Affinage

DPY30

Protein dpy-30 homolog · UniProt Q9C005

Length
99 aa
Mass
11.2 kDa
Annotated
2026-06-09
36 papers in source corpus 23 papers cited in narrative 23 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 6/6 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

DPY30 is a conserved core subunit of SET1/MLL-family COMPASS histone methyltransferase complexes that controls genome-wide H3K4 trimethylation and thereby governs lineage-specific gene expression programs (PMID:21335234, PMID:27647347). Mechanistically, its dimerization/docking (D/D) domain anchors the COMPASS complex by engaging an amphipathic α-helix at the C-terminus of ASH2L through hydrophobic contacts; DPY30 stabilizes ASH2L and promotes compaction of the MLL1 complex, both through a nucleosome-independent stabilization mechanism and by enabling ASH2L to form additional interfaces with histone H3 and nucleosomal DNA that boost methyltransferase activity on chromatin (PMID:25456412, PMID:36065180). The ASH2L-binding groove is functionally critical: peptides occluding it block H3K4 methylation and the ASH2L-DPY30 interface is required for H3K4me3 at developmental loci, while reciprocally DPY30 protein is stabilized by ASH2L and degraded via the ubiquitin-proteasome pathway when ASH2L is lost (PMID:25456412, PMID:31251903, PMID:35563756). Through this activity DPY30 directs differentiation of embryonic stem cells, hematopoietic stem/progenitor cells, and osteoclasts by enabling H3K4me3 deposition and induction at lineage-regulatory genes (PMID:21335234, PMID:27647347, PMID:35307321). In C. elegans the ortholog DPY-30 is a ubiquitous nuclear protein essential for dosage compensation, required for stable chromatin binding and X-chromosome recruitment of the dosage compensation complex via DPY-27 in a manner largely independent of H3K4 methylation (PMID:7982580, PMID:7588066, PMID:21998734). DPY30 has also been localized to stressed DNA replication forks where it promotes H3K4me3 deposition to safeguard replication fork stability (PMID:41941748).

Mechanistic history

Synthesis pass · year-by-year structured walk · 9 steps
  1. 1995 High

    Established the ortholog DPY-30 as a ubiquitous nuclear factor whose role in dosage compensation is to recruit the dosage compensation complex rather than to act directly on the X chromosome, defining it as an assembly/recruitment factor.

    Evidence Molecular cloning, immunofluorescence localization, and genetic rescue with a defined temporal window in C. elegans (extending earlier null-mutant genetics)

    PMID:7588066 PMID:7982580

    Open questions at the time
    • Molecular mechanism by which DPY-30 promotes DPY-27/DCC recruitment not resolved
    • Did not connect DPY-30 to histone methylation
  2. 2011 High

    Showed mammalian DPY30 is a core COMPASS subunit that directly modulates genome-wide H3K4me3 and is required for stem cell differentiation but not self-renewal, defining its developmental rather than housekeeping role.

    Evidence In vitro H3K4 methylation assay, genome-wide ChIP, and siRNA knockdown with differentiation assays in ESCs

    PMID:21335234

    Open questions at the time
    • Structural basis of DPY30 incorporation into COMPASS not yet defined
    • Lineage selectivity mechanism unexplained
  3. 2011 Medium

    Demonstrated that among Set1/MLL subunit homologs DPY-30 is uniquely required for stable DCC chromatin binding independently of H3K4 methylation, separating its scaffolding function from its methylation-promoting function.

    Evidence Genetic loss-of-function and epistasis with htz-1 and Set1/MLL subunit mutants, with DCC immunofluorescence in C. elegans

    PMID:21998734

    Open questions at the time
    • How DPY-30 stabilizes DCC binding mechanistically is unknown
    • Generality to mammalian non-COMPASS functions unclear
  4. 2014 High

    Provided the structural mechanism: the DPY-30 D/D domain binds an amphipathic ASH2L helix via hydrophobic contacts, and disrupting this interface reduces H3K4me3 and delays erythroid differentiation, linking complex assembly to function.

