Affinage

MYH11

Myosin-11 · UniProt P35749

Length
1972 aa
Mass
227.3 kDa
Annotated
2026-06-10
100 papers in source corpus 36 papers cited in narrative 36 extracted findings
Cross-family judge faithfulness: 9/9 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

MYH11 encodes smooth muscle myosin heavy chain (SMMHC), a contractile motor whose ATPase activity drives actin filament sliding and smooth muscle contraction (PMID:22511748). Biochemical and genetic analysis of the R247C variant established that impaired ATPase activity, slowed phosphate/ADP release, and reduced actin sliding velocity translate in vivo into decreased aortic contraction and a dedifferentiated smooth muscle cell phenotype with reduced Rho activation and loss of nuclear myocardin-related transcription factor-A, a defect rescuable by Rho activation (PMID:22511748); transcription of the MYH11 promoter is itself repressed by CHF1/Hey2 acting through GATA-6 (PMID:16293227). MYH11 dysfunction causes human disease across two organ systems: compound heterozygous null/missense alleles disrupting the motor ATP-binding pocket cause megacystis-microcolon-intestinal hypoperistalsis syndrome (MMIHS) (PMID:31044419), and a K1256del allele produces angiotensin II-driven aortic dissection accompanied by weakened cell adhesion and downregulation of integrin alpha2 (PMID:35614093). The bulk of the corpus concerns the inv(16) leukemic fusion CBFβ-SMMHC, in which the SMMHC tail is fused to CBFβ; the fusion binds the RUNX1 Runt domain with higher affinity than wild-type CBFβ through both CBFβ and SMMHC coiled-coil contacts (PMID:12172539), and requires both the CBFα-interaction domain and the SMMHC multimerization/C-terminal domain for cellular transformation, CBF inhibition, and leukemogenesis (PMID:7892201, PMID:9813068, PMID:23152542). Mechanistically the fusion sequesters RUNX1/CBFα in the cytoplasm and at aberrant high-molecular-weight nuclear structures, inhibiting CBF DNA-binding and transactivation, blocking the G1-to-S transition, and dominantly phenocopying loss of CBF function during definitive hematopoiesis (PMID:8929537, PMID:9315100, PMID:9632809, PMID:12239155). Genome-wide, CBFβ-SMMHC co-occupies RUNX1 target promoters with TAL1, FLI1, ERG, GATA2, PU.1, EP300 and HDAC1 and maintains active stem-cell gene expression rather than acting solely as a repressor (PMID:24002588); together with RUNX1 it functions as a co-activator whose target genes are downregulated upon Runx1 loss, and Runx1 activity is genetically required for leukemogenesis (PMID:25742748, PMID:32929473). The fusion sustains MYC expression by displacing RUNX1 from MYC enhancers — a switch enforced by exchange of SWI/SNF BRG1 for polycomb RING1B upon pharmacologic disruption (PMID:29958106) — recruits HDAC1 and CHD7 to drive target-gene transcription (PMID:29018080, PMID:30814129), and prevents RUNX1-dependent DNMT3A recruitment, yielding hypomethylation at target loci (PMID:34336831). Cooperating lesions including KIT D816V (via MAPK/STAT3) and NrasG12D (via MEK/ERK/Bim) accelerate transformation (PMID:22160378, PMID:24894773). The small-molecule AI-10-49 selectively disrupts the CBFβ-SMMHC/RUNX1 interaction and kills inv(16) blasts, and the fusion junction is presented as an HLA-B*40:01 neoantigen targetable by engineered T cells (PMID:25678665, PMID:32831296).

Mechanistic history

Synthesis pass · year-by-year structured walk · 24 steps
  1. 1995 High

    Established that the leukemic CBFβ-SMMHC fusion transforms cells only when both the CBFβ (CBFα-association) and SMMHC tail (multimerization) domains are intact, defining the bipartite domain logic of the oncoprotein.

    Evidence NIH 3T3 transformation assay with deletion mutants plus EMSA

    PMID:7892201

    Open questions at the time
    • Did not define the in vivo target genes
    • Mechanism of multimerization-dependent transformation unresolved
  2. 1996 High

    Showed the fusion acts as a dominant-negative on CBF in vivo, blocking definitive hematopoiesis by phenocopying Cbfb/Cbfa2 loss.

    Evidence Cbfb-MYH11 knock-in mouse embryo phenotyping with genetic epistasis

    PMID:8929537

    Open questions at the time
    • Embryonic lethality precluded study of adult leukemogenesis
    • Did not identify silenced target genes
  3. 1996 Medium

    Localized the fusion to nuclei of patient cells as novel high-molecular-weight nuclear structures, framing where its dominant-negative activity occurs.

    Evidence Immunofluorescence and EMSA on inv(16) patient nuclear extracts

    PMID:8818654

    Open questions at the time
    • Single study
    • Did not resolve nuclear vs cytoplasmic site of action
  4. 1998 High

    Defined the cell-biological mechanism: the fusion both sequesters CBFα in the cytoplasm and requires both functional domains to inhibit CBF DNA-binding, transactivation, and G1-to-S progression — nuclear localization alone being insufficient.

    Evidence GR-LBD nuclear translocation assay, deletion mutagenesis, EMSA, luciferase and cell-cycle assays

    PMID:9315100 PMID:9632809 PMID:9813068

    Open questions at the time
    • Reconciliation of cytoplasmic sequestration vs nuclear action incomplete
    • p53 and cytoskeletal effects described separately
  5. 1999 High

    Provided a structural basis for CBFα sequestration by solving the CBFβ fold and mapping its Runt-domain contact surface.

    Evidence NMR solution structure and ternary RD-β-DNA complex analysis

    PMID:10404215

    Open questions at the time
    • Did not include the SMMHC portion in the structure
    • Affinity differences vs wild-type not quantified here
  6. 2002 High

    Quantified the higher RUNX1-binding affinity of the fusion and identified SMMHC coiled-coil contacts, explaining its dominant-negative phenotype at the biophysical level.

    Evidence Isothermal titration calorimetry and NMR

    PMID:12172539

    Open questions at the time
    • In-cell consequence of higher affinity not directly tested here
    • Multimerization contribution to affinity not isolated
  7. 2002 High

    Pinpointed the hematopoietic stem/progenitor cell as the level at which the fusion blocks embryonic hematopoiesis.

