Affinage

MEIS1

Homeobox protein Meis1 · UniProt O00470

Length
390 aa
Mass
43.0 kDa
Annotated
2026-04-28
100 papers in source corpus 44 papers cited in narrative 44 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

MEIS1 is a TALE-class homeodomain transcription factor that orchestrates cell fate decisions across hematopoiesis, cardiac development, limb patterning, and neural differentiation by forming cooperative DNA-binding complexes with PBX and HOX family proteins. MEIS1 heterodimerizes with PBX proteins through a conserved N-terminal domain distinct from the HOX-interaction interface, and assembles trimeric MEIS1–PBX–HOXA9 complexes on composite DNA elements to activate target genes including FLT3, cyclin D3, HLF, SYTL1, TAL1, FLI1, PAX6, and SKOR1; GSK-3 promotes recruitment of CREB/CBP/TORC coactivators to MEIS1, and PBX binding stabilizes MEIS1 protein by preventing CDC20-mediated ubiquitin–proteasome degradation (PMID:9343407, PMID:10082572, PMID:20541704, PMID:29719258). MEIS1 is essential for definitive hematopoiesis, megakaryopoiesis, and HSC quiescence; its deletion causes embryonic lethality with hemorrhage and vascular defects, while in adult HSCs it maintains self-renewal and glycolytic metabolism (PMID:14713950, PMID:24498346, PMID:30884246). MEIS1 is a rate-limiting driver of MLL-fusion leukemia stem cell self-renewal and independently controls cardiomyocyte cell-cycle arrest through activation of p15/p16/p21, sympathetic neuron survival via endosomal trafficking, cerebellar granule cell differentiation via PAX6–BMP signaling, and proximodistal limb patterning (PMID:17942707, PMID:23594737, PMID:26857994, PMID:29317485, PMID:10586884).

Mechanistic history

Synthesis pass · year-by-year structured walk · 17 steps
  1. 1995 High

    Identification of MEIS1 as a TALE-class homeobox gene at a retroviral insertion site in myeloid leukemia established it as a candidate oncogene and founding member of a new homeodomain subfamily.

    Evidence cDNA cloning, Northern blot, and retroviral insertional mutagenesis in BXH-2 mice

    PMID:7565694

    Open questions at the time
    • No DNA-binding specificity or partner proteins yet identified
    • Mechanism of leukemogenic activation unknown
  2. 1997 High

    Demonstration that MEIS1 forms cooperative DNA-binding heterodimers with both AbdB-like HOX proteins and PBX1 via distinct interaction interfaces defined the two-partner binding logic that underlies all subsequent MEIS1 function.

    Evidence EMSA with purified proteins, cooperative binding kinetics, deletion mapping distinguishing PBX- vs HOX-interaction domains

    PMID:9343407 PMID:9405651

    Open questions at the time
    • No trimeric complex yet demonstrated
    • In vivo relevance of these interactions not established
  3. 1999 High

    Reconstitution of a trimeric HOXA9–PBX2–MEIS1 complex in myeloid nuclei and demonstration that MEIS1/Hth drives PBX/EXD nuclear import established the core transcriptional unit and explained how MEIS1 controls partner activity in vivo.

    Evidence Co-IP from myeloid nuclear extracts, EMSA for trimeric complex, Drosophila hth genetic epistasis, chick limb ectopic expression

    PMID:10082572 PMID:10586884 PMID:9463350

    Open questions at the time
    • Genome-wide target genes unknown
    • Relative contribution of PBX nuclear import vs direct transcriptional activation not resolved
  4. 2001 High

    Showing that PREP1 cannot substitute for MEIS1 in HOXA9-induced AML despite shared PBX-binding ability revealed that MEIS1 leukemogenic function extends beyond PBX nuclear retention to include unique transactivation or target-gene selection.

    Evidence Retroviral co-expression and bone marrow transplantation leukemia model

    PMID:11113197

    Open questions at the time
    • Unique MEIS1 domains responsible for leukemogenic specificity not mapped
    • Direct transcriptional targets in leukemia unknown
  5. 2004 High

    Germline Meis1 knockout and identification of Meis1 as a critical downstream effector of MLL-ENL together established MEIS1 as essential for definitive hematopoiesis, megakaryopoiesis, angiogenesis, and HSC function, and as a key mediator of MLL-fusion leukemogenesis.

    Evidence Meis1-/- mouse embryonic lethality with hemorrhage and HSC failure; inducible MLL-ENL system showing Hoxa9+Meis1 substitutes for MLL-ENL

    PMID:14701735 PMID:14713950

    Open questions at the time
    • Cell-autonomous vs non-cell-autonomous contributions not fully separated
    • Direct MEIS1 target genes in HSCs not yet identified
  6. 2005 High

    Structure–function analysis showed that MEIS1 programs leukemia stem cell identity through PBX-dependent induction of HSC genes (FLT3, CD34), requiring PBX binding, DNA binding, and a C-terminal transactivation domain.

    Evidence Domain deletion mutants in retroviral transformation and leukemia transplantation assays

    PMID:15755900

    Open questions at the time
    • Whether FLT3 alone is sufficient for MEIS1 leukemogenic effect unclear
    • Structural basis of C-terminal domain function unknown
  7. 2006 High

    ChIP demonstration that MEIS1 and HOXA9 co-occupy the FLT3 promoter, combined with VP16-Meis1 acting as an autonomous oncogene that activates endogenous HOX genes, proved direct promoter co-occupancy and revealed bidirectional HOX-MEIS1 regulatory feedback.

    Evidence VP16/engrailed fusion proteins, ChIP on Flt3 promoter, retroviral transformation assays

    PMID:16648484

    Open questions at the time
    • Genome-wide co-occupancy maps not yet available
    • Mechanism of endogenous HOX activation by VP16-Meis1 not defined
  8. 2007 High

    Multiple loss-of-function approaches established MEIS1 as the rate-limiting factor for MLL leukemia stem cell self-renewal, quantitatively controlling LSC frequency, and identified Pbx2/Pbx3 redundancy as the PBX partner requirement.

    Evidence Conditional knockout, shRNA, dominant-negative in MLL-transformed cells with in vivo LSC frequency assay

    PMID:17942707

    Open questions at the time
    • Specific MEIS1 target genes mediating self-renewal vs differentiation arrest not separated
    • Whether MEIS1 is druggable in this context unknown
  9. 2010 High

    Discovery that GSK-3 promotes CREB/TORC/CBP coactivator assembly on MEIS1 provided the first cofactor-recruitment mechanism for MEIS1 transcriptional activation in HOX-dependent leukemia, while identification of cyclin D3 as a direct target linked MEIS1 to the cell cycle machinery.

