinetics not quantified
  13. 2011 High

    Demonstrated requirement of MTG16 for T-cell development through dual capacity to suppress E2A-dependent activation and bind Notch ICD.

    Evidence Mtg16 KO mice, competitive BMT, Notch-driven differentiation with domain complementation

    PMID:21536648

    Open questions at the time
    • Direct E2A/Notch co-target genes in T-progenitors not mapped
  14. 2011 High

    Positioned ETO2 within the NLI/Ldb1 complex at the BGL3 region with BCL11A to repress γ-globin, mechanistically tying ETO2 to hemoglobin switching via chromatin looping.

    Evidence ChIP of NLI members, chromosome conformation capture, ETO2 knockdown

    PMID:22010104

    Open questions at the time
    • Causal order of ETO2 loss vs looping not fully separated
    • Direct ETO2-BCL11A interaction not shown
  15. 2012 High

    Showed ETO2 directly occupies GATA1 globin loci and that its early peak/decline times hemoglobin gene activation in human erythroblasts.

    Evidence Microarray, ChIP-seq integration, quantitative ChIP, shRNA and overexpression in primary erythroblasts

    PMID:23127762

    Open questions at the time
    • Mechanism setting ETO2 protein dynamics not defined
  16. 2012 High

    Identified Kaiso (ZBTB33) as a sequence-specific recruiter directing MTG16 to repress targets like MMP-7, expanding its partner repertoire.

    Evidence Yeast two-hybrid, co-IP, ChIP, reporter assay with binding-site mutants

    PMID:23251453

    Open questions at the time
    • Genome-wide Kaiso/MTG16 co-targets not mapped
  17. 2012 Medium

    Revealed CRM1-dependent nucleocytoplasmic shuttling of MTG16, indicating localization is regulated and may control availability for nuclear repression.

    Evidence Immunofluorescence with validated antibodies, leptomycin-B inhibition, fractionation

    PMID:36267145

    Open questions at the time
    • Functional consequence of shuttling untested
    • Signals/conditions controlling export unknown
    • Abstract-level detail only
  18. 2014 High

    Established that Mtg16 directs dendritic cell subset balance by directly repressing Id2, with genetic rescue confirming the target.

    Evidence Mtg16 KO mice, genome-wide ChIP/expression, Mtg16/Id2 double-KO epistasis

    PMID:24980046

    Open questions at the time
    • Other DC-relevant direct targets not detailed
  19. 2015 Medium

    Implicated MTG16 in intestinal stem cell function and the DNA-damage response, shifting crypt cells between apoptosis and repair after radiation.

    Evidence Mtg16 KO mice, radiation model, DNA-damage flow cytometry, crypt enteroid assays

    PMID:25573176

    Open questions at the time
    • Direct transcriptional targets controlling repair-vs-apoptosis not identified
  20. 2019 Medium

    Showed CBFA2T3 establishes leukemia stem cell signatures in non-CBF AML and that its promoter is activated by GCN5 and repressed by RUNX1-RUNX1T1, with knockdown arresting cell cycle.

    Evidence GSEA, shRNA in vitro and xenograft, promoter analysis

    PMID:31040112

    Open questions at the time
    • Direct CBFA2T3 leukemic targets incompletely defined
    • Whether it acts as repressor or activator here unresolved
  21. 2019 Medium

    Identified PRDM14 as a partner and demonstrated CBFA2T3 is genetically required for PRDM14-driven T-ALL, an oncogenic dependency distinct from its corepressor partners.

    Evidence MS interaction screen, co-IP, Cbfa2t3 KO/heterozygous leukemia models

    PMID:31015254

    Open questions at the time
    • Target genes of the PRDM14-CBFA2T3 complex not mapped
  22. 2020 High

    Defined the NuRD-recruitment mechanism (hydrophobic heptad repeat) by which ETO2 controls histone acetylation, nucleosome occupancy, and LCR/γ-globin looping, and showed its requirement for erythroid commitment via PU.1/GATA2 downregulation.

    Evidence Eto2 KO mice (β-globin transgenic), human CD34+ reduction, ChIP-seq, 3C, NuRD interaction with heptad-deletion mutant

    PMID:32960220

    Open questions at the time
    • Precise NuRD subunit contact not yet resolved at this stage
  23. 2020 High

    Extended MTG16 function to intestinal epithelium, repressing stem-cell (Lgr5, Ascl2) and ATOH1 secretory-lineage genes downstream of Notch, controlling crypt proliferation and differentiation.

    Evidence Lgr5-GFP profiling, Mtg16/Mtg8 KO organoids, RNA-seq, ChIP-seq of crypts

    PMID:32553763

    Open questions at the time
    • Cooperation/redundancy with MTG8 partially resolved
  24. 2021 High

    Showed CBFA2T3 potentiates rather than represses RUNX1 in BCP-ALL within a feedforward enhancer loop, and that an NHR2-mimicking peptide disrupts the interaction and reduces tumor growth.

    Evidence ChIP-seq, co-IP, PLA, reporter assay, xenograft

    PMID:33743795

    Open questions at the time
    • Mechanism switching CBFA2T3 from repressor to coactivator context-dependent and not fully defined
  25. 2022 High

    Used a separation-of-function point mutant (P209T) to prove that E protein repression is a central mechanism of MTG16 in colonic differentiation and tumor suppression.

