Affinage

DDX20

Probable ATP-dependent RNA helicase DDX20 · UniProt Q9UHI6

Length
824 aa
Mass
92.2 kDa
Annotated
2026-06-09
43 papers in source corpus 27 papers cited in narrative 28 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

DDX20 (Gemin3/DP103) is a DEAD-box RNA helicase that functions as a core component of the SMN complex, directly binding SMN through its unique C-terminal domain and contacting Sm proteins (SmB, SmD2, SmD3) to drive spliceosomal snRNP assembly (PMID:10601333, PMID:18923150). Genetic loss in Drosophila codepletes SMN, blocks Sm-core snRNP assembly, and produces larval lethality and motor and neuromuscular defects, with Gemin3 loss—not secondary SMN loss—being the primary cause of death (PMID:18923150, PMID:19023405). Its intact protein possesses ATP-dependent RNA-unwinding (helicase) activity, while a discrete C-terminal domain confers autonomous transcriptional repression of multiple transcription factors including SF-1, the Egr family, and p53, acting through SUMO-dependent and partially HDAC-dependent mechanisms (PMID:12482992, PMID:14699164, PMID:15713642, PMID:22335944). Beyond the spliceosome, DDX20 participates in miRNA loading into RISC (PMID:22445758) and engages signaling pathways: it enhances TAK1-mediated IKK2 phosphorylation to amplify NF-κB and MMP9-driven metastasis in a feedback loop (PMID:25083991), bridges TBK1 and IRF3 to promote IRF3 phosphorylation and antiviral interferon signaling (PMID:38552910), and interacts with GSK3β to potentiate Wnt/β-catenin activation independently of helicase activity (PMID:42248871). DDX20 is essential for early development and tissue-specific cell-cycle control: homozygous null mice die before the four-cell stage (PMID:18258677), CNS-specific deletion triggers p53-dependent apoptosis with Mdm2 mis-splicing in neural and oligodendrocyte progenitors (PMID:34974536), and germ-cell deletion impairs prospermatogonial cell-cycle reentry by controlling translation of cell-cycle regulators (PMID:38657611). DDX20 protein stability is set by TRIM25-mediated ubiquitination, which DAPK antagonizes within a DAPK–TRIM25–DDX20 ternary complex (PMID:39558224).

Mechanistic history

Synthesis pass · year-by-year structured walk · 14 steps
  1. 1999 High

    Established DDX20/Gemin3 as a physical and functional member of the SMN complex, placing a previously uncharacterized helicase in the snRNP-assembly machinery.

    Evidence Co-IP, yeast two-hybrid, immunolocalization and mass spectrometry mapping direct SMN binding to the C-terminal domain and binding to Sm proteins

    PMID:10601333

    Open questions at the time
    • Did not establish catalytic contribution of helicase activity to assembly
    • SMA-relevant in vivo consequence not yet tested
  2. 1999 Medium

    Identified DP103 as an EBV nuclear protein interactor with intrinsic/associated ATPase activity residing in high-molecular-weight complexes, hinting at functions beyond snRNP assembly.

    Evidence Co-IP with EBNA2/EBNA3C, ATPase assay, subcellular fractionation

    PMID:10383418

    Open questions at the time
    • ATPase activity not definitively attributed to DP103 itself
    • Functional consequence of viral protein binding unresolved at this stage
  3. 2003 High

    Resolved the domain logic of DDX20: a discrete C-terminal region is necessary and sufficient for transcriptional repression while the full protein supports in vitro RNA unwinding, separating its enzymatic and regulatory functions.

    Evidence In vitro helicase assay, domain deletion, transcriptional reporter assays for SF-1 and Egr-family repression

    PMID:12482992 PMID:14699164

    Open questions at the time
    • RNA substrate specificity of helicase activity undefined
    • Mechanism of HDAC-independent repression not identified
  4. 2005 High

    Defined a SUMO-dependent repression mechanism in which DDX20 reads SUMO-modified SF-1/LRH-1 and cooperates with PIAS ligases, explaining HDAC-independent repression.