    Evidence Co-IP of CREB/TORC/CBP with MEIS1, GSK-3 inhibition, ChIP identifying cyclin D3, M33-Meis1 repressor with rescue

    PMID:20237320 PMID:20541704

    Open questions at the time
    • How GSK-3 kinase activity mechanistically promotes coactivator assembly on MEIS1 not resolved at molecular level
    • Whether cyclin D3 is required for leukemia in vivo not tested
  10. 2011 High

    ChIP-seq revealed extensive genome-wide co-occupancy of MN1 and MEIS1 and showed that cell-of-origin susceptibility to MN1 leukemia is determined by MEIS1/HOX expression levels, establishing MEIS1 as a gatekeeper of oncogenic competence.

    Evidence ChIP-seq, genetic complementation of GMP with MEIS1/AbdB-HOX, in vivo transplantation

    PMID:21741595

    Open questions at the time
    • Whether MN1 and MEIS1 physically interact or just co-bind DNA not determined
    • Full set of co-regulated target genes not defined
  11. 2013 High

    Cardiomyocyte-specific Meis1 deletion extended postnatal proliferation and reactivated adult cardiomyocyte mitosis, while Gfi1b/LSD1/CoREST were shown to repress Meis1 in erythroid cells, revealing MEIS1 as a master regulator of cell-cycle exit and demonstrating lineage-specific epigenetic control of MEIS1 itself.

    Evidence Cardiomyocyte-specific conditional KO and OE with mitosis and cardiac function readouts; ChIP for Gfi1b/LSD1/CoREST at Meis1 promoter in erythroid cells

    PMID:23308270 PMID:23594737

    Open questions at the time
    • Whether MEIS1 deletion enables functional cardiac regeneration after injury not shown
    • Gfi1b repression mechanism limited to erythroid lineage
  12. 2014 High

    Conditional adult Meis1 KO showed HSC exhaustion due to impaired quiescence and self-renewal, PREP1 was found to antagonize MEIS1 by competing for PBX binding and destabilizing MEIS1 protein, and an RLS-associated SNP was shown to reduce MEIS1 enhancer activity via impaired CREB1 binding, broadening MEIS1 biology to stem cell homeostasis and neurological disease.

    Evidence Adult conditional KO with FACS/transplantation; PREP1 competition assays with protein stability readout; enhancer reporter assays with allelic variants and Meis1+/- behavioral phenotyping

    PMID:24498346 PMID:24578510 PMID:24642863

    Open questions at the time
    • Mechanism by which MEIS1 haploinsufficiency produces RLS-like behavior not molecularly defined
    • Identity of DDX3X/DDX5 functional role in MEIS1 tumorigenesis not elaborated
  13. 2015 High

    PBX3 binding was shown to stabilize MEIS1 by preventing ubiquitin-proteasome degradation, PBX3–MEIS1 co-expression alone was sufficient for AML, and MEIS1 was found to regulate a HLF-oxidative-stress axis and SYTL1-CXCR4 trafficking in leukemia, defining protein stability control and multiple downstream effector pathways.

    Evidence Ubiquitination assays with proteasome inhibition; PBX3+MEIS1 co-expression leukemia model; ChIP for HLF and SYTL1; oxidative stress and migration rescue experiments

    PMID:25740828 PMID:25911551 PMID:26747896 PMID:27018596

    Open questions at the time
    • E3 ligase responsible for MEIS1 ubiquitination not identified (CDC20 link came later)
    • Whether HLF and SYTL1 pathways are independent or convergent unknown
  14. 2016 High

    Neural crest-specific Meis1 knockout revealed a requirement for sympathetic neuron survival and endosomal trafficking regulation, linking MEIS1 to Rab5+ endosome function and cardiac autonomic control including susceptibility to sudden cardiac death.

    Evidence Neural crest-specific conditional KO, sympathetic neuron apoptosis assay, Rab5 endosome trafficking analysis, cardiac electrophysiology

    PMID:26857994

    Open questions at the time
    • Direct transcriptional targets mediating endosomal machinery regulation not fully identified
    • Whether this mechanism operates in other neuronal populations unknown
  15. 2018 High

    Multiple studies defined new MEIS1 transcriptional targets and regulatory axes: PPM1K was shown to maintain MEIS1 protein by opposing CDC20-mediated ubiquitination in HSCs; MEIS1 was found to drive hemogenic endothelium specification via TAL1 and megakaryopoiesis via FLI1; MEIS1 directly activates SKOR1 at an RLS SNP-modifiable promoter; and MEIS1 acts as an AR corepressor recruiting NCoR/SMRT.

    Evidence CDC20 ubiquitination assays, PPM1K conditional KO; hPSC differentiation with ChIP for TAL1/FLI1; SKOR1 promoter ChIP and allele-specific reporter; AR co-IP, GST pulldown, ChIP at PSA promoter

    PMID:25158280 PMID:29358086 PMID:29719258 PMID:30111810

    Open questions at the time
    • PPM1K–CDC20–MEIS1 axis not confirmed in leukemia context
    • AR corepressor function studied in prostate cancer cells only
    • SKOR1 regulation link to RLS pathophysiology not mechanistically complete
  16. 2019 High

    Metabolic flux analysis in cardiomyocytes demonstrated that MEIS1 actively suppresses oxidative phosphorylation and promotes glycolysis, establishing the mechanistic basis for the perinatal metabolic switch accompanying cardiomyocyte cell-cycle arrest.

    Evidence siRNA knockdown in primary fetal cardiomyocytes with Seahorse metabolic flux analysis

    PMID:30884246

    Open questions at the time
    • Direct transcriptional targets mediating metabolic reprogramming not identified
    • Whether metabolic shift is separable from cell-cycle arrest not tested
  17. 2022 High

    Epigenetic silencing of MEIS1 by EZH2–DNMT3a recruited by lncRNA ELFN1-AS1 was shown to drive oxaliplatin resistance in colorectal cancer through FEN1 upregulation, revealing an MLL-independent mechanism of MEIS1 suppression with therapeutic implications.