    Evidence Mtg16-/- and Mtg16P209T knock-in mice, colitis and colitis-associated cancer models, transcriptomics, ChIP

    PMID:35503250

    Open questions at the time
    • Full set of E protein targets in colon not enumerated
  26. 2024 Medium

    Revealed an unexpected activating role in which ETO2 colocalizes with EP300 and MYB at enhancers in a feedforward loop, with EP300 acetyltransferase activity stabilizing ETO2 protein and chromatin binding.

    Evidence Transcriptomics, ChIP/CUT&RUN, ETO2 depletion, EP300 small-molecule and PROTAC inhibition

    PMID:38903535

    Open questions at the time
    • Cellular context determining activation vs repression unresolved
    • Direct EP300-ETO2 contact not biochemically mapped
  27. 2024 Medium

    Demonstrated the CBFA2T3-GLIS2 fusion drives leukemia through NHR2-dependent homodimerization and direct binding of transcription factor regulatory elements, activating NOTCH/Hedgehog/TGFβ/WNT/JAK-STAT networks.

    Evidence CBFA2T3-GLIS2 mouse model, genome-wide binding, NHR2 deletion mutant

    PMID:39384814

    Open questions at the time
    • Direct vs indirect targets within the network not fully separated
  28. 2024 High

    Provided biochemical resolution of the ETO2-NuRD interface: NHR4 binds multivalent polyproline-leucine motifs in GATAD2A, with NHR3 oligomerization boosting affinity, and a disrupting peptide elevates γ-globin.

    Evidence Biochemical binding assays, peptide competition, enforced peptide expression in HUDEP-2/K562

    PMID:40421803

    Open questions at the time
    • In vivo validation of the peptide's therapeutic potential pending
  29. 2025 High

    Defined the NHR1 residue F210 as critical for E protein binding and lymphopoiesis using a separation-of-function knock-in, distinguishing E protein-dependent from -independent ETO2 functions in hematopoietic stress.

    Evidence Mtg16F210A and P209T knock-in mice, competitive BMT, phenylhydrazine hemolysis model, colony assays

    PMID:40316246

    Open questions at the time
    • Identity of E protein-independent functions contributing to severe anemia unresolved
  30. 2025 Medium

    Identified ETO2 as a MYB-induced repressor of ζ-globin via NuRD-mediated histone deacetylation, extending its globin-switching role to the α-cluster with therapeutic relevance for hemoglobin H disease.

    Evidence MYB KO mouse and cell models, ETO2 KO in patient CD34+ cells, multiomics, NuRD interaction analysis

    PMID:39757769

    Open questions at the time
    • Direct ETO2 occupancy at ζ-globin locus quantification limited
  31. 2025 Medium

    Showed the ETO2::GLIS2 fusion progressively rewires chromatin by activating DLX3, which redistributes ETS/GATA motif accessibility and is required for leukemia initiation.

    Evidence CRISPR-engineered iPSC ETO2::GLIS2 model, single-cell multi-omics, DLX3 KO epistasis

    PMID:39656971

    Open questions at the time
    • How DLX3 mechanistically alters factor accessibility not fully defined
    • Single-lab model system

Open questions

Synthesis pass · forward-looking unresolved questions
  • What molecular switch converts CBFA2T3 between corepressor (NuRD/N-CoR-recruiting) and coactivator (EP300/RUNX1-potentiating) modes, and what regulates its protein-level dynamics and CRM1-dependent localization, remains unresolved.
  • Context-determinant for activation vs repression unknown
  • Post-translational control of ETO2 protein abundance undefined
  • Structural basis for switching not established

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0140110 transcription regulator activity 8 GO:0060090 molecular adaptor activity 4 GO:0003677 DNA binding 3 GO:0042393 histone binding 2
Localization
GO:0005634 nucleus 2 GO:0005730 nucleolus 1 GO:0005829 cytosol 1
Pathway
R-HSA-1266738 Developmental Biology 5 R-HSA-74160 Gene expression (Transcription) 5 R-HSA-1643685 Disease 4 R-HSA-168256 Immune System 4 R-HSA-4839726 Chromatin organization 4 R-HSA-162582 Signal Transduction 2
Complex memberships
N-CoR corepressor complexNLI/LDB1 complexNuRD complexSCL/TAL1 transcription complex