    Evidence X-ray crystallography of the D/D–ASH2L helix complex, pull-down, site-directed mutagenesis, ChIP, and erythroid differentiation assays

    PMID:25456412

    Open questions at the time
    • Functional significance of the BAP18/NURF interaction not pursued
    • Did not address nucleosome substrate engagement
  5. 2016 High

    Demonstrated in vivo that Dpy30 is required for HSC differentiation and lineage gene induction, establishing its role in hematopoietic stem cell function through selective H3K4me3 control.

    Evidence Conditional knockout mouse, transplantation chimeras, ChIP-seq, RNA-seq, and flow cytometry of hematopoietic compartments

    PMID:27647347

    Open questions at the time
    • Determinants of gene selectivity for H3K4me3 control not defined
    • Relationship to leukemic dependency not directly addressed here
  6. 2022 High

    Reconstituted the dual mechanism by which DPY30 stimulates MLL1 activity: ASH2L stabilization/complex compaction plus nucleosome-specific interfaces with H3 and DNA, mechanistically explaining its catalytic enhancement.

    Evidence In vitro histone methyltransferase assays with free H3 and nucleosomes, biochemical reconstitution, and protein stability assays

    PMID:36065180

    Open questions at the time
    • Structure of the full nucleosome-bound complex not determined
    • Quantitative contribution of each mechanism in cells unknown
  7. 2022 Medium

    Defined the reciprocal dependency: the ASH2L SDI domain is required to bind and stabilize DPY30, and DPY30 is otherwise degraded by the proteasome, while DPY30 overexpression rescues ASH2L-loss phenotypes, indicating ASH2L-independent DPY30 functions.

    Evidence Conditional Ash2l knockout, proteasome inhibitor assays, SDI-domain mutagenesis, Co-IP, ChIP-seq, RNA-seq, and DPY30 overexpression rescue

    PMID:35563756

    Open questions at the time
    • Identity of the E3 ligase targeting free DPY30 unknown
    • Nature of ASH2L-independent DPY30 complexes undefined
  8. 2022 Medium

    Extended DPY30's H3K4me3 function to terminal cell lineages by showing it drives osteoclast differentiation via H3K4me3 at the NFATc1 promoter, controlling bone mass.

    Evidence LysM-Cre conditional knockout mouse, bone histomorphometry, ex vivo osteoclast assays, and ChIP at the NFATc1 promoter

    PMID:35307321

    Open questions at the time
    • Whether DPY30 acts within canonical COMPASS at NFATc1 not tested
    • Upstream signal coupling DPY30 to osteoclast program unknown
  9. 2026 Medium

    Revealed a non-transcriptional genome-protective role: DPY30 localizes to stressed replication forks and deposits H3K4me3 to safeguard fork stability, with loss causing fork degradation, chromosomal instability, and immune sensitization.

    Evidence ChIP-seq at replication forks, DNA fiber assays, chromosomal instability analysis, immunocompetent PDAC models with anti-PD-1, and patient RNA-seq correlation

    PMID:41941748

    Open questions at the time
    • Mechanism of DPY30/COMPASS recruitment to stalled forks unknown
    • How fork-associated H3K4me3 stabilizes forks mechanistically unresolved

Open questions

Synthesis pass · forward-looking unresolved questions
  • It remains unresolved how DPY30 achieves locus and lineage selectivity for H3K4me3 deposition, what its non-COMPASS and ASH2L-independent activities are at the molecular level, and how it is recruited to specialized chromatin contexts such as replication forks.
  • No mechanism for target-gene selectivity
  • Recruitment to stressed forks uncharacterized
  • Composition of ASH2L-independent DPY30 complexes unknown