    Evidence ChIP for EZH2/DNMT3a at MEIS1 promoter, lncRNA–protein interaction assays, FEN1 expression, xenograft drug resistance model

    PMID:35351858

    Open questions at the time
    • Whether MEIS1 directly represses FEN1 or acts indirectly not resolved
    • Generalizability to other cancer types not established

Open questions

Synthesis pass · forward-looking unresolved questions
  • A high-resolution structural model of the MEIS1–PBX–HOX trimeric complex on DNA, the full catalog of direct MEIS1 genomic targets across normal tissues, and the mechanism by which MEIS1 haploinsufficiency causes restless legs syndrome-related neuronal phenotypes remain undefined.
  • No crystal or cryo-EM structure of MEIS1-containing trimeric complex
  • Genome-wide MEIS1 target maps in non-leukemic tissues largely absent
  • Neuronal cell types and circuits through which MEIS1 contributes to RLS not identified

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0140110 transcription regulator activity 9 GO:0003677 DNA binding 6
Localization
GO:0005634 nucleus 3
Pathway
R-HSA-74160 Gene expression (Transcription) 11 R-HSA-1643685 Disease 7 R-HSA-1266738 Developmental Biology 5 R-HSA-168256 Immune System 3 R-HSA-1640170 Cell Cycle 2 R-HSA-4839726 Chromatin organization 2
Partners
ARCBPCREB1DDX3XHOXA9PBX1PBX2PBX3
Complex memberships
MEIS1-CREB-CBP-TORC coactivator complexMEIS1-PBX heterodimerMEIS1-PBX-HOXA9 trimer