Evidence

Reading pass · 36 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1999 ETO-2 (CBFA2T3) is a nuclear protein that forms homodimers and heterodimers with other ETO family members (ETO/MTG8, MTGR1) through a conserved region containing domain II; nuclear localization does not require domain III or the zinc-finger region. Northern analysis, nuclear localization studies, dimerization mapping by domain deletion Oncogene Medium 10022820
2002 CBFA2T3 functions as a transcriptional repressor when tethered to a GAL4 DNA-binding domain in reporter assays, and its re-introduction into breast cancer cell lines with reduced CBFA2T3 expression reduces colony growth on plastic and in soft agar, suggesting tumor suppressor activity. GAL4-fusion reporter assay, colony formation assay, soft agar assay after re-expression Cancer research Medium 12183414
2004 CBFA2T3 (ETO-2/MTG16) interacts with the nuclear receptor corepressor N-CoR through its MYND domain; AML1-ETO competitively occupies the ETO-2 binding site on N-CoR, reducing ETO-2/N-CoR interaction and thereby impairing granulocyte differentiation. Overexpression of ETO-2 rescues AML1-ETO-induced granulocyte differentiation arrest. Co-immunoprecipitation, overexpression rescue in 32Dcl3 and human CD34+ cells, MYND domain competition assay Cancer research Medium 15231665
2005 AML1-MTG16 fusion protein blocks myeloid differentiation and proliferation in 32D/WT1 cells and induces epigenetic repressive changes (histone and DNA methylation) at the AML1 target gene Csf1r (c-fms), correlating with loss of myeloid differentiation in response to GM-CSF. Myeloid differentiation assays, chromatin/epigenetic analysis of Csf1r locus in 32D/WT1 cells expressing AML1-MTG16 Oncogene Medium 16007222
2005 ETO-2 (CBFA2T3) associates with SCL in erythroid and megakaryocytic cells; in erythroid cells it additionally interacts with Gfi-1b to form a tri-partite corepressor complex; this SCL/ETO-2/Gfi-1b complex is lost during erythroid differentiation. ETO-2 exerts repressor effects on SCL target genes. Proteomic characterization of SCL complexes, co-immunoprecipitation of endogenous proteins in primary cells, genetic epistasis/knockdown in erythroid cells Molecular and cellular biology High 16287841
2006 ETO2 is recruited into TAL-1/SCL complexes through interaction with E2A/HEB; ETO2 actively represses erythroid TAL-1 target genes and governs expansion of erythroid progenitors. At the onset of differentiation, a change in stoichiometry of ETO2 within the TAL-1 complex de-represses erythroid-specific target genes including Gfi-1b and p21Cip. Tagging/proteomics of TAL-1 complexes, ectopic expression and siRNA knockdown in hematopoietic progenitor cells, gene expression analysis The EMBO journal High 16407974
2006 ErbB-4 s80 intracellular domain translocates to the nucleus, colocalizes and interacts with ETO2, and blocks ETO2-mediated transcriptional repression of a heterologous promoter. This effect does not require s80 kinase activity and is mediated by the C-terminal region of s80. Co-immunoprecipitation, co-localization, transcriptional reporter assay, kinase-dead mutant analysis The Journal of biological chemistry Medium 16815842
2006 ZNF652 specifically interacts with CBFA2T3 through the C-terminal 109 amino acids of ZNF652; this interaction is substantially stronger than ZNF652 interactions with the other two ETO family members (CBFA2T1 and CBFA2T2). The CBFA2T3-ZNF652 complex represses transcription in reporter assays. Yeast two-hybrid screen, co-immunoprecipitation, transcriptional reporter assay Molecular cancer research : MCR Medium 16966434
2008 CBFA2T3 interacts with ZNF652 via its NHR3 and NHR4 domains binding a conserved proline-rich region in the C-terminus of ZNF652; the CBFA2T3-ZNF652 corepressor complex directly represses HEB (E-box gene) by binding a single ZNF652 response element within the HEB promoter. Domain mapping, chromatin immunoprecipitation, transcriptional reporter assay, co-immunoprecipitation The Journal of biological chemistry High 18456661
2008 Inactivation of Mtg16 in mice skews early myeloid progenitor cells toward granulocytic/macrophage lineage while reducing megakaryocyte-erythroid progenitors, and impairs rapid expansion of short-term stem cells and multipotent progenitors under hematopoietic stress. This proliferative defect is rescued by c-Myc but not Bcl2. Mtg16 knockout mice, flow cytometry of progenitor populations, rescue by c-Myc/Bcl2 complementation Molecular and cellular biology High 18710942
2008 ETO2 (CBFA2T3) interacts with GATA1 in megakaryocytes; knockdown of ETO2 promotes megakaryocyte differentiation and enhances expression of terminal megakaryocyte genes including Pf4. ETO2 directly represses the Pf4 proximal promoter through GATA-binding sites and an E-Box motif, and endogenous ETO2, GATA1, and the SCL pentameric complex all occupy this promoter in vivo. Biotinylated GATA1 pull-down/proteomics, co-immunoprecipitation, ETO2 knockdown, chromatin immunoprecipitation, reporter assay Blood High 18625887
2009 Eto2/Mtg16 and Mtgr1 are heteromeric corepressors of TAL1/SCL in murine erythroid progenitors; they interact through the bHLH domain of Tal1 and the TAF110 domain of Eto2. Mtgr1 and Eto2 enhance each other's association with Tal1. Enforced Eto2 expression inhibits the Protein 4.2 (P4.2) gene promoter (a direct TAL1 target), and Eto2 chromatin occupancy at the P4.2 promoter decreases during differentiation in parallel with declining Eto2 protein. Tandem affinity purification/LC-MS, co-immunoprecipitation in COS-7 and MEL cells, Gal4-fusion domain mapping, GST pull-down, chromatin immunoprecipitation Biochemical and biophysical research communications High 19799863
2009 MTG16a (CBFA2T3) localizes to the nucleolus of breast epithelial cells and functions as a ribosomal RNA (rRNA) transcription repressor that counteracts MYC-driven rRNA activation. Knockdown or nucleolar sequestration of MTG16a impairs acinar morphogenesis and increases rRNA synthesis. RNA interference knockdown, nucleolar localization studies, rRNA transcription assays, 3D acinar morphogenesis assay Journal of cellular and molecular medicine Medium 19961547