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0140096 catalytic activity, acting on a protein 3 GO:0060090 molecular adaptor activity 2 GO:0098772 molecular function regulator activity 2 GO:0042393 histone binding 1
Localization
GO:0005634 nucleus 2 GO:0005694 chromosome 2
Pathway
R-HSA-1266738 Developmental Biology 3 R-HSA-4839726 Chromatin organization 3 R-HSA-74160 Gene expression (Transcription) 3 R-HSA-73894 DNA Repair 1
Partners
AKAP8ASH2LBAP18BIG1DPY-27
Complex memberships
COMPASS (SET1/MLL H3K4 methyltransferase complex)WRAD moduledosage compensation complex (C. elegans, recruitment factor)

Evidence

Reading pass · 23 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2011 Mammalian DPY30, a core subunit of SET1/MLL histone methyltransferase complexes, modulates H3K4 methylation in vitro and directly regulates chromosomal H3K4 trimethylation (H3K4me3) genome-wide. Depletion of DPY30 does not affect ESC self-renewal but significantly alters differentiation potential, particularly along the neural lineage, accompanied by defects in gene induction and H3K4 methylation at key developmental loci. In vitro H3K4 methylation assay, genome-wide ChIP, siRNA knockdown in ESCs with differentiation assays Cell High 21335234
1994 C. elegans DPY-30 is an essential component of the dosage compensation machinery; loss-of-function mutations disrupt dosage compensation and cause XX-specific lethality, and DPY-30 is also required for normal development of XO animals (coordinated movement, body size, tail morphology). DPY-30 mutations can influence sexual fate determination. Genetic analysis, null mutant characterization, phenotypic rescue experiments in C. elegans Genetics High 7982580
1995 C. elegans DPY-30 is a ubiquitous nuclear protein (123 aa) present in both hermaphrodites and males throughout development. DPY-30 is required for the sex-specific association of DPY-27 with hermaphrodite X chromosomes (dosage compensation complex recruitment), but DPY-30 itself is not associated with X chromosomes. Rescue of both XX lethality and XO morphological defects requires dpy-30 expression only through end of gastrulation. Molecular cloning, nuclear localization by immunofluorescence, genetic rescue experiments, dosage compensation complex localization assays Development (Cambridge, England) High 7588066
2014 Crystal structure of the DPY-30 dimerization/docking (D/D) module in complex with an amphipathic α-helix from the C-terminus of ASH2L reveals that DPY-30 incorporation into COMPASS-like complexes is mediated by hydrophobic interactions between this ASH2L helix and the inner surface of the DPY-30 D/D domain. Mutations impairing ASH2L–DPY-30 interaction reduce H3K4me3 at the β-globin locus control region and delay erythroid terminal differentiation. DPY-30 also interacts with BAP18, a subunit of the NURF nucleosome remodeling complex, via the same D/D surface. X-ray crystallography, overlay/pull-down binding assays, site-directed mutagenesis, ChIP for H3K4me3, erythroid differentiation assays Structure (London, England : 1993) High 25456412
2014 DPY30 promotes ex vivo proliferation and myelomonocytic differentiation of human CD34+ hematopoietic progenitor cells while its knockdown potently promotes hemoglobin production and alters erythroid differentiation kinetics. In vivo, morpholino-mediated dpy30 knockdown in zebrafish causes severe hematopoietic defects rescued by dpy30 mRNA co-injection. DPY30 knockdown also impairs growth of MLL1-fusion leukemia cell lines. shRNA/siRNA knockdown in human CD34+ HPCs, colony and differentiation assays, zebrafish morpholino knockdown with mRNA rescue, leukemia cell line growth assays Blood High 25139354