    Evidence Co-IP, SENP1 rescue, lysine mutagenesis, nuclear-body relocalization assays

    PMID:15713642

    Open questions at the time
    • Whether DDX20 itself is SUMOylated not addressed
    • Breadth of SUMO-dependent target repertoire unknown
  5. 2008 High

    Demonstrated organismal essentiality and tissue roles, showing DDX20 is required for the earliest embryonic divisions and modulates steroidogenesis and ovarian physiology.

    Evidence Constitutive knockout mouse phenotyping; heterozygote endocrine analysis

    PMID:18258677

    Open questions at the time
    • Early lethality precludes mechanistic dissection of which DDX20 function is essential
    • Molecular basis of endocrine phenotype not mapped
  6. 2008 High

    Provided genetic epistasis proof that Gemin3 loss—not secondary SMN depletion—drives motor and lethality phenotypes, while confirming its requirement for Sm-core snRNP assembly.

    Evidence Drosophila transposon/RNAi loss-of-function, in vitro snRNP assembly assay, transgenic rescue (Gem3 rescues, SMN does not)

    PMID:18923150 PMID:19023405

    Open questions at the time
    • Catalytic requirement of the helicase domain in vivo not isolated
    • Relevance to human SMA pathology indirect
  7. 2011 High

    Identified p53 as a direct DDX20 target whose DNA-binding and transactivation are repressed, linking DDX20 to apoptosis control and EBV-mediated oncogenesis.

    Evidence Co-IP, GST pull-down, EMSA, luciferase reporter, shRNA knockdown with apoptosis readout

    PMID:22174681 PMID:22335944

    Open questions at the time
    • Whether repression requires helicase or RNA binding unclear
    • Generality beyond EBV-driven contexts not established
  8. 2012 Medium

    Connected the helicase to RNA silencing by showing DDX20 is required for species-specific miRNA loading into RISC, with miR-140 loading controlling NF-κB output.

    Evidence RNAi knockdown, RISC loading assay, NF-κB luciferase reporter

    PMID:22445758

    Open questions at the time
    • Determinants of miRNA species selectivity unknown
    • Direct biochemical role in RISC loading not reconstituted
  9. 2014 High

    Placed DDX20 as a pro-metastatic signaling amplifier, enhancing TAK1-dependent IKK2 phosphorylation and NF-κB/MMP9 output within a positive feedback loop.

    Evidence Gain/loss-of-function, phosphorylation assay, reporter assay, xenograft model

    PMID:25083991

    Open questions at the time
    • Direct enzymatic mechanism by which DDX20 enhances TAK1 activity unclear
    • Helicase dependence not tested
  10. 2022 High

    Showed DDX20 is indispensable for progenitor survival in the CNS, with deletion activating p53 via Mdm2 mis-splicing and SMN complex disruption, tying snRNP function to cell-fate control.

    Evidence CNS conditional knockout, splicing analysis, p53 pathway assays, Olig2–Ddx20 Co-IP

    PMID:34974536

    Open questions at the time
    • Whether p53 activation is solely splicing-driven or also via direct repression loss unresolved
    • Olig2-mediated stabilization mechanism not detailed
  11. 2024 High

    Extended DDX20 function to translational control in germ cells, where it is required for prospermatogonial cell-cycle reentry by engaging the translational machinery to regulate cell-cycle regulator mRNAs.

    Evidence Germ-cell conditional knockout, ribosome/translational-machinery Co-IP, mRNA target identification

    PMID:38657611

    Open questions at the time
    • Specific translation-machinery contacts not fully enumerated
    • Relationship to canonical SMN-complex role unclear
  12. 2024 High

    Identified DDX20 as a positive regulator of antiviral interferon signaling by bridging TBK1 and IRF3 to promote IRF3 phosphorylation.