2010 MTG16 interacts with both CSL and the intracellular domains of Notch receptors; the Notch1 intracellular domain disrupts the MTG16-CSL interaction. Ex vivo Notch-dependent cell fate specification is impaired in Mtg16-/- hematopoietic progenitors and restored by MTG16 expression but not by an MTG16 derivative lacking the Notch intracellular domain binding site. Co-immunoprecipitation, Mtg16 knockout hematopoietic progenitor fate assays, MTG16 re-expression rescue with domain mutants Molecular and cellular biology High 20123979
2010 CBFA2T3 forms a corepressor complex with ZNF651 (a ZNF652 paralogue) that shares the same consensus DNA binding sequence as ZNF652 and represses target gene expression, performing functionally similar roles to the CBFA2T3-ZNF652 complex in a tissue-specific manner. Reporter assay, co-immunoprecipitation, DNA binding sequence analysis FEBS letters Low 20116376
2011 ETO2 (CBFA2T3) participates in the NLI (Ldb1 homolog) complex at a site downstream of the Aγ-globin gene (BGL3 region) in human erythroid cells. When β-globin is expressed, ETO2 and BCL11A co-occupy BGL3 sequences to repress γ-globin; when γ-globin is reactivated, ETO2 participation in the NLI complex at BGL3 is diminished, LCR proximity to the BGL3/γ-globin region is established, and both BGL3 and γ-globin are transcribed. ChIP of NLI complex members, chromatin conformation capture (chromosome conformation assays), knockdown of ETO2 Blood High 22010104
2011 Mtg16 is required for T-cell development; Mtg16-/- LSK cells fail to produce CD4+/CD8+ cells in response to Notch signal in vitro. Complementation shows that the capacity of Mtg16 to suppress E2A-dependent transcriptional activation and to bind the Notch intracellular domain are both required for T-cell fate specification. Mtg16 knockout mice, competitive bone marrow transplantation, in vitro Notch-driven differentiation assay, domain complementation Molecular and cellular biology High 21536648
2012 ETO2 directly regulates globin genes (HBB, HBA, ALAS2) in human erythroid cells by occupying GATA-1 target loci; ETO2 protein peaks early in erythroid differentiation and its decline contributes to activation of these targets. ETO2 overexpression represses, and shRNA knockdown de-represses, hemoglobin gene expression in primary erythroblasts. Microarray gene expression profiling, ChIP-seq integration, quantitative ChIP, shRNA knockdown and retroviral overexpression in primary erythroblasts Experimental hematology High 23127762
2012 Kaiso (ZBTB33) interacts with MTG16 through its zinc finger domains; MTG16 is required for efficient repression of Kaiso target genes including MMP-7. ChIP shows MTG16 occupies the Kaiso binding site at the MMP-7 promoter, and this repression requires Kaiso to bind its DNA binding site. Yeast two-hybrid screen, co-immunoprecipitation, chromatin immunoprecipitation, transcriptional reporter assay with Kaiso binding site mutants PloS one High 23251453
2014 Mtg16 promotes plasmacytoid dendritic cell (pDC) differentiation and restricts classical DC (cDC) development in part by directly repressing Id2; Mtg16-deficient pDCs and cDC progenitors show aberrant Id2 induction, and Id2 deletion partially rescues impaired pDC development in Mtg16-/- mice. Mtg16 knockout mice, genome-wide expression and DNA-binding analysis (ChIP), Id2 genetic epistasis (Mtg16/Id2 double KO rescue) The Journal of experimental medicine High 24980046
2015 MTG16 loss promotes radioresistance in intestinal crypts and impacts intestinal stem cell function, shifting cellular response away from DNA damage-induced apoptosis toward DNA repair. Mtg16-/- crypts show increased Wnt3a-driven enterosphere formation but delayed maturation into enteroids. Mtg16 knockout mice, radiation injury model, flow cytometry for DNA damage markers, ex vivo crypt enteroid culture assays American journal of physiology. Gastrointestinal and liver physiology Medium 25573176
2019 CBFA2T3 regulates cell-fate genes establishing leukemia stem cell gene expression signatures; its transcription is activated via the NM_005187 promoter by GCN5 in non-CBF AML. The RUNX1-RUNX1T1 fusion protein transcriptionally represses this CBFA2T3 promoter. ShRNA-mediated CBFA2T3 knockdown arrests G1/S progression and attenuates AML cell proliferation in vitro and in vivo. Gene set enrichment analysis of primary samples, shRNA knockdown (in vitro and xenograft), promoter analysis with GCN5 activation and RUNX1-RUNX1T1 repression Blood advances Medium 31040112
2019 CBFA2T3 associates with PRDM14 in mouse leukemic cells independently of the related family member CBFA2T2; Prdm14-induced T-ALL does not occur in Cbfa2t3-deficient mice and develops with longer latency in heterozygotes, establishing that CBFA2T3 is required for PRDM14-driven leukemogenesis. Mass spectrometry protein interaction screen, co-immunoprecipitation, Cbfa2t3 knockout and heterozygous mouse leukemia model Molecular cancer research : MCR Medium 31015254
2020 ETO2 (CBFA2T3) absence in mice interferes with downregulation of PU.1 and GATA2 in fetal liver, impeding commitment to erythroid maturation. ETO2 recruits the NuRD complex via its hydrophobic heptad repeat region to regulate histone acetylation and nucleosome occupancy at the β-globin locus control region and γ-globin gene; loss of ETO2 elevates LDB1, MED1, and Pol II and facilitates fetal γ-globin/LCR looping and γ-globin transcription. Eto2 knockout mice (including human β-globin transgenic), human CD34+ cells with ETO2 reduction, ChIP-seq, chromatin conformation capture, NuRD interaction assays with hydrophobic heptad repeat deletion mutant Nucleic acids research High 32960220