    Evidence Cbfb-GFP knock-in flow cytometry in fusion-heterozygous embryos

    PMID:12239155

    Open questions at the time
    • Did not address adult leukemia initiation
    • Target genes at the HSPC level unresolved
  8. 2005 High

    Extended the mechanism to translational control and to primary cells, showing the fusion represses CEBPA protein via calreticulin and directly inhibits normal myeloid progenitor proliferation requiring both fusion domains.

    Evidence Conditional expression with siRNA rescue; transduction of murine and human CD34+ progenitors with deletion mutants

    PMID:15815715 PMID:15855281

    Open questions at the time
    • Link between calreticulin induction and RUNX1 inhibition not fully traced
    • Did not establish whether CEBPA repression is required for leukemia
  9. 2006 High

    Defined the cellular phenotype of the preleukemic state — abnormal myeloid progenitors with leukemic predisposition and lineage-specific maturation blocks.

    Evidence Conditional knock-in mouse with competitive transplantation and progenitor phenotyping

    PMID:16413472

    Open questions at the time
    • Molecular driver of AMP expansion not yet defined
    • Additional mutations needed for overt leukemia not identified here
  10. 2007 Medium

    Connected fusion activity to specific silenced loci (INK4b displacement of RUNX1) and to lymphoid differentiation/V(D)J defects, broadening the target-gene repertoire.

    Evidence ChIP and reporter assays in U937; conditional knock-in B-cell progenitor analysis

    PMID:17283131 PMID:17940206

    Open questions at the time
    • INK4b finding from single lab
    • Causal contribution of INK4b silencing to leukemia not isolated
  11. 2009 High

    Demonstrated RUNX1-independent activities of the fusion, revising the purely dominant-negative model.

    Evidence Cbfb-MYH11 knock-in crossed to Cbfb/Runx1 null backgrounds with expression profiling

    PMID:20007544

    Open questions at the time
    • Molecular basis of RUNX1-independent gene dysregulation unresolved
    • Did not identify the effector mediating Gata2/Il1rl1 maintenance
  12. 2010 High

    Overturned the assumption that RUNX1 dominant inhibition is the critical leukemogenic step, showing HABD-deleted fusion accelerates leukemia despite inefficient RUNX1 binding.

    Evidence HABD-deleted knock-in mice with transplantation and LIC frequency analysis

    PMID:20478528

    Open questions at the time
    • MN1 upregulation mechanism not defined
    • Apparent contradiction with later RUNX1-requirement findings unresolved at the time
  13. 2012 High

    Established the wild-type SMMHC motor function and its role in vascular disease: the R247C variant impairs ATPase and motility and drives SMC dedifferentiation via reduced Rho/MRTF-A signaling.

    Evidence In vitro ATPase and motility assays; knock-in mouse aortic contraction and SMC culture with Rho rescue

    PMID:22511748

    Open questions at the time
    • Mechanistic link between motor defect and Rho signaling not fully traced
    • Distinct from the leukemic fusion biology
  14. 2012 High

    Showed the SMMHC C-terminus (multimerization plus repression) is essential in vivo for both embryonic defects and leukemogenesis.

    Evidence C-terminally truncated CBFβ-SMMHCΔC95 knock-in mice with mutagen challenge

    PMID:23152542

    Open questions at the time
    • Specific repression partners recruited via the C-terminus not identified here
    • Did not separate multimerization from repression functions
  15. 2013 High

    Recast the fusion as a transcriptional maintenance factor co-occupying RUNX1 promoters with a hematopoietic TF/coactivator network and sustaining active stem-cell gene expression.

    Evidence ChIP-seq, quantitative interaction proteomics, and shRNA knockdown transcriptomics

    PMID:24002588

    Open questions at the time
    • Direct vs indirect interactions within the TF network not all resolved
    • Which interactions are leukemogenically essential not established
  16. 2014 High

    Identified cooperating oncogenic signaling lesions (KIT D816V via MAPK/STAT3; NrasG12D via MEK/ERK/Bim survival) that complete transformation.

    Evidence Retroviral KIT mutant and compound Nras/Cbfb knock-in mouse models with phospho-signaling and MEK inhibition

    PMID:22160378 PMID:24894773

    Open questions at the time
    • Whether these pathways converge on fusion target genes unresolved
    • Relative contribution of each pathway in human inv(16) AML not quantified
  17. 2014 Medium

    Linked the fusion to ribosomal gene regulation via RUNX-factor-dependent NOR association.

    Evidence Fluorescence microscopy, chromatin fractionation, and ChIP

    PMID:25079347

    Open questions at the time
    • Single lab with limited functional follow-up
    • Contribution of rDNA regulation to leukemia not established
  18. 2015 High

    Demonstrated therapeutic targetability and confirmed RUNX1 dependence: AI-10-49 disrupts the fusion-RUNX1 interaction to kill inv(16) blasts, while genetic Runx1 loss rescues defects and delays leukemia.

    Evidence Small-molecule binding/disruption assay with mouse model and primary blasts; compound Runx1-null knock-in epistasis

    PMID:25678665 PMID:25742748

    Open questions at the time
    • Reconciliation with the earlier HABD-deletion result not fully settled
    • Resistance mechanisms to AI-10-49 not addressed
  19. 2018 High

    Resolved the chromatin mechanism of MYC maintenance: the fusion keeps MYC enhancers active, and its disruption lets RUNX1 swap BRG1 for RING1B to repress MYC.

    Evidence AI-10-49, ChIP-seq, Hi-C, and CRISPR editing of enhancer-promoter connections

    PMID:29958106

    Open questions at the time
    • Generality of the BRG1/RING1B switch across target genes not established
    • Kinetics of complex exchange not defined
  20. 2019 High

    Identified HDAC1 as a required fusion-complex partner and validated HDAC inhibition as therapy.

    Evidence Co-IP, ChIP, and in vivo entinostat treatment of knock-in mice

    PMID:30814129

    Open questions at the time
    • How HDAC1 reconciles with the fusion's activating role unresolved
    • Direct vs RUNX1-mediated HDAC1 recruitment not separated
  21. 2019 Medium

    Established a non-leukemic Mendelian disease role: biallelic MYH11 loss disrupting the motor ATP pocket causes MMIHS.