2016 Conditional knockout of Dpy30 in the adult hematopoietic system (mouse) causes severe pancytopenia with striking HSC/early HPC accumulation. Dpy30-deficient HSCs cannot differentiate or efficiently upregulate lineage-regulatory genes, fail to sustain long-term, and lose HSC signature gene expression. Molecular analyses show Dpy30 directly and preferentially controls H3K4 methylation and expression of hematopoietic development-associated genes including key transcriptional and chromatin regulators. Conditional knockout mouse, bone marrow chimera transplantation, ChIP-seq for H3K4me3, RNA-seq, flow cytometry of hematopoietic progenitor populations The Journal of experimental medicine High 27647347
2018 The PKA-binding domain of AKAP8 and the C-terminal Dpy-30 motif of DPY30 are required for their interaction. A single amino acid substitution L69D in DPY30 abolishes dimerization and completely abrogates interaction with both AKAP8 and BIG1 (another AKAP domain-containing protein). AKAP8 interacts with DPY30 and RIIα regulatory subunit of PKA in both interphase and mitotic cells. Co-immunoprecipitation, site-directed mutagenesis (L69D), pull-down assays, confocal microscopy in interphase and mitotic cells The FEBS journal Medium 29288530
2019 Cell-penetrating peptides derived from ASH2L that bind the ASH2L-binding groove of DPY30 specifically inhibit DPY30's interaction with ASH2L and its enhancement of H3K4 methylation. These peptides significantly inhibit growth of MLL-rearranged leukemia and MYC-dependent hematologic cancer cells, demonstrating the ASH2L-binding groove of DPY30 as a functionally critical domain. Peptide design and cell-penetrating delivery, co-immunoprecipitation competition assay, H3K4 methylation measurement, cancer cell growth assays, gene expression analysis Experimental cell research Medium 31251903
2022 DPY30 stimulates MLL1 complex methyltransferase activity via two complementary mechanisms: (1) a nucleosome-independent mechanism in which DPY30 functions as an ASH2L-specific stabilizer, increasing ASH2L stability and promoting compaction/stabilization of the MLL1 complex; (2) a nucleosome-specific mechanism in which DPY30-stabilized ASH2L acquires additional interfaces with H3 and nucleosomal DNA to boost methyltransferase activity on nucleosomes. In vitro histone methyltransferase assays, biochemical reconstitution, protein stability assays, nucleosome substrate assays iScience High 36065180
2022 The ASH2L SDI (Sdc1-DPY30 interaction) domain is essential for DPY30 binding; three specific amino acids in this domain are required for DPY30 recognition. In Ash2l-depleted cells, DPY30 protein levels decrease significantly due to degradation via the ubiquitin-mediated proteasomal pathway (not through transcriptional or translational regulation). Overexpression of DPY30 in Ash2l-depleted cells rescues decreased Ccnd1 and abnormal cell cycle, indicating DPY30 can function in complexes independent of ASH2L. Conditional Ash2l knockout mouse model, ChIP-seq, RNA-seq, proteasome inhibitor assays, site-directed mutagenesis of ASH2L SDI domain, co-immunoprecipitation, DPY30 overexpression rescue Cells Medium 35563756