2020 MTG8 and MTG16 are expressed by +4/5 early intestinal progenitors (repressed by Notch/ATOH1 signaling) and repress transcription of stem cell-specific genes (Lgr5, Ascl2) and ATOH1-regulated secretory-lineage genes; MTG16-KO intestines show crypt hyperproliferation, ISC expansion, and impaired enterocyte differentiation. Lgr5-GFP sorted cell expression profiling, Mtg16/Mtg8 knockout intestinal organoids, histology, immunohistochemistry, RNA-seq, ChIP-seq of intestinal crypts Gastroenterology High 32553763
2021 CBFA2T3 and RUNX1 form a complex in BCP-ALL cells; RUNX1 drives expression of both RUNX1 and CBFA2T3 via an enhancer ~2 kb upstream of the CBFA2T3 promoter. CBFA2T3 strongly potentiates RUNX1 transcriptional activity (activation loop). A CBFA2T3 NHR2-mimicking peptide inhibits the RUNX1-CBFA2T3 interaction and reduces BCP-ALL proliferation in vitro and in xenograft models. ChIP-seq, co-immunoprecipitation, proximity ligation assay, luciferase reporter assay, xenograft mouse model Journal of hematology & oncology High 33743795
2022 MTG16 controls colonic epithelial differentiation and regeneration by repressing E protein-mediated transcription; a point mutation (P209T) that attenuates MTG16:E protein interactions partially phenocopies MTG16 deficiency with increased tumorigenicity, demonstrating that E protein repression is a key functional mechanism of MTG16 in the colon. Mtg16-/- and Mtg16P209T knock-in mice, DSS colitis model, azoxymethane/DSS colitis-associated cancer model, transcriptomic analysis, chromatin immunoprecipitation JCI insight High 35503250
2024 ETO2 (CBFA2T3) directly activates transcription of MYB (among other genes) at enhancers by colocalizing with EP300 and MYB, forming an ETO2/MYB feedforward transcription activation loop. EP300 acetyltransferase inhibition strongly reduces ETO2 protein, chromatin binding, and ETO2-activated transcripts. Transcriptomic and chromatin binding analyses (ChIP/CUT&RUN), controlled ETO2 depletion models, EP300 inhibition (small molecule and PROTAC) HemaSphere Medium 38903535
2024 CBFA2T3 is a PPARA-sensitive gene in mouse liver; hepatic CBFA2T3 modulates expression of Cidea, Cd36, and Fabp1 (lipid accumulation genes) and Hspa1b and Ca5a. Loss of Cbfa2t3 in mice leads to increased insulin resistance and fasting-induced hepatic lipid accumulation. Cbfa2t3 knockout mice, PPARA ligand (WY14643) treatment, glucose and insulin tolerance tests, hepatic histology, gene expression analysis Cells Medium 38786053
2025 ETO2 NHR4 domain interacts with multiple polyproline-leucine motifs within GATAD2A (a NuRD complex component); oligomerization of ETO2 NHR3 enhances binding affinity for peptides containing ≥2 polyproline-leucine motifs (multivalent interaction). A peptide disrupting this interaction elevates γ-globin expression and induces differentiation of HUDEP-2 and K562 cells. Biochemical binding assays, peptide competition, enforced peptide expression in cell lines with γ-globin expression readout Nucleic acids research High 40421803
2025 Mtg16 interaction with E proteins (via NHR1 domain residue F210) is critical for B and T lymphopoiesis; F210A knock-in mice show impaired lymphopoiesis after competitive bone marrow transplant equivalent to Mtg16-/- mice. The Mtg16:E protein interaction is also required for normal burst-forming unit-erythroid (BFU-E) response after hemolytic stress, though Mtg16-/- mice are more severely anemic. Mtg16F210A knock-in mice, Mtg16P209T knock-in mice, competitive bone marrow transplantation, phenylhydrazine-induced hemolytic anemia model, colony-forming assays Experimental hematology High 40316246
2025 ETO2 (via the ETO2::GLIS2 fusion) drives progressive chromatin rewiring during leukemogenesis: it aberrantly activates the osteogenic homeobox factor DLX3, which in turn increases accessibility to ETS factor motifs and reduces GATA motif accessibility. DLX3 knockout abrogates leukemia initiation in an iPSC model expressing ETO2::GLIS2. CRISPR-Cas9 genome editing of human iPSCs to create the ETO2::GLIS2 inversion, single-cell transcriptomics and chromatin accessibility profiling, DLX3 KO epistasis Blood Medium 39656971
2024 CBFA2T3-GLIS2 fusion protein binds genome-wide through its NHR2 domain (ETO moiety)-dependent homodimerization; loss of the NHR2 domain abrogates leukemia development and downregulates JAK/STAT, Hedgehog, and NOTCH transcriptional signatures. The fusion upregulates a network of transcription factor genes (NOTCH, Hedgehog, TGFβ, WNT pathways) by directly binding their regulatory elements. CBFA2T3-GLIS2 mouse model, genome-wide ChIP/binding mapping, NHR2 deletion mutant functional studies Nature communications Medium 39384814
2017 ETO2-GLIS2 fusion oncoprotein confers megakaryocytic identity via the GLIS2 moiety while both ETO2 and GLIS2 domains are required to drive increased self-renewal. ETO2-GLIS2 directly binds DNA and controls transcription by upregulating expression and interacting with ERG at enhancer elements. Interference with ETO2-GLIS2 oligomerization reverses transcriptional activation at enhancers and promotes megakaryocytic differentiation. Domain-specific functional studies, ChIP/enhancer occupancy assays, oligomerization inhibition experiments Cancer cell High 28292442
2012 MTG16 is concentrated in the cytoplasm of erythroleukemia cell lines (human and mouse), and treatment with the CRM1 antagonist leptomycin-B causes MTG16 levels to rise in the nucleus and decline in the cytoplasm, indicating bidirectional CRM1-dependent nucleocytoplasmic shuttling. Immunofluorescence with validated α-MTG16 antibodies, leptomycin-B CRM1 inhibition, subcellular fractionation Antibody technology journal Medium 36267145
2025 MYB represses ζ-globin expression by upregulating ETO2; ETO2 functions as a novel repressor of ζ-globin through coordination with the NuRD complex to modulate histone deacetylation at the ζ-globin locus. ETO2 knockout in primary CD34+ cells from non-deletional hemoglobin H patients significantly increases ζ-globin expression. MYB knockout mouse models, MYB-knockout human cell lines, ETO2 knockout in primary CD34+ cells, multiomics (RNA-seq, ChIP), NuRD interaction analysis Acta biochimica et biophysica Sinica Medium 39757769