    Evidence Whole-exome sequencing, arrayCGH, molecular modeling, and patient-tissue Western blot

    PMID:31044419

    Open questions at the time
    • No direct enzymatic assay of the mutant motor
    • Genotype-phenotype relationship from single family
  22. 2020 High

    Reframed the fusion-RUNX1 relationship as a co-activator partnership essential for the abnormal myeloid progenitor and for leukemia, and demonstrated a targetable fusion neoantigen.

    Evidence Conditional Runx1-knockout × Cbfb-MYH11 mice with CUT&RUN/RNA-seq; HLA-B*40:01 neoantigen T-cell killing and PDX model

    PMID:32831296 PMID:32929473

    Open questions at the time
    • Mechanism switching the fusion between repressor and co-activator roles unresolved
    • Neoantigen approach limited to a single HLA allele
  23. 2021 Medium

    Connected cytoplasmic RUNX1 sequestration to an epigenetic consequence: loss of RUNX1-dependent DNMT3A recruitment producing hypomethylation at target loci.

    Evidence Co-IP of RUNX1-DNMT3A, sequestration assay, and bisulfite sequencing

    PMID:34336831

    Open questions at the time
    • Single lab; reciprocal validation limited
    • Functional impact of hypomethylation on leukemia not established
  24. 2022 High

    Defined a vascular disease mechanism for the K1256del allele: weakened SMC adhesion and integrin alpha2 loss underlying reduced contractility and dissection susceptibility.

    Evidence Knock-in mice with angiotensin II challenge, aortic contraction, electron microscopy, and iPSC-SMC model

    PMID:35614093

    Open questions at the time
    • Causal link between Itga2 downregulation and dissection not directly tested
    • How K1256del alters motor mechanics not defined

Open questions

Synthesis pass · forward-looking unresolved questions
  • How CBFβ-SMMHC switches between dominant-negative RUNX1 inhibition and RUNX1-dependent co-activation, and how its essential SMMHC multimerization domain mechanistically enables both, remains unresolved.
  • No unified model reconciling cytoplasmic sequestration, nuclear co-activation, and the HABD-deletion acceleration
  • Structural basis for multimerization-dependent leukemogenesis not solved
  • Connection between wild-type SMMHC motor biology and fusion oncology unexplored

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0098772 molecular function regulator activity 3 GO:0140110 transcription regulator activity 3 GO:0008092 cytoskeletal protein binding 2 GO:0140657 ATP-dependent activity 2 GO:0003774 cytoskeletal motor activity 1
Localization
GO:0005634 nucleus 3 GO:0005829 cytosol 2 GO:0005730 nucleolus 1 GO:0005856 cytoskeleton 1
Pathway
R-HSA-1266738 Developmental Biology 3 R-HSA-1643685 Disease 3 R-HSA-4839726 Chromatin organization 3 R-HSA-74160 Gene expression (Transcription) 3 R-HSA-397014 Muscle contraction 2 R-HSA-1640170 Cell Cycle 1
Partners
ACTACHD7DNMT3AEP300GATA2GATA6HDAC1RUNX1
Complex memberships
CBFβ-SMMHC/HDAC1 repressor complexCBFβ-SMMHC/RUNX1 (core binding factor)