Evidence

Reading pass · 44 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1995 MEIS1 was identified as a novel TALE-class homeobox gene whose homeodomain is most closely related to PBX/exd family proteins, suggesting cooperative binding with HOX proteins; viral integration at the Meis1 locus in BXH-2 murine myeloid leukemias produces an additional truncated transcript, implicating altered MEIS1 expression in myeloid leukemogenesis. Northern blot, cDNA cloning, retroviral insertional mutagenesis in BXH-2 mice Molecular and cellular biology High 7565694
1997 MEIS1 proteins form heterodimeric DNA-binding complexes with AbdB-like HOX proteins (HOXA9, HOXA10, HOXA11, HOXD12, HOXB13) on a composite DNA target containing a MEIS1 site (TGACAG) and an AbdB-like HOX site; HOX proteins dramatically stabilize MEIS1 DNA binding, as shown by slower dissociation kinetics of the complex compared to MEIS1 alone. In vitro DNA-binding assay (EMSA), gel mobility shift, cooperative binding analysis Molecular and cellular biology High 9343407
1997 MEIS1 and its relative pKNOX1 dimerize with PBX1 on a TGATTGAC motif; the MEIS1/pKNOX1 interaction domain maps to a conserved N-terminal PBX domain that is deleted in the leukemic oncoprotein E2a-PBX1, explaining why MEIS1 fails to dimerize with E2a-PBX1. The interaction interface on MEIS1 is distinct from the tryptophan motif used by HOX proteins. EMSA, cooperative DNA-binding assays, deletion mapping, comparison with E2a-PBX1 Proceedings of the National Academy of Sciences of the United States of America High 9405651
1998 MEIS1 cooperatively binds the cAMP-responsive sequence CRS1 of bovine CYP17 together with PBX1; neither protein binds alone. Mutagenesis shows a dedicated MEIS1 binding site adjacent to the PBX site, and the conserved tryptophan N-terminal to the MEIS1 homeodomain is NOT required for Pbx cooperative binding, distinguishing the PBX-MEIS1 interaction from the PBX-HOX interaction. The interaction is evolutionarily conserved with Drosophila extradenticle and C. elegans ceh-20. CRS1 affinity chromatography purification of MEIS1 from adrenal cell extracts, EMSA, site-directed mutagenesis The Journal of biological chemistry High 9525891
1998 Homothorax (hth), the Drosophila orthologue of MEIS1, is required for nuclear localization of Extradenticle (EXD, orthologue of PBX); ectopic HTH drives ectopic nuclear EXD. In hth mutants, EXD protein remains cytoplasmic; in exd mutants, HTH protein levels are severely reduced, establishing a mutual dependency. Genetic epistasis in Drosophila, immunostaining, ectopic expression experiments Development (Cambridge, England) High 9463350
1999 MEIS1 promotes nuclear import of PBX1 in vertebrate limb cells; Meis1/2 expression is restricted to the proximal limb domain coinciding with nuclear PBX1; ectopic Meis1 in chicken limb or hth in Drosophila abolishes distal limb structures and causes distal-to-proximal identity transformations, demonstrating that restriction of Meis1/Hth to proximal regions is essential for proximodistal limb patterning. In situ hybridization, immunostaining, ectopic overexpression in chick and Drosophila, Drosophila genetics Nature High 10586884
1999 HOXA9, PBX2, and MEIS1 form trimeric complexes in myeloid cell nuclei: MEIS1 enhances in vitro HOXA9-PBX protein complex formation in the absence of DNA and forms a trimeric EMSA complex on PBX-HOXA9 oligonucleotides. Immunoprecipitation of HOXA9 from myeloid cell extracts co-precipitates PBX2 and MEIS1. The three proteins co-localize in nuclear speckles. In vitro EMSA, co-immunoprecipitation from myeloid cell nuclear extracts, immunofluorescence co-localization Molecular and cellular biology High 10082572
1999 Pbx-Meis1/Prep1 heterodimers bind DNA cooperatively with myogenic bHLH transcription factors (MyoD, myogenin, Mrf-4, Myf-5) through a conserved tryptophan motif N-terminal to the bHLH DNA-binding domain; this tryptophan motif is required for MyoD to remodel chromatin at the Myogenin promoter and activate Myogenin transcription in vivo. EMSA, tryptophan motif mutagenesis, chromatin remodeling assay, transactivation assay Nucleic acids research High 10471746
2001 MEIS1 genetically collaborates with both HOXA9 and HOXB3 to induce AML, but PREP1 overexpression cannot substitute for MEIS1 in HOXA9-induced AML despite shared ability to retain PBX in the nucleus, demonstrating that MEIS1 leukemogenic function extends beyond PBX nuclear retention. Murine bone marrow transplantation leukemia model, retroviral overexpression, genetic epistasis Molecular and cellular biology High 11113197
2003 MEIS1, PBX1B, and PBX2 bind as MEIS1/PBX complexes to the TME (tandem repeat of MEIS1 binding element) in the platelet factor 4 (PF4) promoter to activate PF4 transcription in megakaryocytic cells; disruption of MEIS1 binding sites reduces promoter activity by approximately half in megakaryocytic HEL cells. EMSA, DNA affinity chromatography, Western blot, supershift assay, promoter reporter assay, dominant-negative inhibition Blood High 12609849
2004 Meis1-deficient mouse embryos die by E14.5 with failure to produce megakaryocytes, extensive hemorrhaging, lack of well-formed capillaries, and severely reduced colony-forming hematopoietic cells; Meis1-/- fetal liver cells fail to radioprotect irradiated mice and compete poorly in repopulation assays, establishing Meis1 as required for definitive hematopoiesis, megakaryocyte production, angiogenesis, and hematopoietic stem cell function. Germline knockout mouse, fetal liver transplantation, radioprotection assay, competitive repopulation, histology The EMBO journal High 14713950
2004 Hoxa9 and Meis1 are key transcriptional targets upregulated by MLL-ENL; enforced co-expression of Hoxa9 with Meis1 is sufficient to substitute for MLL-ENL function and maintain continuous proliferation and differentiation arrest of hematopoietic cells. Inducible MLL-ENL-ERtm system, microarray expression profiling, retroviral co-expression, proliferation and differentiation assays Molecular and cellular biology High 14701735
2005 Meis1 programs expression of FLT3 and CD34 (HSC-specific genes) in Hoxa9-immortalized myeloid progenitors, converting them to AML-initiating cells. Meis1 leukemogenic activity requires PBX binding, DNA binding, and a conserved C-terminal tail function. Meis1 establishes leukemia stem cell character through induction of HSC-associated genes. Retroviral transduction, in vitro progenitor culture, leukemia transplantation assay, domain deletion mutants Blood High 15755900
2006 A dominant transactivating VP16-Meis1 fusion acts as an autonomous oncogene without co-expressed HOX genes and all resulting leukemias show activation of endogenous Hoxa9/Hoxa7, indicating HOX gene activation is a key downstream event. ChIP confirmed co-occupancy of Hoxa9 and Meis1 on the Flt3 promoter, demonstrating Meis1-Pbx and Hox-Pbx complexes co-occupy leukemogenic promoters. VP16/engrailed fusion proteins, retroviral transformation, chromatin immunoprecipitation (ChIP) on Flt3 promoter Molecular and cellular biology High 16648484
2007 Meis1 is an essential and rate-limiting regulator of MLL leukemia stem cell potential; knockout, knockdown, and dominant-negative approaches show that MLL transformation requires Meis1 and is co-dependent on redundant contributions of Pbx2 and Pbx3. Meis1 quantitatively controls self-renewal extent, differentiation arrest, cycling, and in vivo LSC generation rate. Conditional knockout, shRNA knockdown, dominant-negative genetic approaches, in vivo LSC frequency assay Genes & development High 17942707