    Evidence Knockdown/overexpression, TBK1–IRF3 Co-IP, IRF3 phosphorylation assay, IFN-β reporter, KO mouse VSV/HSV-1 infection

    PMID:38552910

    Open questions at the time
    • Whether RNA-binding or helicase activity is required for bridging unknown
    • Structural basis of the TBK1-IRF3 scaffolding undefined
  13. 2024 High

    Established the regulatory circuit controlling DDX20 abundance: TRIM25 ubiquitinates the 1-244 region for degradation while DAPK antagonizes this within a DAPK–TRIM25–DDX20 ternary complex.

    Evidence Co-IP, ubiquitination assay, domain mapping, knockdown, protein stability assay

    PMID:39558224

    Open questions at the time
    • Physiological signals controlling this switch not defined
    • Functional output of stabilized DDX20 in this context not mapped
  14. 2026 Medium

    Defined a helicase-independent role in Wnt signaling, with DDX20 binding GSK3β to promote LRP6 phosphorylation and nuclear β-catenin in a feedforward loop.

    Evidence Co-IP, LRP6 phosphorylation assay, Wnt reporter, xenograft and Drosophila models

    PMID:42248871

    Open questions at the time
    • Mechanism by which DDX20 promotes GSK3β-dependent modifications unclear
    • Reconciliation with GSK3β's canonical inhibitory role in Wnt not detailed

Open questions

Synthesis pass · forward-looking unresolved questions
  • It remains unresolved how DDX20's enzymatic helicase activity is mechanistically partitioned across its many roles—snRNP assembly, miRNA loading, transcriptional repression, and signaling scaffolding—and which functions require catalysis versus protein-scaffolding.
  • No structure-function map separating catalytic from scaffolding functions across pathways
  • No high-resolution structure of DDX20 within the SMN complex reported in the corpus

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0140110 transcription regulator activity 4 GO:0060089 molecular transducer activity 3 GO:0003723 RNA binding 2 GO:0140657 ATP-dependent activity 2 GO:0140098 catalytic activity, acting on RNA 1
Localization
GO:0005634 nucleus 2 GO:0005829 cytosol 2 GO:0031410 cytoplasmic vesicle 2
Pathway
R-HSA-74160 Gene expression (Transcription) 4 R-HSA-1266738 Developmental Biology 3 R-HSA-162582 Signal Transduction 3 R-HSA-8953854 Metabolism of RNA 3 R-HSA-168256 Immune System 2 R-HSA-392499 Metabolism of proteins 2
Partners
DAPK1EBNA3CGSK3BP53SMN1TAK1TBK1TRIM25
Complex memberships
DAPK-TRIM25-DDX20 ternary complexRISCSMN complex