Evidence

Reading pass · 36 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1995 CBFβ-SMMHC fusion protein requires both the CBFβ domain (for CBFα association) and the SMMHC tail domain (for multimerization into filaments) to transform NIH 3T3 cells; deletion of either domain abolished focus formation, soft-agar growth, and tumor formation in nude mice. NIH 3T3 transformation assay with deletion mutants; electrophoretic mobility-shift assay Proceedings of the National Academy of Sciences of the United States of America High 7892201
1996 Mouse embryos heterozygous for a knocked-in Cbfb-MYH11 gene lacked definitive hematopoiesis and developed lethal hemorrhages (~E12.5), a phenotype consistent with dominant-negative inhibition of CBF function, as it phenocopies homozygous deletion of Cbfb or Cbfa2. Homologous recombination knock-in mouse model; embryonic phenotype analysis; genetic epistasis Cell High 8929537
1996 The CBFβ-SMMHC chimeric protein is localized primarily in the nuclei of inv(16) leukemic cells and forms a very high molecular weight protein/DNA complex in nuclear extracts; immunofluorescence shows it is organized into novel nuclear structures. Immunofluorescence staining; EMSA with nuclear extracts from patient cells; antibody against C-terminus of SMMHC and fusion junction peptide Genes, chromosomes & cancer Medium 8818654
1997 CBFβ-SMMHC reduced endogenous CBF DNA-binding ~5-fold in myeloid (32D cl3) and lymphoid (Ba/F3) cells, increased G1 fraction ~1.7-fold, decreased S-phase cells, and induced hypophosphorylated Rb, demonstrating a G1-to-S cell cycle block via CBF inhibition. Inducible metallothionein promoter expression system; EMSA; flow cytometry cell cycle analysis; BrdU incorporation; Rb phosphorylation by immunoblot Oncogene High 9315100
1998 CBFβ-SMMHC requires both the CBFα interaction domain (aa 2–11) and the SMMHC multimerization domain (C-terminal 283 residues) to inhibit CBF DNA binding, slow cell cycle progression from G1 to S, and inhibit CBF-dependent transactivation; nuclear localization alone of a CBFα-interaction-deficient mutant was insufficient to slow growth. Deletion mutagenesis; CBF DNA-binding EMSA; cell cycle analysis; luciferase transactivation assay in Ba/F3 cells The Journal of biological chemistry High 9813068
1998 CBFβ-SMMHC sequesters the CBFα (PEBP2α) subunit in the cytoplasm, blocking its nuclear translocation and thereby inhibiting PEBP2/CBF-mediated transcriptional activation; cytoplasmic sequestration was demonstrated using a glucocorticoid receptor ligand-binding domain fusion that rendered nuclear entry dexamethasone-dependent. Luciferase transactivation assay; GR-LBD fusion nuclear translocation assay; immunofluorescence microscopy Molecular and cellular biology High 9632809
1998 CBFβ-SMMHC expression reduces p53 induction 3-4-fold in response to DNA damage (ionizing radiation or etoposide) via a CBF genetic target that regulates p53 mRNA levels, and transiently slows apoptosis; a CBFα-interaction-deficient variant did not reduce p53, indicating the effect requires CBF inhibition. Inducible expression in Ba/F3 cells; p53 protein and mRNA quantification; apoptosis assays; deletion mutant analysis Blood Medium 9834241
1998 CBFβ-SMMHC disorganizes cytoplasmic stress fibers and alters F-actin organization when expressed in tissue culture cells; a significant fraction is retained in the cytoskeleton after detergent extraction; both the CBFβ and SMMHC domains are required for morphological alteration. Transfection; immunocytochemistry; double fluorescent labeling for F-actin; detergent extraction/fractionation; deletion mutant analysis Oncogene Medium 9715271
1999 NMR solution structure of PEBP2/CBFβ reveals a fold related to the β-barrel oligomer-binding (OB) motif; direct analysis of the ternary RD-β-DNA complex identifies the likely surface of CBFβ in contact with the Runt domain (RD), providing a structural basis for how CBFβ-SMMHC can sequester CBFα in the cytoplasm. NMR structure determination; ternary complex analysis by NMR Nature structural biology High 10404215
2000 PEBP2β/CBFβ-SMMHC is localized both in the nuclear fraction (co-fractionating with Runt domain proteins in high-salt DNA pellet) and in a cytoplasmic membrane fraction in inv(16) leukemic cells, suggesting the dominant-negative effect on CBF occurs inside the nucleus. Subcellular fractionation; immunoblot analysis of nuclear, DNA-pellet, and membrane fractions from patient leukemic cells Leukemia Medium 10914550
2002 CBFβ-SMMHC binds the Runt domain of RUNX1 (CBFα) with higher affinity than wild-type CBFβ, as measured by isothermal titration calorimetry; NMR identifies interactions in both the CBFβ portion and the SMMHC coiled-coil domain, explaining the dominant-negative phenotype. Isothermal titration calorimetry; NMR spectroscopy Nature structural biology High 12172539
2002 Cbfb-MYH11 blocks embryonic hematopoiesis at the hematopoietic stem/progenitor cell level, demonstrated by absence of the stem/progenitor population (marked by Cbfb-GFP knock-in) in Cbfb-MYH11 heterozygous embryos. Cbfb-GFP knock-in mouse model; flow cytometric analysis of hematopoietic stem/progenitor populations Blood High 12239155
2005 CBFβ-SMMHC suppresses CEBPA protein expression (not mRNA) in U937 cells and in inv(16) AML patient samples by inducing calreticulin, a translational inhibitor of CEBPA; siRNA knockdown of calreticulin restored CEBPA levels, establishing a calreticulin-mediated translational repression mechanism. Conditional expression in U937 cells; protein and mRNA quantification; siRNA knockdown; calreticulin siRNA rescue Blood High 15855281
2006 Cbfβ-SMMHC expression reduces multilineage repopulating capacity of HSCs while maintaining HSC numbers, induces abnormal myeloid progenitors (AMPs) with limited proliferative potential but leukemic predisposition, and blocks megakaryocytic maturation at the CFU-Meg to megakaryocyte transition. Conditional Cbfb-MYH11 knock-in mouse; competitive transplantation; flow cytometric progenitor characterization Cancer cell High 16413472
2007 CBFβ-SMMHC displaces RUNX1 from a CBF-binding site in the INK4b (p15) promoter, silencing INK4b expression through a methylation-independent mechanism in inv(16) AML. Chromatin immunoprecipitation; reporter assay; inducible expression in U937 cells; bisulfite methylation analysis of patient samples Cancer research Medium 17283131
2007 Cbfβ-SMMHC impairs differentiation of common lymphoid progenitors, blocks B-cell development at pre-pro-B stage via apoptosis, reduces expression of Ebf1, Tcfe2a, Pax5, Rag1, and Rag2, and impairs V(D)J recombination in a cell-autonomous manner. Conditional Cbfb-MYH11 knock-in mice; flow cytometric B-cell progenitor analysis; gene expression analysis; Lck-Cre conditional activation Blood High 17940206
2009 Cbfb-MYH11 induces hematopoietic defects (sustained Gata2, Il1rl1, Csf2rb expression; differentiation block) that are independent of Cbfb/Runx1 repression, as these defects are not found in Cbfb or Runx1 knockout mice, indicating additional RUNX1-independent activities of the fusion protein. Conditional Cbfb-MYH11 knock-in mice crossed with Cbfb/Runx1 null backgrounds; flow cytometric progenitor analysis; gene expression profiling Blood High 20007544
2010 Accelerated leukemia development in mice expressing CBFβ-SMMHC with the RUNX1 high-affinity binding domain (HABD) deleted, despite partial rescue of hematopoietic defects, accompanied by larger pool of leukemia-initiating cells and increased MN1 expression; type I CBFβ-SMMHC (lacking HABD) binds RUNX1 inefficiently, indicating RUNX1 dominant inhibition is not the critical step for leukemogenesis. Knock-in mice expressing HABD-deleted CBFβ-SMMHC; transplantation assays; flow cytometry; leukemia-initiating cell frequency analysis Cancer cell High 20478528
2011 KIT with D816V/Y mutations cooperates with CBFB-MYH11 for leukemogenesis; signaling analysis showed p44/42 MAPK and Stat3, but not AKT or Stat5, were strongly phosphorylated in resulting leukemia cells. Retroviral transduction of KIT mutants into conditional Cbfb-MYH11 knock-in bone marrow; transplantation assays; signaling pathway analysis by phospho-immunoblot Blood High 22160378