Source papers

Stage 0 corpus · 89 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2012 An Inv(16)(p13.3q24.3)-encoded CBFA2T3-GLIS2 fusion protein defines an aggressive subtype of pediatric acute megakaryoblastic leukemia. Cancer cell 225 23153540
2005 ETO-2 associates with SCL in erythroid cells and megakaryocytes and provides repressor functions in erythropoiesis. Molecular and cellular biology 122 16287841
2006 ETO2 coordinates cellular proliferation and differentiation during erythropoiesis. The EMBO journal 120 16407974
2013 CBFA2T3-GLIS2 fusion transcript is a novel common feature in pediatric, cytogenetically normal AML, not restricted to FAB M7 subtype. Blood 116 23407549
2017 ETO2-GLIS2 Hijacks Transcriptional Complexes to Drive Cellular Identity and Self-Renewal in Pediatric Acute Megakaryoblastic Leukemia. Cancer cell 74 28292442
2008 Deletion of Mtg16, a target of t(16;21), alters hematopoietic progenitor cell proliferation and lineage allocation. Molecular and cellular biology 71 18710942
2019 Comprehensive Transcriptome Profiling of Cryptic CBFA2T3-GLIS2 Fusion-Positive AML Defines Novel Therapeutic Options: A COG and TARGET Pediatric AML Study. Clinical cancer research : an official journal of the American Association for Cancer Research 63 31719049
2018 CBFA2T3-GLIS2-positive acute myeloid leukaemia. A peculiar paediatric entity. British journal of haematology 61 30592296
2002 CBFA2T3 (MTG16) is a putative breast tumor suppressor gene from the breast cancer loss of heterozygosity region at 16q24.3. Cancer research 59 12183414
2011 Distinct Ldb1/NLI complexes orchestrate γ-globin repression and reactivation through ETO2 in human adult erythroid cells. Blood 53 22010104
2008 Characterization of megakaryocyte GATA1-interacting proteins: the corepressor ETO2 and GATA1 interact to regulate terminal megakaryocyte maturation. Blood 51 18625887
2006 ErbB-4 s80 intracellular domain abrogates ETO2-dependent transcriptional repression. The Journal of biological chemistry 51 16815842
2014 ETO family protein Mtg16 regulates the balance of dendritic cell subsets by repressing Id2. The Journal of experimental medicine 46 24980046
2006 ZNF652, a novel zinc finger protein, interacts with the putative breast tumor suppressor CBFA2T3 to repress transcription. Molecular cancer research : MCR 46 16966434
2022 CBFA2T3-GLIS2 model of pediatric acute megakaryoblastic leukemia identifies FOLR1 as a CAR T cell target. The Journal of clinical investigation 43 36136600
1999 ETO-2, a new member of the ETO-family of nuclear proteins. Oncogene 38 10022820
2017 Hh/Gli antagonist in acute myeloid leukemia with CBFA2T3-GLIS2 fusion gene. Journal of hematology & oncology 35 28109323
2008 CBFA2T3-ZNF652 corepressor complex regulates transcription of the E-box gene HEB. The Journal of biological chemistry 33 18456661
2020 The Transcription Co-Repressors MTG8 and MTG16 Regulate Exit of Intestinal Stem Cells From Their Niche and Differentiation Into Enterocyte vs Secretory Lineages. Gastroenterology 26 32553763
2020 Embryonic erythropoiesis and hemoglobin switching require transcriptional repressor ETO2 to modulate chromatin organization. Nucleic acids research 26 32960220
2017 Emerging Roles of MTG16 in Cell-Fate Control of Hematopoietic Stem Cells and Cancer. Stem cells international 26 29358956
2012 Role of transcriptional corepressor ETO2 in erythroid cells. Experimental hematology 26 23127762
2011 Mtg16/Eto2 contributes to murine T-cell development. Molecular and cellular biology 24 21536648
2009 Eto2/MTG16 and MTGR1 are heteromeric corepressors of the TAL1/SCL transcription factor in murine erythroid progenitors. Biochemical and biophysical research communications 24 19799863
2010 Myeloid translocation gene 16 (MTG16) interacts with Notch transcription complex components to integrate Notch signaling in hematopoietic cell fate specification. Molecular and cellular biology 23 20123979
2004 AML1-ETO decreases ETO-2 (MTG16) interactions with nuclear receptor corepressor, an effect that impairs granulocyte differentiation. Cancer research 23 15231665
2024 CBFA2T3::GLIS2 pediatric acute megakaryoblastic leukemia is sensitive to BCL-XL inhibition by navitoclax and DT2216. Blood advances 22 37729615
2009 Loss of MTG16a (CBFA2T3), a novel rDNA repressor, leads to increased ribogenesis and disruption of breast acinar morphogenesis. Journal of cellular and molecular medicine 22 19961547
2019 Myeloid translocation gene CBFA2T3 directs a relapse gene program and determines patient-specific outcomes in AML. Blood advances 21 31040112