Evidence

Reading pass · 28 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1999 Gemin3 (DDX20) was identified as a novel component of the SMN complex. It directly interacts with SMN via its unique C-terminal domain, and also binds SmB, SmD2, and SmD3. Immunolocalization confirmed colocalization with SMN in nuclear gems. SMA patient-derived SMN mutations strongly reduce the Gemin3-SMN interaction. Co-immunoprecipitation, immunolocalization with monoclonal antibodies, yeast two-hybrid, mass spectrometry The Journal of cell biology High 10601333
1999 DP103 (DDX20) binds to Epstein-Barr virus nuclear proteins EBNA2 (via aa 121-213) and EBNA3C (via aa 534-778). An ATPase activity intrinsic to or closely associated with DP103 was detected. DP103 resides in high molecular weight complexes in vivo and is found in both soluble nuclear and insoluble skeletal fractions. Co-immunoprecipitation, ATPase activity assay, subcellular fractionation, monoclonal antibody characterization The Journal of biological chemistry Medium 10383418
2000 The murine homologue of DP103 directly and specifically binds SMN, as demonstrated by isolation from mouse brain, consistent with a role in the SMN complex in neuronal cells. Pull-down assay, direct binding assay from mouse brain extract Human molecular genetics Medium 10767334
2001 DP103 directly interacts with the proximal repression domain of the nuclear receptor SF-1 (steroidogenic factor-1) via yeast two-hybrid and direct binding assays. DP103 exhibits autonomous transcriptional repression activity localized to its C-terminal region and represses wild-type but not mutant (repression-domain) SF-1 activity. Yeast two-hybrid, direct binding assay, transcriptional reporter assay, point mutagenesis Molecular endocrinology (Baltimore, Md.) High 11145740
2003 A discrete C-terminal domain of DP103 is necessary and sufficient for transcriptional repression of SF-1. Intact DP103 exhibits RNA helicase (unwinding) activity in vitro, and the C-terminal domain is obligatory but not sufficient for this helicase activity. In vitro helicase activity assay, domain deletion analysis, transcriptional reporter assay Molecular and cellular biology High 12482992
2003 Ddx20 (DP103/Gemin3) interacts with Egr2/Krox-20 and all four Egr family members (Egr1, Egr2, Egr3, Egr4). It represses Egr2-mediated transcriptional activation with promoter specificity, including repression of the endogenous IGF2 gene. The C-terminal segment lacking the DEAD-box domain is sufficient for repression. This repression is partially but not fully dependent on histone deacetylase activity, indicating an additional HDAC-independent repression mechanism. Yeast two-hybrid, mammalian two-hybrid, transcriptional reporter assay, endogenous gene expression assay, HDAC inhibitor (trichostatin A) treatment The Journal of biological chemistry High 14699164
2005 DP103 (DDX20) directly interacts with SUMO-modified SF-1 and liver receptor homolog 1 (LRH-1), mediating SUMO-dependent transcriptional repression. PIASy and PIASxα promote SF-1 sumoylation, and DP103 enhances PIAS-dependent sumoylation and SF-1 relocalization to discrete nuclear bodies. This repression is largely histone deacetylase independent. Co-immunoprecipitation, transcriptional reporter assay, SUMO isopeptidase (SENP1) functional assay, lysine mutagenesis, fluorescence localization Molecular and cellular biology High 15713642
2005 FOXL2 interacts with DP103 by co-immunoprecipitation. Overexpression of DP103 alone does not affect cell viability, but co-expression with FOXL2 potentiates FOXL2-induced apoptosis in CHO and rat granulosa cells. Co-immunoprecipitation, overexpression, cell viability assay Biochemical and biophysical research communications Medium 16153597
2008 Homozygous Dp103-null mice die before the four-cell stage of embryonic development. Heterozygous females show larger ovaries, altered estrous cycle, and reduced basal ACTH secretion, indicating roles in early embryogenesis and steroidogenesis. Gene knockout (homologous recombination), phenotypic analysis of null and heterozygous mice Endocrinology High 18258677