2012 MYH11 R247C variant reduces steady-state ATPase activity, rates of phosphate and ADP release, and actin filament sliding velocity; knock-in Myh11(R247C/R247C) mice show decreased aortic contraction, dedifferentiated SMC phenotype with increased proliferation, altered focal adhesions, decreased Rho activation, and reduced nuclear localization of myocardin-related transcription factor-A; Rho activator rescued the dedifferentiated SMC phenotype. In vitro ATPase assay; in vitro motility assay; knock-in mouse model; aortic contraction assay; vascular injury model; primary SMC culture; Rho activation assay; rescue experiment Circulation research High 22511748
2012 The C-terminus of CBFβ-SMMHC (containing self-multimerization and transcriptional repression domains) is essential for inducing embryonic hematopoietic defects and leukemogenesis; mice expressing C-terminally truncated CBFβ-SMMHCΔC95 did not develop leukemia even after mutagen treatment. Knock-in mice expressing C-terminally truncated CBFβ-SMMHC; hematopoietic phenotyping; mutagen challenge Blood High 23152542
2013 Genome-wide binding analysis shows CBFβ-SMMHC localizes to RUNX1-occupied promoters where it interacts (by quantitative interaction proteomics) with TAL1, FLI1, TBP-associated factors (TAFs), ERG, GATA2, PU.1/SPI1, EP300, and HDAC1; fusion protein knockdown revealed that the majority of its target genes (including ID1, LMO1, JAG1) are actively transcribed and repressed upon knockdown, indicating CBFβ-SMMHC maintains stem-cell gene expression. ChIP-seq (genome-wide binding); quantitative interaction proteomics (AP-MS); shRNA knockdown with transcriptional analysis Leukemia High 24002588
2014 NrasG12D cooperates with Cbfβ-SMMHC to increase survival of preleukemic short-term HSCs and myeloid progenitors via activation of the MEK/ERK/Bim axis; pharmacologic MEK/ERK inhibition increased apoptosis and Bim levels in Nras(G12D); Cbfb(56M) leukemic cells. Nras(LSL-G12D); Cbfb(56M) compound knock-in mice; competitive transplantation; MEK inhibitor treatment; Bim protein quantification Blood High 24894773
2014 CBFβ and CBFβ-SMMHC associate with nucleolar organizing regions (NORs) during mitosis and regulate RUNX-dependent ribosomal gene expression; CBFβ-SMMHC also associates with ribosomal genes in interphase chromatin via RUNX factor interactions, epigenetically sustaining ribosomal gene regulation. Fluorescence microscopy; biochemical chromatin fractionation; ChIP Journal of cellular biochemistry Medium 25079347
2015 The small-molecule inhibitor AI-10-49 selectively binds CBFβ-SMMHC and disrupts its binding to RUNX1, restoring RUNX1 transcriptional activity and delaying leukemia progression in mice; it selectively kills primary inv(16) AML patient blasts. Protein-protein interaction inhibitor design; binding assay; RUNX1 transcriptional activity assay; mouse leukemia model; primary AML patient blast cytotoxicity Science (New York, N.Y.) High 25678665
2015 Runx1 activity is required for Cbfb-MYH11-induced hematopoietic defects and leukemogenesis; loss of Runx1 rescued differentiation defects and greatly delayed leukemia onset in Cbfb-MYH11 knock-in mice. Compound Cbfb-MYH11 knock-in × Runx1 null/hypomorphic mice; competitive transplantation; hematopoietic phenotyping Leukemia High 25742748
2017 CHD7 interacts with CBFβ-SMMHC through RUNX1 (Co-IP) and enhances transcriptional activity of RUNX1 and CBFβ-SMMHC on the Csf1r target gene; Chd7 deficiency delayed Cbfb-MYH11-induced leukemia and reduced proliferation of the LK progenitor population. Co-immunoprecipitation; luciferase transcriptional assay; conditional Chd7 knockout × Cbfb-MYH11 knock-in mice; RNA-seq; BrdU labeling Blood High 29018080
2018 CBFβ-SMMHC maintains cell viability by neutralizing RUNX1-mediated repression of MYC; upon pharmacologic disruption of the CBFβ-SMMHC/RUNX1 interaction, RUNX1 binds MYC distal enhancers and represses MYC by replacing SWI/SNF component BRG1 with polycomb-repressive complex component RING1B; genome editing confirmed enhancer-MYC promoter functional connections. Pharmacologic inhibition (AI-10-49); ChIP-seq; Hi-C enhancer interaction analysis; CRISPR genome editing; SWI/SNF/PRC complex component analysis Cell High 29958106
2019 HDAC1 forms a complex with CBFβ-SMMHC, co-localizes with RUNX1 and CBFβ-SMMHC at promoters of fusion protein target genes, and is required for expression of these genes; in vivo treatment with HDAC1 inhibitor entinostat decreased leukemic burden and induced differentiation and apoptosis. Co-immunoprecipitation; ChIP; conditional knock-in mouse treatment with entinostat; gene expression analysis Molecular cancer research : MCR High 30814129
2020 RUNX1 and CBFβ-SMMHC function together as transcriptional activators of target genes in abnormal myeloid progenitors (AMPs); conditional Runx1 knockout eliminated AMPs and prevented Cbfb-MYH11-induced leukemia in a cell-autonomous manner; CUT&RUN-seq showed RUNX1/CBFβ-SMMHC target genes are mainly downregulated upon Runx1 loss. Conditional Runx1 knockout × conditional Cbfb-MYH11 knock-in mice; Mx1-Cre activation; RNA-seq; CUT&RUN-seq; flow cytometric AMP quantification Blood High 32929473
2021 CBFB-MYH11 fusion protein sequesters RUNX1 in the cytoplasm, thereby preventing RUNX1 from interacting with and recruiting DNMT3A to its target genes, resulting in DNA hypomethylation at RUNX1 target loci; RUNX1 was shown to directly interact with DNMT3A by Co-IP. Co-immunoprecipitation (RUNX1-DNMT3A interaction); cytoplasmic sequestration assay; bisulfite sequencing; gene expression analysis Frontiers in cell and developmental biology Medium 34336831
2005 CHF1/Hey2 suppresses the smooth muscle myosin heavy chain (MYH11) promoter activity through direct interaction with GATA-6 (demonstrated by Co-IP); the bHLH domain of CHF1/Hey2 is required for transcriptional repression of the SMMHC promoter; p300 overexpression could not overcome the repression. Co-immunoprecipitation; promoter-luciferase assay; co-transfection; bHLH domain mutagenesis Biochemical and biophysical research communications Medium 16293227
2022 Myh11 K1256del knock-in mice develop aortic dissections and intramural haematomas upon angiotensin II stimulation; the Myh11ΔK/ΔK aorta shows reduced contractility in response to phenylephrine, ultrastructural abnormalities with weakened cell adhesion, and downregulation of integrin subunit alpha2 (Itga2), suggesting defective cell adhesion underlies reduced aortic contractility and susceptibility to dissection. Knock-in mouse model; angiotensin II challenge; aortic contraction assay; electron microscopy; iPSC-derived SMC differentiation; gene expression analysis Scientific reports High 35614093
2005 CBFβ-SMMHC directly inhibits proliferation of normal murine and human myeloid progenitors (3-4-fold reduction) via inhibition of AML1/RUNX1; both the CBFα-interaction domain and the assembly-competence (multimerization) domain are required, as mutants lacking either domain did not slow proliferation or reduce myeloid colonies. Retroviral/lentiviral transduction of murine marrow and human CD34+ cells; liquid culture proliferation assay; colony assay; cell cycle analysis; deletion mutant analysis Leukemia High 15815715
2019 Compound heterozygosity for MYH11 null alleles (microdeletion + missense p.Pro127Ser) causes MMIHS; Pro127 is crucial for ATP binding pocket formation in the MYH11 motor domain, and molecular modeling indicated the missense alters nucleotide binding properties. Whole-exome sequencing; arrayCGH; molecular modeling of ATP binding domain; Western blot showing reduced MYH11 protein in patient tissue Clinical genetics Medium 31044419
2020 CBFβ-SMMHC fusion neoantigen peptide (from the CBFB-MYH11 junction) is naturally presented on HLA-B*40:01 on AML blasts; high-avidity CD8+ T cell clones and TCR-transduced T cells killed CBFB-MYH11+ HLA-B*40:01+ AML cell lines and primary AML samples in vitro and controlled AML in a patient-derived xenograft model. T cell clone isolation and killing assays; TCR transduction; patient-derived xenograft mouse model; primary AML sample cytotoxicity The Journal of clinical investigation High 32831296