2015 Transcriptional corepressor MTG16 regulates small intestinal crypt proliferation and crypt regeneration after radiation-induced injury. American journal of physiology. Gastrointestinal and liver physiology 21 25573176
2012 MTG16 contributes to colonic epithelial integrity in experimental colitis. Gut 21 22833394
2012 Kaiso directs the transcriptional corepressor MTG16 to the Kaiso binding site in target promoters. PloS one 21 23251453
2008 RUNX1-MTG16 fusion gene in acute myeloblastic leukemia with t(16;21)(q24;q22): case report and review of the literature. Cancer genetics and cytogenetics 20 18656694
2016 Med19 promotes breast cancer cell proliferation by regulating CBFA2T3/HEB expression. Breast cancer (Tokyo, Japan) 19 27572702
2018 Myeloid neoplasms with t(16;21)(q24;q22)/RUNX1-RUNX1T3 mimics acute myeloid leukemia with RUNX1-RUNX1T1. Annals of hematology 18 29872884
2013 DHH-RHEBL1 fusion transcript: a novel recurrent feature in the new landscape of pediatric CBFA2T3-GLIS2-positive acute myeloid leukemia. Oncotarget 18 24127550
2012 The CBFA2T3/ACSF3 locus is recurrently involved in IGH chromosomal translocation t(14;16)(q32;q24) in pediatric B-cell lymphoma with germinal center phenotype. Genes, chromosomes & cancer 17 22420028
2022 Screening of ETO2-GLIS2-induced Super Enhancers identifies targetable cooperative dependencies in acute megakaryoblastic leukemia. Science advances 15 35138899
2022 MTG16 regulates colonic epithelial differentiation, colitis, and tumorigenesis by repressing E protein transcription factors. JCI insight 15 35503250
2005 Myeloid maturation block by AML1-MTG16 is associated with Csf1r epigenetic downregulation. Oncogene 15 16007222
2023 CBFA2T3-GLIS2-dependent pediatric acute megakaryoblastic leukemia is driven by GLIS2 and sensitive to navitoclax. Cell reports 13 37716355
2021 Reduction of RUNX1 transcription factor activity by a CBFA2T3-mimicking peptide: application to B cell precursor acute lymphoblastic leukemia. Journal of hematology & oncology 12 33743795
2021 CD56, HLA-DR, and CD45 recognize a subtype of childhood AML harboring CBFA2T3-GLIS2 fusion transcript. Cytometry. Part A : the journal of the International Society for Analytical Cytology 12 33811445
2010 CBFA2T3-ZNF651, like CBFA2T3-ZNF652, functions as a transcriptional corepressor complex. FEBS letters 12 20116376
2022 High caspase 3 and vulnerability to dual BCL2 family inhibition define ETO2::GLIS2 pediatric leukemia. Leukemia 11 36585521
2002 A pediatric case of secondary leukemia associated with t(16;21)(q24;q22) exhibiting the chimeric AML1-MTG16 gene. Leukemia & lymphoma 11 11999578
2023 The NFIA-ETO2 fusion blocks erythroid maturation and induces pure erythroid leukemia in cooperation with mutant TP53. Blood 10 36735909
2019 Kaiso is required for MTG16-dependent effects on colitis-associated carcinoma. Oncogene 10 30858547
2012 The leukemia associated nuclear corepressor ETO homologue genes MTG16 and MTGR1 are regulated differently in hematopoietic cells. BMC molecular biology 9 22443175
2024 Clinical Analysis of Pediatric Acute Megakaryocytic Leukemia With CBFA2T3-GLIS2 Fusion Gene. Journal of pediatric hematology/oncology 8 38315896
2019 The Pluripotency Regulator PRDM14 Requires Hematopoietic Regulator CBFA2T3 to Initiate Leukemia in Mice. Molecular cancer research : MCR 8 31015254
2024 CBFA2T3 Is PPARA Sensitive and Attenuates Fasting-Induced Lipid Accumulation in Mouse Liver. Cells 7 38786053
2023 CBFA2T3::GLIS2-positive acute leukemia with RAM and mixed T/megakaryocytic phenotype. EJHaem 7 37601875
2016 Clinical Courses of Two Pediatric Patients with Acute Megakaryoblastic Leukemia Harboring the CBFA2T3-GLIS2 Fusion Gene. Turkish journal of haematology : official journal of Turkish Society of Haematology 7 27094503
2019 Genome-wide association study identifies CBFA2T3 affecting the rate of CSF Aβ42 decline in non-demented elders. Aging 6 31370031
2017 MTG16 is a tumor suppressor in colitis-associated carcinoma. JCI insight 6 28814670
2024 CBFA2T3-GLIS2 mediates transcriptional regulation of developmental pathways through a gene regulatory network. Nature communications 5 39384814
2022 A direct comparison between AML1-ETO and ETO2-GLIS2 leukemia fusion proteins reveals context-dependent binding and regulation of target genes and opposite functions in cell differentiation. Frontiers in cell and developmental biology 4 36158200
2024 The ETO2 transcriptional cofactor maintains acute leukemia by driving a MYB/EP300-dependent stemness program. HemaSphere 3 38903535
2022 Acute megakaryoblastic leukemia with trisomy 3 and CBFA2T3::GLIS2: A case report. Genes, chromosomes & cancer 3 35294081