2011 In C. elegans, DPY-30 is required for stable chromatin binding of the dosage compensation complex (DCC). Among all Set1/MLL complex subunit homologs, only DPY-30 is required for stable DCC binding to chromatin. This function of DPY-30 in DCC localization is largely independent of H3K4 methylation, as loss of H3K4 methylation does not enhance DCC mislocalization in htz-1 animals. Genetic loss-of-function in C. elegans, immunofluorescence of DCC localization, epistasis analysis with htz-1 and Set1/MLL complex subunit mutants PloS one Medium 21998734
2012 The DPY-30 domain (D/D module) in radial spoke protein 2 (RSP2) of Chlamydomonas flagella is required for firm attachment of spokehead subunits to the spokestalk and for normal flagellar motility. Deletion of only the DPY-30 domain from RSP2 causes paralyzed flagella, while deletion of the calmodulin-binding C-terminal region restores motility but impairs steering under bright light. This establishes that D/D domains can function as conserved two-prong linkers to organize duplicated subunits in macromolecular complexes. Site-directed mutagenesis/deletion transgenic strains in Chlamydomonas, motility assays, flagellar protein fractionation/immunoblot Molecular and cellular biology Medium 22851692
2022 In glioblastoma stem cells, DPY30 regulates H3K4me3 deposition on angiogenesis and hypoxia pathway genes (including FOS, NFκB, and PDE family members) in an intracranial in vivo context but is dispensable for cultured GSCs in vitro. PDE4B is a key downstream effector of DPY30, and DPY30 loss reduces H3K4me3 at PDE4B-regulated loci. In vivo genetic screening and ChIP analysis establish the DPY30–H3K4me3–PDE4B axis as a context-specific dependency. In vivo genetic screening (intracranial PDX), H3K4me3 ChIP-seq comparison of in vivo vs. in vitro GSCs, transcriptome analysis, PDE4B functional validation, PDE4 inhibitor (rolipram) treatment in PDX mouse model Science translational medicine Medium 34985972
2022 Conditional deletion of Dpy30 in myeloid cells (LysM-Cre) impairs osteoclast differentiation and suppresses osteoclast activity, resulting in increased bone mass. Dpy30 deficiency decreases H3K4me3 enrichment at the NFATc1 promoter, thereby reducing NFATc1 expression and osteoclast-related gene transcription. Conditional knockout mouse (Dpy30F/F; LysM-Cre), bone histomorphometry, ex vivo osteoclast differentiation assays, ChIP for H3K4me3 at NFATc1 promoter Bone Medium 35307321
2023 DPY30 promotes colorectal cancer cell proliferation and cell cycle progression by facilitating H3K4me3 deposition on the promoters of PCNA, Ki67, and Cyclin A2, thereby driving their transcription. DPY30 knockdown induces S-phase cell cycle arrest with downregulation of Cyclin A2. siRNA knockdown, ChIP assay for H3K4me3 at target promoters, RNA-seq, in vitro and in vivo proliferation assays International journal of medical sciences Medium 37324189
2018 DPY30 regulated H3K4me3 recruitment controls expression of Hif1α and targeted glycolytic genes. DPY30 also promotes H3K9Ac recruitment via inhibiting SIRT6 occupancy on glycolytic gene promoters, linking DPY30 to glucose homeostasis through coordinated epigenetic regulation. ChIP assay for H3K4me3 and H3K9Ac at gene promoters, SIRT6 occupancy measurement, knockdown experiments Biochemical and biophysical research communications Low 30448059