Source papers

Stage 0 corpus · 100 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
1996 Failure of embryonic hematopoiesis and lethal hemorrhages in mouse embryos heterozygous for a knocked-in leukemia gene CBFB-MYH11. Cell 249 8929537
2007 MYH11 mutations result in a distinct vascular pathology driven by insulin-like growth factor 1 and angiotensin II. Human molecular genetics 223 17666408
2011 Novel MYH11 and ACTA2 mutations reveal a role for enhanced TGFβ signaling in FTAAD. International journal of cardiology 130 21937134
2006 Cbf beta-SMMHC induces distinct abnormal myeloid progenitors able to develop acute myeloid leukemia. Cancer cell 117 16413472
2004 Plag1 and Plagl2 are oncogenes that induce acute myeloid leukemia in cooperation with Cbfb-MYH11. Blood 112 15585652
2004 Identification of genes that synergize with Cbfb-MYH11 in the pathogenesis of acute myeloid leukemia. Proceedings of the National Academy of Sciences of the United States of America 111 15044690
1995 Detection of the chromosome 16 CBF beta-MYH11 fusion transcript in myelomonocytic leukemias. Blood 103 7858261
2015 Chemical biology. A small-molecule inhibitor of the aberrant transcription factor CBFβ-SMMHC delays leukemia in mice. Science (New York, N.Y.) 102 25678665
1995 Heterogeneity in CBF beta/MYH11 fusion messages encoded by the inv(16)(p13q22) and the t(16;16)(p13;q22) in acute myelogenous leukemia. Blood 93 7780153
2012 Rare, nonsynonymous variant in the smooth muscle-specific isoform of myosin heavy chain, MYH11, R247C, alters force generation in the aorta and phenotype of smooth muscle cells. Circulation research 81 22511748
2005 CBFB-SMMHC is correlated with increased calreticulin expression and suppresses the granulocytic differentiation factor CEBPA in AML with inv(16). Blood 80 15855281
1998 Inversion of chromosome 16 and uncommon rearrangements of the CBFB and MYH11 genes in therapy-related acute myeloid leukemia: rare events related to DNA-topoisomerase II inhibitors? Journal of clinical oncology : official journal of the American Society of Clinical Oncology 75 9586906
1995 Detection of CBFB/MYH11 transcripts in patients with inversion and other abnormalities of chromosome 16 at presentation and remission. British journal of haematology 75 7577615
2009 Runx2 induces acute myeloid leukemia in cooperation with Cbfbeta-SMMHC in mice. Blood 74 19179305
2020 CBFB-MYH11 fusion neoantigen enables T cell recognition and killing of acute myeloid leukemia. The Journal of clinical investigation 73 32831296
1997 CBF beta-SMMHC, expressed in M4Eo AML, reduced CBF DNA-binding and inhibited the G1 to S cell cycle transition at the restriction point in myeloid and lymphoid cells. Oncogene 72 9315100
2013 CBFB-MYH11/RUNX1 together with a compendium of hematopoietic regulators, chromatin modifiers and basal transcription factors occupies self-renewal genes in inv(16) acute myeloid leukemia. Leukemia 69 24002588
1998 Cytoplasmic sequestration of the polyomavirus enhancer binding protein 2 (PEBP2)/core binding factor alpha (CBFalpha) subunit by the leukemia-related PEBP2/CBFbeta-SMMHC fusion protein inhibits PEBP2/CBF-mediated transactivation. Molecular and cellular biology 68 9632809
2018 CBFβ-SMMHC Inhibition Triggers Apoptosis by Disrupting MYC Chromatin Dynamics in Acute Myeloid Leukemia. Cell 65 29958106
2008 Germ line activation of the Tie2 and SMMHC promoters causes noncell-specific deletion of floxed alleles. Physiological genomics 62 18612081
1995 RT-PCR diagnosis of patients with acute nonlymphocytic leukemia and inv(16)(p13q22) and identification of new alternative splicing in CBFB-MYH11 transcripts. Blood 60 7795233
2002 Altered affinity of CBF beta-SMMHC for Runx1 explains its role in leukemogenesis. Nature structural biology 55 12172539
1996 Identification of the chimeric protein product of the CBFB-MYH11 fusion gene in inv(16) leukemia cells. Genes, chromosomes & cancer 55 8818654
2000 Cytogenetically cryptic AML1-ETO and CBF beta-MYH11 gene rearrangements: incidence in 412 cases of acute myeloid leukaemia. British journal of haematology 54 11167739
2006 A critical developmental role for tgfbr2 in myogenic cell lineages is revealed in mice expressing SM22-Cre, not SMMHC-Cre. Journal of molecular and cellular cardiology 49 16887142
2015 Runx1 is required for hematopoietic defects and leukemogenesis in Cbfb-MYH11 knock-in mice. Leukemia 47 25742748
2002 Role of Cbfb in hematopoiesis and perturbations resulting from expression of the leukemogenic fusion gene Cbfb-MYH11. Blood 46 12239155
1998 Detection of CBFbeta/MYH11 fusion transcripts in patients with inv(16) acute myeloid leukemia after allogeneic bone marrow or peripheral blood progenitor cell transplantation. Bone marrow transplantation 46 9489633
2011 KIT with D816 mutations cooperates with CBFB-MYH11 for leukemogenesis in mice. Blood 43 22160378
2009 Cbfb/Runx1 repression-independent blockage of differentiation and accumulation of Csf2rb-expressing cells by Cbfb-MYH11. Blood 43 20007544
2007 Rare CBFB-MYH11 fusion transcripts in AML with inv(16)/t(16;16) are associated with therapy-related AML M4eo, atypical cytomorphology, atypical immunophenotype, atypical additional chromosomal rearrangements and low white blood cell count: a study on 162 patients. Leukemia 43 17287858
1999 Molecular insights into PEBP2/CBF beta-SMMHC associated acute leukemia revealed from the structure of PEBP2/CBF beta. Nature structural biology 43 10404215