2008 Meis1 directly occupies regulatory sequences of Trib2, Flt3, Dlk1, Ccl3, Ccl4, Pf4, and Rgs1 as shown by ChIP; the PBX-interaction domain, homeodomain, and C-terminal domain are all required for Meis1 leukemogenic collaboration with NUP98-HOXD13, while the N-terminal domain is required for Flt3 upregulation but dispensable for leukemia, indicating Flt3-independent leukemogenic pathways. ChIP, structure-function deletion analysis, murine bone marrow transplantation, gene expression profiling Experimental hematology High 18375036
2009 Meis1 regulates proximodistal patterning of the mouse limb in a Pbx1-independent manner; Msx2:Meis1 transgenic mice display altered P-D patterning and shifted Hox gene expression domains similar to chick, but Pbx1 deficiency does not modify this phenotype, suggesting Pbx1 is dispensable or another Pbx paralog provides the Meis1 partner function in this context. Transgenic mouse overexpression (Msx2 promoter-driven Meis1), Pbx1 knockout cross, limb Hox gene expression analysis The International journal of developmental biology Medium 19247936
2009 HOXA9 modulates Meis1 expression indirectly through upregulation of CREB1 and PKNOX1: ChIP showed HOXA9 does not directly bind the Meis1 promoter, but HOXA9 directly activates CREB1 and PKNOX1 transcription, and forced CREB1 expression in Hoxa9-/- bone marrow restores Meis1 mRNA levels, identifying CREB1 as a mediator of HOXA9 regulation of Meis1. ChIP, gene expression analysis in Hoxa9-/- mice, retroviral CREB1 overexpression rescue experiment Molecular and cellular biology High 19620287
2010 GSK-3 promotes conditional association of CREB and its coactivators TORC and CBP with MEIS1 to facilitate HOX-mediated transcription and transformation in MLL leukemia; this mechanism is required for maintenance of the MLL leukemia stem cell transcriptional program and applies broadly to HOX-associated leukemias. Co-immunoprecipitation of CREB/TORC/CBP with MEIS1, GSK-3 inhibition, reporter gene assays, leukemia transformation assays Cancer cell High 20541704
2010 Meis1 directly activates cyclin D3 transcription; a transcriptional repressor form (M33-Meis1) blocks G1-to-S phase progression by reducing cyclin D3 levels and inhibiting Rb hyperphosphorylation; overexpression of cyclin D3 partially rescues M33-Meis1-induced growth suppression, linking Meis1 growth-promoting activity to the cyclin D-Rb cell cycle axis. ChIP identifying cyclin D3 as direct target, M33-Meis1 repressor fusion, cell cycle analysis, Rb phosphorylation assay, cyclin D3 rescue experiment Blood High 20237320
2010 Meis1 and Pbx act upstream of gata1 in the erythropoietic transcription factor hierarchy in zebrafish; morpholino knockdown of Meis1 and Pbx causes severe reduction in gata1 expression and failure to produce circulating erythrocytes with increased myeloid cells; gata1 overexpression rescues hemoglobin expression in Pbx/Meis1-depleted embryos. Morpholino knockdown in zebrafish, genetic rescue by gata1 mRNA injection, in situ hybridization Developmental biology High 20123093
2010 ELF1, an ETS transcription factor, directly binds a conserved site 289 bp upstream of the human MEIS1 transcription start site and is required for MEIS1 promoter activity; ELF1 ChIP confirms enrichment at the MEIS1 promoter in MEIS1-expressing cells, and siRNA knockdown of ELF1 reduces MEIS1 expression. Phylogenetic sequence analysis, promoter reporter assay with truncation/mutation, EMSA, ChIP, siRNA knockdown Experimental hematology High 20600580
2011 MN1-induced leukemogenesis requires the MEIS1/AbdB-like HOX-protein complex; ChIP-seq shows extensive overlap of MN1 and MEIS1 chromatin binding sites; common myeloid progenitors (CMP) but not granulocyte-macrophage progenitors (GMP) can be transformed by MN1, and complementation of GMP with MEIS1/AbdB-like HOX genes restores susceptibility, demonstrating cell-of-origin susceptibility is determined by MEIS1/HOX expression. ChIP-seq, complementation assay in primary bone marrow cells, in vivo leukemia transplantation Cancer cell High 21741595
2013 Meis1 is a critical transcriptional regulator of cardiomyocyte cell cycle arrest; cardiomyocyte-specific Meis1 deletion extends the postnatal proliferative window and reactivates cardiomyocyte mitosis in adult heart without deleterious cardiac function effects; Meis1 overexpression decreases neonatal myocyte proliferation and inhibits neonatal heart regeneration. Meis1 is required for transcriptional activation of CDK inhibitors p15, p16, and p21. Cardiomyocyte-specific conditional knockout, Meis1 overexpression in neonatal heart, cardiomyocyte mitosis assay, cardiac function assessment, target gene expression analysis Nature High 23594737
2014 PREP1 and MEIS1 competitively heterodimerize with PBX1 in mouse embryonic fibroblasts; MEIS1 alone transforms Prep1-deficient fibroblasts; PREP1 overexpression inhibits MEIS1 tumorigenicity by sequestering PBX1, which destabilizes MEIS1 protein post-translationally. MEIS1 interaction with DDX3X and DDX5 (identified by Prep1-competition reducing these interactions) is essential for MEIS1-driven tumorigenesis. Co-immunoprecipitation, transformation assay in MEFs, protein stability assay, transcriptomic analysis Proceedings of the National Academy of Sciences of the United States of America High 24578510
2014 Conditional Meis1 knockout in adult hematopoietic cells causes significant reduction in hematopoietic stem/progenitor cells due to impaired self-renewal and reduced quiescence in a cell-autonomous manner, resulting in stem cell exhaustion. Meis1 deficiency downregulates Pbx1-dependent HSC signature genes, indicating functional cooperation with Pbx1 in HSC maintenance. Conditional knockout in adult mice (tamoxifen-inducible), FACS enumeration of HSPCs, competitive transplantation, BrdU quiescence assay, gene expression profiling PloS one High 24498346
2014 C/EBPα is a critical collaborator required for Hoxa9/Meis1-mediated leukemogenesis; over 50% of Hoxa9 genome-wide binding sites are co-bound by C/EBPα; Hoxa9 represses the Cdkn2a/b locus in concert with C/EBPα to overcome G1 cell cycle arrest; C/EBPα loss greatly improves survival in Hoxa9/Meis1-induced leukemia models. ChIP-seq, in vitro transformation assay, murine leukemia model, loss-of-function genetic approach Proceedings of the National Academy of Sciences of the United States of America High 24958854
2014 An RLS-associated intronic SNP (rs12469063) in MEIS1 reduces enhancer activity in the ganglionic eminences of the developing mouse forebrain; CREB1 binds this enhancer and the risk SNP affects CREB1 binding in vitro; heterozygous Meis1-deficient mice exhibit circadian hyperactivity resembling RLS phenotype. Zebrafish and mouse enhancer reporter assays, EMSA for CREB1 binding with allelic variants, heterozygous Meis1 KO behavioral phenotyping Genome research High 24642863
2015 Pbx3 and Meis1 must dimerize to support Hox-induced leukemia; in the absence of Pbx3, Meis1 is rapidly ubiquitinated and degraded via the proteasome. The Meis1 Pbx-binding domain is required to prevent ubiquitination; Pbx3 binding stabilizes Meis1. Additionally, Pbx3 overexpression induces endogenous Meis1 transcription. Meis1/Pbx3 dimerization is required for high-affinity DNA/Hoxa9/Meis1/Pbx3 complex formation in vitro. Deletion analysis, protein half-life assay, proteasome inhibition, in vitro EMSA for quaternary complex, murine leukemia transplantation Haematologica High 25911551