2022 BPA exposure decreases DPY30 expression, which reduces H3K4me3 recruitment at the PIK3CA transcriptional start site, attenuating PI3K/AKT signaling in spermatogonial cells. Adenovirus-mediated DPY30 overexpression rescues PI3K/AKT activity, restores H3K4me3 at the PIK3CA TSS, and promotes DPY30 localization to round and elongated spermatids for energy accumulation. ChIP assay for H3K4me3 at PIK3CA TSS, adenoviral DPY30 overexpression rescue, in vitro cell proliferation assays, in vivo mouse model Ecotoxicology and environmental safety Low 36030680
2023 DPY30 promotes CRC metastasis by increasing H3K4me3 levels at the ZEB1 promoter, thereby upregulating ZEB1 transcription and driving EMT. DPY30 knockdown reduces ZEB1 expression, suppresses EMT markers, and impairs in vitro migration/invasion and in vivo lung metastasis. ChIP assay for H3K4me3 at ZEB1 promoter, siRNA knockdown, in vitro migration/invasion assays, in vivo lung metastasis xenograft model Cancer cell international Low 38115111
2024 DPY30 knockdown in colorectal cancer cells promotes MST2-induced apoptosis by inhibiting Raf1 transcriptional activity through reduction of H3K4me3 at the Raf1 promoter, establishing a DPY30/Raf1/MST2 apoptosis signaling axis. RNA-seq, ChIP assay for H3K4me3 at Raf1 promoter, siRNA knockdown, caspase activation assays, xenograft mouse model Heliyon Low 38314299
2026 DPY30 (as part of the WRAD/COMPASS complex) localizes to stressed DNA replication forks and promotes H3K4me3 deposition at these sites to safeguard DNA replication stability. Loss of DPY30 destabilizes stalled replication forks causing fork degradation, chromosomal instability, and inflammation without reducing cancer cell proliferation, and induces T-cell infiltration that sensitizes PDAC tumors to immune checkpoint blockade. ChIP-seq for H3K4me3 at replication forks, DNA fiber assay for fork stability, chromosomal instability analysis, immunocompetent mouse PDAC models, anti-PD-1 treatment experiments, patient RNA-seq correlation Cancer research Medium 41941748
2024 DPY30 knockdown in colorectal cancer cells attenuates aerobic glycolysis and reduces H3K4me3 on promoters of glycolytic genes HK1, PFKL, and ALDOA, while also broadly altering the PI3K-AKT signaling pathway as revealed by proteomic analysis. Knockdown + TMT-labeled quantitative proteomics, Seahorse ECAR glycolysis assay, ChIP for H3K4me3 at HK1/PFKL/ALDOA promoters Translational cancer research Low 39262496
2022 DPY30 silencing by siRNA in melanoma cells significantly inhibits PD-L1 expression. ChIP analysis reveals H3K4me3 is enriched at the proximal PD-L1 promoter in tumor cells, and DPY30 knockdown reduces this enrichment. DPY30 knockdown also reduces apoptosis of PD1+ T-cells in co-culture. siRNA knockdown, ChIP for H3K4me3 at PD-L1 promoter, RT-PCR, flow cytometry, co-culture apoptosis assay Journal of inflammation research Low 36185638
2010 A genomic deletion in a Japanese SPG4 family removes exons 1–3 of DPY30 in addition to exons 1–4 of SPAST (~70 kb deletion), demonstrating that DPY30 is located immediately upstream of SPAST in a head-to-head orientation and that partial heterozygous deletion of DPY30 may modify SPG4 clinical phenotype. Real-time quantitative PCR for exonic copy number, breakpoint mapping by sequencing Neurogenetics Low 20857310