2008 Drosophila Gemin3 physically interacts with SMN in vivo. Loss of gemin3 causes larval lethality, motor dysfunction, and expanded neuromuscular junctions. Knockdown in mesoderm causes lethality; less severe disruption in muscles causes flight muscle degeneration. In vivo genetic loss-of-function (transposon insertion, RNAi), co-immunoprecipitation, neuromuscular junction morphology, behavioral assay PLoS genetics High 19023405
2008 Drosophila Gemin3 colocalizes and interacts with dSMN in vitro and in vivo. RNAi for dGem3 codepletes dSMN and inhibits efficient Sm core snRNP assembly in vitro. Transposon mutations cause larval lethality and motor defects. Overexpression of dGem3 rescues lethality, but overexpression of dSMN does not, indicating Gemin3 loss—not secondary SMN loss—is the primary cause of death. RNAi, transposon insertion, in vitro snRNP assembly assay, in vivo colocalization, transgenic rescue Molecular biology of the cell High 18923150
2010 HspB8 interacts with Ddx20 (gemin3). Disease-associated HspB8 mutants show abnormally increased binding to Ddx20 compared to wild-type HspB8. RNase treatment affects the mutant HspB8–Ddx20 interaction, suggesting RNA involvement. Yeast two-hybrid, co-immunoprecipitation, chemical cross-linking, quantitative FRET Cell stress & chaperones Medium 20157854
2010 SMN, Gemin2, and Gemin3 associate with beta-actin mRNA in the cytoplasm of human neuroblastoma (SHSY5Y) cells, providing direct evidence that Gemin3 is part of cytoplasmic mRNA complexes involved in axonal mRNA transport. Targeted RNA pull-down/immunoprecipitation screen, RT-PCR Journal of molecular biology Medium 20620147
2010 Gemin3 localizes to U bodies (cytoplasmic RNA granules containing U snRNPs) in Drosophila egg chambers, colocalizing with SMN, Gemin2, and Gemin5. U bodies consistently associate with P bodies but Gemin3 is excluded from P bodies themselves. Immunofluorescence/cytological colocalization in Drosophila egg chambers Experimental cell research Medium 20452345
2011 EBNA3C directly interacts with Gemin3 through its C-terminal domain, stabilizing Gemin3 protein and increasing its accumulation in B lymphoma and EBV-transformed cells. EBNA3C promotes formation of a Gemin3–p53 complex that blocks p53 DNA-binding affinity. Gemin3 knockdown attenuates EBNA3C-mediated suppression of p53 transcriptional activity on p21 and Bax, and increases apoptosis. Co-immunoprecipitation, shRNA knockdown, EMSA (p53 DNA binding), luciferase reporter assay, flow cytometry for apoptosis PLoS pathogens High 22174681
2011 Gemin3 binds p53 via its C-terminal domain interacting with the DNA binding domain of p53, forming a complex in vivo. Gemin3 represses p53 transcriptional activity, and Gemin3 knockdown increases p53, p21, and Bax expression and increases apoptosis. Co-immunoprecipitation, GST pull-down, luciferase reporter assay, shRNA knockdown, qRT-PCR, flow cytometry Zhonghua zhong liu za zhi [Chinese journal of oncology] Medium 22335944
2011 NANOS1 and PUMILIO2 interact with GEMIN3 as detected by yeast two-hybrid and co-immunoprecipitation. These three proteins colocalize within the chromatoid body (CB) of human and mouse round spermatids, identified by co-staining with the CB marker VASA protein. Yeast two-hybrid, co-immunoprecipitation, double immunofluorescence colocalization Histochemistry and cell biology Medium 21800163
2012 DDX20 deficiency impairs loading of specific miRNAs (including miR-140) into RISC in a miRNA-species-specific manner, leading to reduced suppression of NF-κB by miR-140 and consequently enhanced NF-κB activity. RNAi knockdown, luciferase NF-κB reporter assay, RISC loading assay Biochemical and biophysical research communications Medium 22445758
2014 DP103 enhances TAK1-mediated phosphorylation of IKK2, leading to increased NF-κB activity and elevated MMP9 expression. NF-κB in turn positively activates DP103 expression, forming a positive feedback loop. Reduction of DP103 reduces IKK2 phosphorylation and abrogates NF-κB-mediated MMP9 expression, impeding metastasis in xenograft models. Knockdown/overexpression, phosphorylation assay, luciferase reporter assay, xenograft mouse model The Journal of clinical investigation High 25083991