2015 PBX3 and MEIS1 co-expression, without a HOX gene, is sufficient to transform normal mouse hematopoietic stem/progenitor cells and cause AML in vivo, recapitulating the MLL-fusion core transcriptome including endogenous Hoxa gene upregulation; disruption of MEIS1-PBX3 binding abolishes transformation and HOX gene upregulation. Retroviral co-expression in primary mouse HSPC, in vitro transformation assay, in vivo transplantation AML model, gene expression profiling, interaction-disrupting mutants Cancer research High 26747896
2015 MEIS1 binds an upstream sequence of Pax6 to enhance its transcription in cerebellar granule cell precursors; this Meis1-Pax6 cascade upregulates Smad proteins to enhance BMP signaling, leading to Atoh1 protein degradation in the inner EGL and promoting GCP-to-GC differentiation. Conditional Meis1 KO in the GC lineage causes smaller cerebella with disorganized lobules and ectopic Atoh1-positive GCPs. Conditional cerebellar KO, ChIP for Pax6 upstream sequence, in vitro promoter assay, Smad/BMP pathway analysis, Atoh1 expression analysis The Journal of neuroscience High 29317485
2015 Sequential and mutually exclusive binding of MEIS1 and NKX2-5 to overlapping sites on the Popdc2 cardiac gene enhancer provides a mechanism for spatiotemporal regulation: as cardiac progenitors differentiate, they sequentially experience high MEIS1 then increasing NKX2-5, whose binding displaces MEIS1 from shared target sites to switch transcriptional output. ChIP, reporter assays, in vitro binding competition assay, expression profiling during cardiac differentiation Cell reports High 26411676
2015 Meis1 regulates a HLF-oxidative stress axis in MLL leukemia: Meis1 loss leads to increased oxidative stress, oxygen flux, and apoptosis in leukemic cells; ChIP and gene expression studies identify HLF as a direct Meis1 target gene; hypoxia or HLF expression rescues leukemia development in Meis1-deficient cells. Inducible Meis1-knockout crossed with MLL-AF9 knockin mice, ChIP for HLF promoter, oxidative stress measurement, HLF rescue experiment Blood High 25740828
2015 MEIS1 promoter is hypomethylated and transcriptionally reactivated in DNMT3A-mutant AML patients; whole-genome bisulfite sequencing and DNA methylation microarrays identify MEIS1 as the key gene undergoing promoter hypomethylation-associated reactivation, providing an alternative (MLL-fusion-independent) mechanism for engaging MEIS1-dependent oncogenic transcription. Whole-genome bisulfite sequencing, DNA methylation microarrays in patient samples Oncogene Medium 26434589
2016 MEIS1 promotes leukemic cell homing and engraftment in bone marrow through transactivation of synaptotagmin-like 1 (SYTL1/SLP1); ChIP in leukemic cells shows MEIS1 directly binds the SYTL1 gene; SYTL1 replacement in MEIS1-deficient cells restores cell migration and engraftment; SYTL1 activates CXCL12/CXCR4 signaling by regulating intracellular trafficking of CXCR4. ChIP for SYTL1 promoter, MEIS1 deficiency murine model, SYTL1 rescue experiment, CXCR4 trafficking assay, migration assay The Journal of clinical investigation High 27018596
2017 Hoxa9 and Meis1 cooperatively suppress miR-146a to upregulate Syk expression and activity in AML; Meis1 regulates Syk indirectly through PU.1-dependent regulation of miR-146a, which directly targets Syk; Syk signaling in turn induces Meis1 in the context of Hoxa9, creating a regulatory feedback loop; Syk inhibition disrupts this loop and prolongs survival of Hoxa9/Meis1 AML mice. (Phospho)proteomic analysis, miR-146a target validation for Syk, ChIP/reporter assays for PU.1-miR-146a axis, Syk inhibitor treatment in murine AML model Cancer cell High 28399410
2018 PPM1K (a mitochondrial Ser/Thr phosphatase promoting BCAA catabolism) maintains MEIS1 and p21 protein levels by decreasing CDC20-mediated ubiquitination and degradation; PPM1K deficiency reduces MEIS1/p21 signaling, impairs HSC glycolysis and quiescence, and decreases repopulation; PPM1K deletion also extends survival in a murine leukemia model. Genetically encoded BCAA fluorescent sensor, conditional KO, ubiquitination assay, HSC functional assays Cell reports High 29719258
2018 MEIS1 controls human hematopoiesis from pluripotent stem cells in a stage-specific manner: it is required for specification of APLNR+ mesoderm progenitors to functional hemogenic endothelial progenitors (via TAL1 as downstream mediator), and is separately required for megakaryopoiesis/thrombopoiesis (via FLI1 as downstream target); mechanistic ChIP or promoter binding for TAL1 and FLI1 within this context was demonstrated. hPSC differentiation, MEIS1 overexpression/knockdown, ChIP for TAL1 and FLI1, functional hematopoietic assays Stem cell reports High 29358086
2018 MEIS1 directly binds two specific sites in the SKOR1 promoter to positively regulate SKOR1 expression; an RLS-associated SNP in the SKOR1 promoter region modifies MEIS1-driven activation, directly linking two GWAS-identified RLS genes through a transcriptional regulatory relationship. MEIS1 ChIP at SKOR1 promoter sites, promoter reporter assay with site mutagenesis, allele-specific reporter assay with RLS SNP Scientific reports High 30111810
2018 MEIS1 interacts directly with the androgen receptor (AR) protein; co-immunoprecipitation and GST pull-down confirm a protein-protein interaction; MEIS1 modulates AR cytoplasm/nucleus translocation, reduces AR recruitment to the PSA gene promoter androgen response element, and promotes recruitment of corepressors NCoR and SMRT in the presence of androgen, acting as a novel AR co-repressor. Co-immunoprecipitation, GST pull-down, nuclear fractionation, ChIP for AR at PSA promoter, reporter assay Experimental cell research High 25158280
2019 MEIS1 suppression in fetal cardiomyocytes (siRNA) increases maximal oxygen consumption and mitochondrial activity while decreasing expression of glycolytic genes, demonstrating that MEIS1 actively suppresses oxidative phosphorylation and promotes glycolysis in the developing cardiomyocyte; the normal developmental downregulation of MEIS1 around birth underlies the perinatal metabolic switch. siRNA knockdown in primary fetal sheep cardiomyocytes, Seahorse metabolic flux analysis, MitoTracker staining, gene expression analysis FASEB journal High 30884246
2016 Meis1 inactivation in mouse neural crest leads to altered sympatho-vagal cardiac regulation and increased susceptibility to sudden cardiac death; Meis1-deficient sympathetic neurons die by apoptosis from embryonic to perinatal stages; Meis1 regulates transcription of key molecules for the endosomal machinery, and Rab5+ endosome trafficking is severely altered in Meis1-inactivated sympathetic neurons. Neural crest-specific conditional Meis1 knockout, cardiac electrophysiology, sympathetic neuron survival assay, endosome trafficking analysis eLife High 26857994
2013 Gfi1b directly represses Meis1 transcription in the erythroid lineage but not in megakaryocytes; Gfi1b and its cofactors LSD1 and CoREST occupy distinct regions of the Meis1 promoter in erythroid cells; LSD1 inhibition upregulates Meis1 specifically in erythroid cells; the repression requires the Gfi1b SNAG domain and DNA binding domain as shown by transfection of mutant forms. ChIP for Gfi1b/LSD1/CoREST at Meis1 promoter, LSD1 inhibitor treatment, gfi1b knockout fetal liver, promoter reporter assay with Gfi1b mutants PloS one High 23308270
2022 MEIS1 transcription is epigenetically suppressed in colorectal cancer by EZH2-DNMT3a recruited by lncRNA ELFN1-AS1 to the MEIS1 promoter; MEIS1 suppression drives oxaliplatin resistance through enhanced FEN1 expression; EZH2 inhibitor GSK126 or ELFN1-AS1 ASO restores MEIS1 expression and reverses resistance. lncRNA-protein complex analysis, ChIP for EZH2/DNMT3a at MEIS1 promoter, FEN1 expression assay, in vivo tumor xenograft, drug resistance assay Signal transduction and targeted therapy High 35351858