Source papers

Stage 0 corpus · 36 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2011 Role for Dpy-30 in ES cell-fate specification by regulation of H3K4 methylation within bivalent domains. Cell 235 21335234
1994 The dpy-30 gene encodes an essential component of the Caenorhabditis elegans dosage compensation machinery. Genetics 79 7982580
1995 DPY-30, a nuclear protein essential early in embryogenesis for Caenorhabditis elegans dosage compensation. Development (Cambridge, England) 69 7588066
2014 The DPY30 subunit in SET1/MLL complexes regulates the proliferation and differentiation of hematopoietic progenitor cells. Blood 54 25139354
2016 Dpy30 is critical for maintaining the identity and function of adult hematopoietic stem cells. The Journal of experimental medicine 51 27647347
2014 Molecular basis for DPY-30 association to COMPASS-like and NURF complexes. Structure (London, England : 1993) 38 25456412
2017 Diverse roles of WDR5-RbBP5-ASH2L-DPY30 (WRAD) complex in the functions of the SET1 histone methyltransferase family. Journal of biosciences 35 28229975
2022 Glioblastoma stem cells reprogram chromatin in vivo to generate selective therapeutic dependencies on DPY30 and phosphodiesterases. Science translational medicine 27 34985972
2022 Bisphenol A exposure causes testicular toxicity by targeting DPY30-mediated post-translational modification of PI3K/AKT signaling in mice. Ecotoxicology and environmental safety 23 36030680
2018 DPY30 is required for the enhanced proliferation, motility and epithelial-mesenchymal transition of epithelial ovarian cancer cells. International journal of molecular medicine 22 30221689
2019 Specific inhibition of DPY30 activity by ASH2L-derived peptides suppresses blood cancer cell growth. Experimental cell research 18 31251903
2015 Roles of DPY30 in the Proliferation and Motility of Gastric Cancer Cells. PloS one 17 26147337
2019 DPY30 regulates cervical squamous cell carcinoma by mediating epithelial-mesenchymal transition (EMT). OncoTargets and therapy 16 31564898
2012 The DPY-30 domain and its flanking sequence mediate the assembly and modulation of flagellar radial spoke complexes. Molecular and cellular biology 16 22851692
2023 DPY30 Promotes Proliferation and Cell Cycle Progression of Colorectal Cancer Cells via Mediating H3K4 Trimethylation. International journal of medical sciences 12 37324189
2010 Partial SPAST and DPY30 deletions in a Japanese spastic paraplegia type 4 family. Neurogenetics 12 20857310
2018 PKA-binding domain of AKAP8 is essential for direct interaction with DPY30 protein. The FEBS journal 11 29288530
2022 DPY30 acts as an ASH2L-specific stabilizer to stimulate the enzyme activity of MLL family methyltransferases on different substrates. iScience 8 36065180
2022 Overexpression of miR-493-3p suppresses ovarian cancer cell proliferation, migration and invasion through downregulating DPY30. Reproductive biology 7 35313261
2022 The DPY30-H3K4me3 Axis-Mediated PD-L1 Expression in Melanoma. Journal of inflammation research 7 36185638
2018 DPY30 functions in glucose homeostasis via integrating activated histone epigenetic modifications. Biochemical and biophysical research communications 7 30448059
2011 Regulation of DCC localization by HTZ-1/H2A.Z and DPY-30 does not correlate with H3K4 methylation levels. PloS one 7 21998734
2022 Role of chromatin modulator Dpy30 in osteoclast differentiation and function. Bone 6 35307321
2024 The role of chromatin modulator DPY30 in glucose metabolism of colorectal cancer cells. Translational cancer research 3 39262496
2023 DPY30 promotes the growth and survival of osteosarcoma cell by regulating the PI3K/AKT signal pathway. European journal of histochemistry : EJH 3 36546421
2022 The Ash2l SDI Domain Is Required to Maintain the Stability and Binding of DPY30. Cells 3 35563756
2014 Novel SPAST deletion and reduced DPY30 expression in a Spastic Paraplegia type 4 kindred. BMC medical genetics 3 24690193
2023 DPY30 promotes colorectal carcinoma metastasis by upregulating ZEB1 transcriptional expression. Cancer cell international 2 38115111
2024 DPY30 knockdown suppresses colorectal carcinoma progression via inducing Raf1/MST2-mediated apoptosis. Heliyon 1 38314299
2026 Disrupting the ASH2L-DPY30 PPI in cancer: structure, function, and therapeutic opportunities in H3K4 methylation. Epigenetics & chromatin 0 41864982
2026 DPY30 is an epigenetic decoupler linking replication stress to immunoediting in pancreatic cancer. Cancer research 0 41941748
2026 Age-associated miR-30e-3p upregulation drives ovarian follicular granulosa cell senescence by targeting DPY30 in laying hens. Poultry science 0 42150419
2025 Successful cord blood transplantation for a unique case of bone marrow failure presenting t(2;19)(p23;q13.3) translocation suggesting disruption of DPY30. Fukushima journal of medical science 0 39909446
2025 MiR-493-3p suppresses the DPY-30 histone methyltransferase complex regulatory subunit to attenuate gefitinib resistance in lung cancer. Translational oncology 0 41145012
2025 Serum miR-493-3p as a diagnostic biomarker and epigenetic regulator targeting DPY30 in pediatric acute lymphoblastic leukemia. Annals of hematology 0 41249660
2024 A novel regulatory sex-skewing method that inhibits testicular DPY30 expression to increase female rate of dairy goat offspring. Journal of animal science 0 38167777

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