2021 CTCF: A novel fusion partner of ETO2 in a multiple relapsed acute myeloid leukemia patient. Journal of leukocyte biology 3 34622967
2026 Compact Differential Photoacoustic Exhaled Gas Sensor for Online ETCO2 and ETO2 Monitoring. ACS sensors 2 41591257
2025 Myeloid sarcomas with CBFA2T3 : GLIS2 fusion: clinicopathologic characterization of 4 cases mimicking small round cell tumors. American journal of clinical pathology 2 39418128
2025 Progressive chromatin rewiring by ETO2::GLIS2 revealed in a genome-edited human iPSC model of pediatric leukemia initiation. Blood 2 39656971
2024 Pediatric Erythroid Sarcoma Diagnostically Confirmed by Identification of a Recurrent NFIA::CBFA2T3 Fusion. Genes, chromosomes & cancer 2 38884198
2024 Developmental interplay between transcriptional alterations and a targetable cytokine signaling dependency in pediatric ETO2::GLIS2 leukemia. Molecular cancer 2 39304903
2023 Chromatin Profiling of CBFA2T3-GLIS2 AMLs Identifies Key Transcription Factor Dependencies and BRG1 Inhibition as a Novel Therapeutic Strategy. bioRxiv : the preprint server for biology 2 37693371
2022 Identification of novel PIEZO1::CBFA2T3 and INO80C::SETBP1 fusion genes in an acute myeloid leukemia patient by RNA-seq. Molecular biology reports 2 36472727
2013 Expression profiling of ETO2-regulated miRNAs in erythroid cells: Possible influence on miRNA abundance. FEBS open bio 2 24251106
2025 MYB represses ζ-globin expression through upregulating ETO2. Acta biochimica et biophysica Sinica 1 39757769
2025 Transcriptional rewiring by enhancer methylation in CBFA2T3-GLIS2-driven pediatric acute megakaryoblastic leukemia. Genes & diseases 1 41141393
2025 Adverse outcomes and high incidence of therapy-related neoplasms in patients with the t(16;21)/RUNX1::RUNX1T3 fusion. Leukemia & lymphoma 1 41424335
2026 Identifying targeted therapies for CBFA2T3::GLIS2 acute myeloid leukemia. Leukemia 0 41507381
2026 Identification of an Elusive CBFA2T3::GLIS2 Fusion Variant in Acute Megakaryoblastic Leukemia by Whole Genome Sequencing. EJHaem 0 41960216
2026 [Acute megakaryoblastic leukemia with CBFA2T3::GLIS2 fusion gene: 3 cases report and literature review]. Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi 0 41991315
2026 The NFIA::CBFA2T3 identifies a molecularly defined subgroup of acute erythroid leukemia/erythroid sarcoma. Frontiers in oncology 0 42158426
2026 Identification of an NFIA::CBFA2T3 fusion in cerebrospinal fluid confirms the diagnosis of pediatric CNS myeloid sarcoma with erythroid differentiation: a case report and literature review. Frontiers in oncology 0 42205757
2025 Mtg16 NHR1 mutations cause defects in lymphopoiesis and the response to anemia. Experimental hematology 0 40316246
2025 The role of multivalency in the association of the eight twenty-one protein 2 (ETO2) with the nucleosome remodeling and deacetylase (NuRD) complex. Nucleic acids research 0 40421803
2025 Identifying Targeted Therapies for CBFA2T3::GLIS2 Acute Myeloid Leukemia. Research square 0 40470252
2025 Extramedullary Relapse of CBFA2T3::GLIS2-Positive Megakaryoblastic Leukemia Mimicking Secondary Ewing Sarcoma: An Exemplary Case for the Diagnostic Trap. International journal of molecular sciences 0 40565358
2025 Two-way inhibition of PAX5 transcriptional activity by PAX5::CBFA2T3. FEBS open bio 0 40643079
2025 A stem cell differentiation model reveals two alternative fates in CBFA2T3::GLIS2-driven acute megakaryoblastic leukemia initiation. Communications biology 0 40866546
2025 BH3 mimetic therapies for CBFA2T3::GLIS2 pediatric acute megakaryoblastic leukemia. Trends in molecular medicine 0 41058336
2025 Guanylate-binding proteins score and a CBFA2T3-included risk model define immune microenvironment and chemosensitivity in lung adenocarcinoma. European journal of medical research 0 41419978
2024 [Mitoxantrone hydrochloride liposome combined with cytarabine for treating pediatric acute myeloid leukemia with RUNX1∷MTG16 fusion gene: a case report and literature review]. Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi 0 39765356
2017 ETO2-GLIS2: A Chimeric Transcription Factor Drives Leukemogenesis through a Neomorphic Transcription Network. Cancer cell 0 28292433
2015 ANTI-MTG16 ANTIBODIES REVEAL MTG16 SUBCELLULAR DISTRIBUTION AND NUCLEOCYTOPLASMIC TRANSPORT IN ERYTHROLEUKEMIA CELLS. Antibody technology journal 0 36267145
2002 [Construction and tumorigenic study on a novel fusion gene AML1-MTG16]. Zhonghua yi xue yi chuan xue za zhi = Zhonghua yixue yichuanxue zazhi = Chinese journal of medical genetics 0 12170460

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