Source papers

Stage 0 corpus · 100 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2013 Meis1 regulates postnatal cardiomyocyte cell cycle arrest. Nature 463 23594737
2004 Hoxa9 and Meis1 are key targets for MLL-ENL-mediated cellular immortalization. Molecular and cellular biology 272 14701735
1995 Meis1, a PBX1-related homeobox gene involved in myeloid leukemia in BXH-2 mice. Molecular and cellular biology 272 7565694
2001 Defining roles for HOX and MEIS1 genes in induction of acute myeloid leukemia. Molecular and cellular biology 247 11113197
2004 Hematopoietic, angiogenic and eye defects in Meis1 mutant animals. The EMBO journal 240 14713950
1999 Conserved regulation of proximodistal limb axis development by Meis1/Hth. Nature 234 10586884
2007 Meis1 is an essential and rate-limiting regulator of MLL leukemia stem cell potential. Genes & development 228 17942707
1997 AbdB-like Hox proteins stabilize DNA binding by the Meis1 homeodomain proteins. Molecular and cellular biology 225 9343407
2002 Differential expression of Hox, Meis1, and Pbx1 genes in primitive cells throughout murine hematopoietic ontogeny. Experimental hematology 224 11823037
1999 HOXA9 forms triple complexes with PBX2 and MEIS1 in myeloid cells. Molecular and cellular biology 205 10082572
1999 Frequent co-expression of the HOXA9 and MEIS1 homeobox genes in human myeloid leukemias. Leukemia 190 10602420
2005 The homeodomain protein Meis1 is essential for definitive hematopoiesis and vascular patterning in the mouse embryo. Developmental biology 183 15882575
1998 Dorsotonals/homothorax, the Drosophila homologue of meis1, interacts with extradenticle in patterning of the embryonic PNS. Development (Cambridge, England) 176 9463350
1997 Meis1 and pKnox1 bind DNA cooperatively with Pbx1 utilizing an interaction surface disrupted in oncoprotein E2a-Pbx1. Proceedings of the National Academy of Sciences of the United States of America 165 9405651
2001 Upregulation of Meis1 and HoxA9 in acute lymphocytic leukemias with the t(4 : 11) abnormality. Oncogene 140 11314021
2022 Downregulation of MEIS1 mediated by ELFN1-AS1/EZH2/DNMT3a axis promotes tumorigenesis and oxaliplatin resistance in colorectal cancer. Signal transduction and targeted therapy 139 35351858
2007 Trib1 and Evi1 cooperate with Hoxa and Meis1 in myeloid leukemogenesis. Blood 131 17227832
2012 miR-196b directly targets both HOXA9/MEIS1 oncogenes and FAS tumour suppressor in MLL-rearranged leukaemia. Nature communications 129 22353710
2010 GSK-3 promotes conditional association of CREB and its coactivators with MEIS1 to facilitate HOX-mediated transcription and oncogenesis. Cancer cell 104 20541704
2016 Deregulation of the HOXA9/MEIS1 axis in acute leukemia. Current opinion in hematology 100 27258906
2002 Nup98-HoxA9 immortalizes myeloid progenitors, enforces expression of Hoxa9, Hoxa7 and Meis1, and alters cytokine-specific responses in a manner similar to that induced by retroviral co-expression of Hoxa9 and Meis1. Oncogene 100 12082612
2005 Meis1 programs transcription of FLT3 and cancer stem cell character, using a mechanism that requires interaction with Pbx and a novel function of the Meis1 C-terminus. Blood 97 15755900
1999 A conserved motif N-terminal to the DNA-binding domains of myogenic bHLH transcription factors mediates cooperative DNA binding with pbx-Meis1/Prep1. Nucleic acids research 97 10471746
2017 Hoxa9 and Meis1 Cooperatively Induce Addiction to Syk Signaling by Suppressing miR-146a in Acute Myeloid Leukemia. Cancer cell 93 28399410
2014 Restless legs syndrome-associated intronic common variant in Meis1 alters enhancer function in the developing telencephalon. Genome research 84 24642863
2008 A role for MEIS1 in MLL-fusion gene leukemia. Blood 84 19109563
2006 Persistent transactivation by meis1 replaces hox function in myeloid leukemogenesis models: evidence for co-occupancy of meis1-pbx and hox-pbx complexes on promoters of leukemia-associated genes. Molecular and cellular biology 81 16648484
2004 Differential and common leukemogenic potentials of multiple NUP98-Hox fusion proteins alone or with Meis1. Molecular and cellular biology 80 14966272
2008 Evidence for an evolutionary conserved role of homothorax/Meis1/2 during vertebrate retina development. Development (Cambridge, England) 79 18216174
2008 MicroRNA 155 modulates megakaryopoiesis at progenitor and precursor level by targeting Ets-1 and Meis1 transcription factors. British journal of haematology 76 18950466
2011 Cell of origin in AML: susceptibility to MN1-induced transformation is regulated by the MEIS1/AbdB-like HOX protein complex. Cancer cell 74 21741595
2011 Restless legs syndrome-associated MEIS1 risk variant influences iron homeostasis. Annals of neurology 70 21710629
2014 C/EBPα is an essential collaborator in Hoxa9/Meis1-mediated leukemogenesis. Proceedings of the National Academy of Sciences of the United States of America 69 24958854
2002 Frequent co-expression of HoxA9 and Meis1 genes in infant acute lymphoblastic leukaemia with MLL rearrangement. British journal of haematology 67 12358913
2019 Super-enhancer-associated MEIS1 promotes transcriptional dysregulation in Ewing sarcoma in co-operation with EWS-FLI1. Nucleic acids research 63 30496486
2018 MEIS1 and MEIS2 Expression and Prostate Cancer Progression: A Role For HOXB13 Binding Partners in Metastatic Disease. Clinical cancer research : an official journal of the American Association for Cancer Research 62 29716922
2015 Pbx3 and Meis1 cooperate through multiple mechanisms to support Hox-induced murine leukemia. Haematologica 61 25911551
2018 PPM1K Regulates Hematopoiesis and Leukemogenesis through CDC20-Mediated Ubiquitination of MEIS1 and p21. Cell reports 60 29719258
2001 The MEIS1 oncogene is highly expressed in neuroblastoma and amplified in cell line IMR32. Genomics 60 11161815
2010 Gfi1 expression is controlled by five distinct regulatory regions spread over 100 kilobases, with Scl/Tal1, Gata2, PU.1, Erg, Meis1, and Runx1 acting as upstream regulators in early hematopoietic cells. Molecular and cellular biology 58 20516218
2016 PBX3 and MEIS1 Cooperate in Hematopoietic Cells to Drive Acute Myeloid Leukemias Characterized by a Core Transcriptome of the MLL-Rearranged Disease. Cancer research 56 26747896
2008 Linkage of Meis1 leukemogenic activity to multiple downstream effectors including Trib2 and Ccl3. Experimental hematology 56 18375036
2011 Down-regulation of homeobox genes MEIS1 and HOXA in MLL-rearranged acute leukemia impairs engraftment and reduces proliferation. Proceedings of the National Academy of Sciences of the United States of America 55 21518888
2017 A tale of TALE, PREP1, PBX1, and MEIS1: Interconnections and competition in cancer. BioEssays : news and reviews in molecular, cellular and developmental biology 53 28322463
2015 DNMT3A mutations mediate the epigenetic reactivation of the leukemogenic factor MEIS1 in acute myeloid leukemia. Oncogene 52 26434589
2018 MEIS1 Regulates Hemogenic Endothelial Generation, Megakaryopoiesis, and Thrombopoiesis in Human Pluripotent Stem Cells by Targeting TAL1 and FLI1. Stem cell reports 50 29358086
2012 Decoupling of tumor-initiating activity from stable immunophenotype in HoxA9-Meis1-driven AML. Cell stem cell 50 22305570
2010 The Hox cofactors Meis1 and Pbx act upstream of gata1 to regulate primitive hematopoiesis. Developmental biology 50 20123093
1998 Members of the meis1 and pbx homeodomain protein families cooperatively bind a cAMP-responsive sequence (CRS1) from bovine CYP17. The Journal of biological chemistry 50 9525891