2012 Incomplete segregation of MYH11 variants with thoracic aortic aneurysms and dissections and patent ductus arteriosus. European journal of human genetics : EJHG 42 22968129
2022 A New Autosomal Myh11-CreER Smooth Muscle Cell Lineage Tracing and Gene Knockout Mouse Model-Brief Report. Arteriosclerosis, thrombosis, and vascular biology 41 36519470
2010 Accelerated leukemogenesis by truncated CBF beta-SMMHC defective in high-affinity binding with RUNX1. Cancer cell 41 20478528
2014 Myh11(R247C/R247C) mutations increase thoracic aorta vulnerability to intramural damage despite a general biomechanical adaptivity. Journal of biomechanics 40 25433566
1998 The core binding factor (CBF) alpha interaction domain and the smooth muscle myosin heavy chain (SMMHC) segment of CBFbeta-SMMHC are both required to slow cell proliferation. The Journal of biological chemistry 39 9813068
1998 CBFbeta-SMMHC, expressed in M4eo acute myeloid leukemia, reduces p53 induction and slows apoptosis in hematopoietic cells exposed to DNA-damaging agents. Blood 39 9834241
2012 inv(16)/t(16;16) acute myeloid leukemia with non-type A CBFB-MYH11 fusions associate with distinct clinical and genetic features and lack KIT mutations. Blood 37 23160462
2015 A deleterious MYH11 mutation causing familial thoracic aortic dissection. Human genome variation 35 27081537
1997 Detection and quantitation of the CBFbeta/MYH11 transcripts associated with the inv(16) in presentation and follow-up samples from patients with AML. Leukemia 34 9067575
2003 Granulocytic sarcoma of the small intestine with CBFbeta/MYH11 fusion gene: report of an aleukaemic case and review of the literature. Leukemia research 32 12859999
2020 RUNX1 and CBFβ-SMMHC transactivate target genes together in abnormal myeloid progenitors for leukemia development. Blood 31 32929473
2019 Identification of a dominant MYH11 causal variant in chronic intestinal pseudo-obstruction: Results of whole-exome sequencing. Clinical genetics 31 31389005
2001 Pseudoxanthoma elasticum: Point mutations in the ABCC6 gene and a large deletion including also ABCC1 and MYH11. Human mutation 31 11439001
1993 Smooth muscle myosin heavy chain locus (MYH11) maps to 16p13.13-p13.12 and establishes a new region of conserved synteny between human 16p and mouse 16. Genomics 31 8276405
2001 Detection and quantification of CBFB/MYH11 fusion transcripts in patients with inv(16)-positive acute myeloblastic leukemia by real-time RT-PCR. Genes, chromosomes & cancer 29 11241787
2019 16p13.11 microdeletion uncovers loss-of-function of a MYH11 missense variant in a patient with megacystis-microcolon-intestinal-hypoperistalsis syndrome. Clinical genetics 28 31044419
2014 NrasG12D oncoprotein inhibits apoptosis of preleukemic cells expressing Cbfβ-SMMHC via activation of MEK/ERK axis. Blood 28 24894773
2008 Somatic mutation analysis of MYH11 in breast and prostate cancer. BMC cancer 28 18796164
1997 Detection of CBFbeta/MYH11 fusion transcripts in acute myeloid leukemia: heterogeneity of cytological and molecular characteristics. Leukemia 28 9180286
2021 Interaction between DNMT3B and MYH11 via hypermethylation regulates gastric cancer progression. BMC cancer 27 34380460
2020 Non-coding variants in MYH11, FZD3, and SORCS3 are associated with dementia in women. Alzheimer's & dementia : the journal of the Alzheimer's Association 27 32966694
2001 Function of the inv(16) fusion gene CBFB-MYH11. Current opinion in hematology 26 11561156
1995 The leukemic core binding factor beta-smooth muscle myosin heavy chain (CBF beta-SMMHC) chimeric protein requires both CBF beta and myosin heavy chain domains for transformation of NIH 3T3 cells. Proceedings of the National Academy of Sciences of the United States of America 26 7892201
2020 Protein-elongating mutations in MYH11 are implicated in a dominantly inherited smooth muscle dysmotility syndrome with severe esophageal, gastric, and intestinal disease. Human mutation 25 31944481
2019 Compound heterozygous variants in MYH11 underlie autosomal recessive megacystis-microcolon-intestinal hypoperistalsis syndrome in a Chinese family. Journal of human genetics 25 31427716
2017 Chd7 deficiency delays leukemogenesis in mice induced by Cbfb-MYH11. Blood 25 29018080
2002 Minimal residual disease quantification in patients with acute myeloid leukaemia and inv(16)/CBFB-MYH11 gene fusion. British journal of haematology 25 12139724
2022 An Myh11 single lysine deletion causes aortic dissection by reducing aortic structural integrity and contractility. Scientific reports 24 35614093
2007 Cbfbeta-SMMHC impairs differentiation of common lymphoid progenitors and reveals an essential role for RUNX in early B-cell development. Blood 22 17940206
2020 Novel Myh11 Dual Reporter Mouse Model Provides Definitive Labeling and Identification of Smooth Muscle Cells-Brief Report. Arteriosclerosis, thrombosis, and vascular biology 21 33356387
2019 IL1RL1 is dynamically expressed on Cbfb-MYH11+ leukemia stem cells and promotes cell survival. Scientific reports 21 30742053
2017 AML associated oncofusion proteins PML-RARA, AML1-ETO and CBFB-MYH11 target RUNX/ETS-factor binding sites to modulate H3ac levels and drive leukemogenesis. Oncotarget 21 28030795
2016 CBFβ-SMMHC creates aberrant megakaryocyte-erythroid progenitors prone to leukemia initiation in mice. Blood 20 27443289
2006 Granulocytic sarcoma of mesentery in acute myeloid leukemia with CBFB/MYH11 fusion gene but not inv(16) chromosome: case report and review of literature. Leukemia research 20 16504290