2015 IDH2 and NPM1 Mutations Cooperate to Activate Hoxa9/Meis1 and Hypoxia Pathways in Acute Myeloid Leukemia. Cancer research 49 25795706
2015 Sequential Binding of MEIS1 and NKX2-5 on the Popdc2 Gene: A Mechanism for Spatiotemporal Regulation of Enhancers during Cardiogenesis. Cell reports 47 26411676
2014 Prep1 and Meis1 competition for Pbx1 binding regulates protein stability and tumorigenesis. Proceedings of the National Academy of Sciences of the United States of America 47 24578510
2003 Homeodomain proteins MEIS1 and PBXs regulate the lineage-specific transcription of the platelet factor 4 gene. Blood 46 12609849
2018 Novel MEIS1-NCOA2 Gene Fusions Define a Distinct Primitive Spindle Cell Sarcoma of the Kidney. The American journal of surgical pathology 45 30179902
2014 Homeodomain transcription factor Meis1 is a critical regulator of adult bone marrow hematopoiesis. PloS one 45 24498346
2021 Recurrent MEIS1-NCOA2/1 fusions in a subset of low-grade spindle cell sarcomas frequently involving the genitourinary and gynecologic tracts. Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc 43 33574497
2009 Ectopic Meis1 expression in the mouse limb bud alters P-D patterning in a Pbx1-independent manner. The International journal of developmental biology 43 19247936
1997 Identification of a conserved family of Meis1-related homeobox genes. Genome research 43 9049632
2015 Retinoic Acid Receptor β Controls Development of Striatonigral Projection Neurons through FGF-Dependent and Meis1-Dependent Mechanisms. The Journal of neuroscience : the official journal of the Society for Neuroscience 41 26511239
2018 Meis1 Coordinates Cerebellar Granule Cell Development by Regulating Pax6 Transcription, BMP Signaling and Atoh1 Degradation. The Journal of neuroscience : the official journal of the Society for Neuroscience 40 29317485
2010 Meis1 specifies positional information in the retina and tectum to organize the zebrafish visual system. Neural development 40 20809932
2016 MEIS1-mediated transactivation of synaptotagmin-like 1 promotes CXCL12/CXCR4 signaling and leukemogenesis. The Journal of clinical investigation 39 27018596
2012 Dual actions of Meis1 inhibit erythroid progenitor development and sustain general hematopoietic cell proliferation. Blood 38 22665933
2015 Meis1 coordinates a network of genes implicated in eye development and microphthalmia. Development (Cambridge, England) 37 26253404
2014 MiR-144 regulates hematopoiesis and vascular development by targeting meis1 during zebrafish development. The international journal of biochemistry & cell biology 37 24448023
2018 Emerging Roles of Meis1 in Cardiac Regeneration, Stem Cells and Cancer. Current drug targets 36 28745213
2009 HOXA9 modulates its oncogenic partner Meis1 to influence normal hematopoiesis. Molecular and cellular biology 36 19620287
2006 Molecular dissection of Meis1 reveals 2 domains required for leukemia induction and a key role for Hoxa gene activation. Blood 36 16469876
2020 The emerging role of MEIS1 in cell proliferation and differentiation. American journal of physiology. Cell physiology 35 33296285
2017 MEIS1 inhibits clear cell renal cell carcinoma cells proliferation and in vitro invasion or migration. BMC cancer 35 28270206
2013 Dynamic expression of MEIS1 homeoprotein in E14.5 forebrain and differentiated forebrain-derived neural stem cells. Annals of anatomy = Anatomischer Anzeiger : official organ of the Anatomische Gesellschaft 33 23756022
2015 Predicting the molecular role of MEIS1 in esophageal squamous cell carcinoma. Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine 31 26314854
2014 Meis1 regulates proliferation of non-small-cell lung cancer cells. Journal of thoracic disease 31 24977012
2010 The role of meis1 in primitive and definitive hematopoiesis during zebrafish development. Haematologica 31 21048033
2005 Transplantable cell lines generated with NUP98-Hox fusion genes undergo leukemic progression by Meis1 independent of its binding to DNA. Leukemia 31 15744344
2019 Down-regulation of MEIS1 promotes the maturation of oxidative phosphorylation in perinatal cardiomyocytes. FASEB journal : official publication of the Federation of American Societies for Experimental Biology 30 30884246
2010 Linkage of the potent leukemogenic activity of Meis1 to cell-cycle entry and transcriptional regulation of cyclin D3. Blood 30 20237320
2016 Correlation Between Meis1 and Msi1 in Esophageal Squamous Cell Carcinoma. Journal of gastrointestinal cancer 28 27142513
2015 MEIS1 regulates an HLF-oxidative stress axis in MLL-fusion gene leukemia. Blood 28 25740828
2011 A conserved tissue-specific homeodomain-less isoform of MEIS1 is downregulated in colorectal cancer. PloS one 28 21858198
2019 MEIS1 and Restless Legs Syndrome: A Comprehensive Review. Frontiers in neurology 27 31551905
2018 PAF1 complex interactions with SETDB1 mediate promoter H3K9 methylation and transcriptional repression of Hoxa9 and Meis1 in acute myeloid leukemia. Oncotarget 27 29774127
2011 MEIS1, PREP1, and PBX4 are differentially expressed in acute lymphoblastic leukemia: association of MEIS1 expression with higher proliferation and chemotherapy resistance. Journal of experimental & clinical cancer research : CR 27 22185299
2021 The Small-Molecule Wnt Inhibitor ICG-001 Efficiently Inhibits Colorectal Cancer Stemness and Metastasis by Suppressing MEIS1 Expression. International journal of molecular sciences 26 34948208
2017 Meis1: effects on motor phenotypes and the sensorimotor system in mice. Disease models & mechanisms 26 28645892
2016 MicroRNAs regulating meis1 expression and inducing cardiomyocyte proliferation. Cardiovascular regenerative medicine 26 28111633
2014 MEIS1 regulates early erythroid and megakaryocytic cell fate. Haematologica 26 25107888
2013 Differential transcriptional regulation of meis1 by Gfi1b and its co-factors LSD1 and CoREST. PloS one 26 23308270
2016 Loss of the transcription factor Meis1 prevents sympathetic neurons target-field innervation and increases susceptibility to sudden cardiac death. eLife 25 26857994
2014 Meis1 regulates epidermal stem cells and is required for skin tumorigenesis. PloS one 25 25013928
2014 MEIS1 functions as a potential AR negative regulator. Experimental cell research 24 25158280
2018 A direct interaction between two Restless Legs Syndrome predisposing genes: MEIS1 and SKOR1. Scientific reports 22 30111810
2016 An ShRNA Screen Identifies MEIS1 as a Driver of Malignant Peripheral Nerve Sheath Tumors. EBioMedicine 22 27333032
2010 Identification of E74-like factor 1 (ELF1) as a transcriptional regulator of the Hox cofactor MEIS1. Experimental hematology 22 20600580
2020 MEIS1 down-regulation by MYC mediates prostate cancer development through elevated HOXB13 expression and AR activity. Oncogene 21 32681068
2018 Meis1 is specifically upregulated in kidney myofibroblasts during aging and injury but is not required for kidney homeostasis or fibrotic response. American journal of physiology. Renal physiology 21 29592525
2007 Flt3 is dispensable to the Hoxa9/Meis1 leukemogenic cooperation. Blood 21 17202314
2020 Transcription Factor ELF1 Activates MEIS1 Transcription and Then Regulates the GFI1/FBW7 Axis to Promote the Development of Glioma. Molecular therapy. Nucleic acids 20 33473327
2019 Role of MEIS1 in restless legs syndrome: From GWAS to functional studies in mice. Advances in pharmacology (San Diego, Calif.) 20 31229170
2019 Homeobox gene Meis1 modulates cardiovascular regeneration. Seminars in cell & developmental biology 19 31623926