2018 Somatic Mutations and Intratumoral Heterogeneity of MYH11 Gene in Gastric and Colorectal Cancers. Applied immunohistochemistry & molecular morphology : AIMM 19 29517504
2017 Transdifferentiation of Human Dermal Fibroblasts to Smooth Muscle-Like Cells to Study the Effect of MYH11 and ACTA2 Mutations in Aortic Aneurysms. Human mutation 19 28074631
2010 Acute myeloid leukemia with inv(16) with CBFB-MYH11, 3'CBFB deletion, variant t(9;22) with BCR-ABL1, and del(7)(q22q32) in a pediatric patient: case report and literature review. Cancer genetics and cytogenetics 19 20513535
2017 An X-linked Myh11-CreERT2 mouse line resulting from Y to X chromosome-translocation of the Cre allele. Genesis (New York, N.Y. : 2000) 18 28845554
2011 Granulocytic sarcoma of the small bowel, greater omentum and peritoneum associated with a CBFβ/MYH11 fusion and inv(16) (p13q22): a case report. International archives of medicine 18 21255400
2011 RAD51 and XRCC3 polymorphisms: impact on the risk and treatment outcomes of de novo inv(16) or t(16;16)/CBFβ-MYH11(+) acute myeloid leukemia. Leukemia research 18 21296419
2006 CBFB-MYH11 hinders early T-cell development and induces massive cell death in the thymus. Blood 18 17185462
1998 The chimeric protein, PEBP2 beta/CBF beta-SMMHC, disorganizes cytoplasmic stress fibers and inhibits transcriptional activation. Oncogene 18 9715271
2020 Myeloid Sarcoma With CBFB-MYH11 Fusion (inv(16) or t(16;16)) Prevails in the Abdomen. American journal of clinical pathology 17 31671434
2019 Gata2 deficiency delays leukemogenesis while contributing to aggressive leukemia phenotype in Cbfb-MYH11 knockin mice. Leukemia 17 31624376
2007 Methylation-independent silencing of the tumor suppressor INK4b (p15) by CBFbeta-SMMHC in acute myelogenous leukemia with inv(16). Cancer research 17 17283131
2005 CHF1/Hey2 suppresses SM-MHC promoter activity through an interaction with GATA-6. Biochemical and biophysical research communications 17 16293227
2003 Structural and functional characterization of Runx1, CBF beta, and CBF beta-SMMHC. Blood cells, molecules & diseases 17 12732176
2000 CBFB/MYH11 fusion in a patient with AML-M4Eo and cytogenetically normal chromosomes 16. Genes, chromosomes & cancer 17 10959099
2020 Intracranial Vessel Stenosis in a Young Patient with an MYH11 Mutation: A Case Report and Review of 2 Prior Cases. World neurosurgery 16 32081817
2019 HDAC1 Is a Required Cofactor of CBFβ-SMMHC and a Potential Therapeutic Target in Inversion 16 Acute Myeloid Leukemia. Molecular cancer research : MCR 16 30814129
2015 Acute myeloid leukaemia (FAB AML-M4Eo) with cryptic insertion of cbfb resulting in cbfb-Myh11 fusion. Hematological oncology 16 28906004
2012 Estrogen-induced maldevelopment of the penis involves down-regulation of myosin heavy chain 11 (MYH11) expression, a biomarker for smooth muscle cell differentiation. Biology of reproduction 15 22976277
2012 The C-terminus of CBFβ-SMMHC is required to induce embryonic hematopoietic defects and leukemogenesis. Blood 15 23152542
2024 Single-cell RNA sequencing reveals the heterogeneity of MYH11+ tumour-associated fibroblasts between left-sided and right-sided colorectal cancer. Journal of cellular and molecular medicine 14 39294858
2021 CBFB-MYH11 Fusion Sequesters RUNX1 in Cytoplasm to Prevent DNMT3A Recruitment to Target Genes in AML. Frontiers in cell and developmental biology 14 34336831
2020 LncRNA Sox2ot modulates the progression of thoracic aortic aneurysm by regulating miR-330-5p/Myh11. Bioscience reports 14 32578852
2007 Investigation of the MYH11 gene in sporadic patients with an isolated persistently patent arterial duct. Cardiology in the young 14 17956658
2000 The PEBP2beta/CBF beta-SMMHC chimeric protein is localized both in the cell membrane and nuclear subfractions of leukemic cells carrying chromosomal inversion 16. Leukemia 14 10914550
2006 Promoter hypermethylation of the retinoic acid receptor beta2 gene is frequent in acute myeloid leukaemia and associated with the presence of CBFbeta-MYH11 fusion transcripts. British journal of haematology 13 16643429
2006 Detection of the CBFB/MYH11 fusion gene in de novo acute myeloid leukemia (AML): a single-institution study of 224 Japanese AML patients. Leukemia research 13 17052753
2005 CBFbeta-SMMHC slows proliferation of primary murine and human myeloid progenitors. Leukemia 13 15815715
2001 Prospective monitoring of minimal residual disease in acute myeloid leukemia with inversion(16) by CBFbeta/MYH11 RT-PCR: implications for a monitoring schedule and for treatment decisions. Leukemia & lymphoma 13 11697647
2006 Cbfbeta reduces Cbfbeta-SMMHC-associated acute myeloid leukemia in mice. Cancer research 12 17145866
1998 Characterization and use of an antibody detecting the CBFbeta-SMMHC fusion protein in inv(16)/t(16;16)-associated acute myeloid leukemias. Blood 12 9490670
1996 The gene product of CBFB-MYH11. Leukemia 12 8751466
2019 Myh11 Lineage Corneal Endothelial Cells and ASCs Populate Corneal Endothelium. Investigative ophthalmology & visual science 11 31826231
2014 CBFβ and the leukemogenic fusion protein CBFβ-SMMHC associate with mitotic chromosomes to epigenetically regulate ribosomal genes. Journal of cellular biochemistry 11 25079347
2014 CBFB-MYH11 hypomethylation signature and PBX3 differential methylation revealed by targeted bisulfite sequencing in patients with acute myeloid leukemia. Journal of hematology & oncology 11 25266220

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