2019 Gemin3 self-interacts; a helicase domain deletion mutant (Gem3ΔN) retains the ability to interact with wild-type Gemin3, and mutant:wild-type dimers are favored over wild-type:wild-type dimers. Disruption of Gemin3 in Drosophila is enhanced by loss of TDP-43 or FUS, genetically linking SMA and ALS pathways through Gemin3. Co-immunoprecipitation (self-interaction), Drosophila genetic epistasis (double mutant analysis), motor behavior and survival assays Scientific reports Medium 31822699
2022 Ddx20 is indispensable for survival of neural progenitor cells (NPCs) and oligodendrocyte progenitor cells (OPCs). CNS-specific Ddx20 conditional knockout causes apoptosis and cell cycle arrest via p53 pathway activation, including abnormal splicing of Mdm2 mRNA and SMN complex disruption. Olig2 contributes to NPC proliferation through Ddx20 protein stabilization. Conditional knockout (CNS-specific Cre), RNA splicing analysis, p53 pathway assays, Co-IP (Olig2–Ddx20 interaction) Cell death and differentiation High 34974536
2022 Gemin3 knockdown in SMA motoneurons reduces SMN, IKKβ, and RelA protein levels and causes neurite degeneration. SMN overexpression increases Gemin3 protein in SMA motoneurons but does not prevent neurite degeneration in Gemin3 knockdown cells, indicating Gemin3 acts downstream or in parallel to SMN in controlling NF-κB (via TAK1) and neuronal integrity. shRNA knockdown, overexpression, Western blot, neuronal morphology quantification Frontiers in cellular neuroscience Medium 36619669
2024 DDX20 is required for cell-cycle reentry of T1-prospermatogonia (T1-ProSG) and formation of the spermatogonial stem cell pool. Mechanistically, DDX20 controls translation of mRNAs encoding cell-cycle-related regulators by interacting with key components of the translational machinery in prospermatogonia. Germ-cell-specific conditional knockout (Ddx20 cKO at E15.5), ribosome/translational machinery interaction (Co-IP), mRNA target identification Developmental cell High 38657611
2024 DDX20 promotes phosphorylation of IRF3 by facilitating the interaction between TBK1 and IRF3, thereby increasing IFN-β expression and downstream ISG induction. Ddx20 gene-deficient mice show increased susceptibility to VSV and HSV-1 infection. RNAi knockdown, overexpression, co-immunoprecipitation (TBK1-IRF3), IRF3 phosphorylation assay, IFN-β reporter, Ddx20 KO mouse viral infection model Antiviral research High 38552910
2024 TRIM25 is the E3 ubiquitin ligase responsible for DDX20 proteasomal degradation, binding and ubiquitinating the 1-244 amino acid region of DDX20. DAPK interacts with this same 1-244 segment, inhibiting TRIM25-mediated ubiquitination of DDX20 and enhancing its stability. DAPK, TRIM25, and DDX20 form a ternary complex, and TRIM25 acts as an intermediate linking DAPK and DDX20. Co-immunoprecipitation, ubiquitination assay, domain mapping (1-244 aa), shRNA knockdown, protein stability assay Cancer cell international High 39558224
2025 A VHL molecular glue degrader (dGEM3) was discovered that targets GEMIN3 for proteasomal degradation. The GEMIN3 degron responsible for VHL-mediated degradation was mapped to the helicase ATP-binding domain, and the kinetics of ternary complex formation were characterized biochemically and biophysically. RNA-seq screening (Picowells), biochemical and biophysical ternary complex assays, domain mapping (degron identification) bioRxivpreprint Medium
2026 DP103 physically interacts with GSK3β to facilitate post-translational modifications essential for Wnt activation. DP103 promotes LRP6 phosphorylation and nuclear β-catenin accumulation, enhancing Wnt transcriptional activity. DP103 is itself a Wnt target gene, forming a positive feedforward loop. This Wnt-modulatory activity occurs independently of its canonical helicase function. Co-immunoprecipitation (DP103-GSK3β), phosphorylation assay (LRP6), luciferase Wnt reporter assay, knockdown/overexpression, xenograft and Drosophila in vivo models Cell death & disease Medium 42248871
2025 A genetic interaction exists between Gemin3 and NAT1 (eIF4G2 orthologue) in Drosophila. Loss of NAT1 function downregulates Gem3 mRNA levels. Transcriptome alterations downstream of Gem3 and NAT1 silencing converge, supporting a functional relationship involving actin cytoskeleton organization and neurodevelopment. Genetic screen in Drosophila, RNAi knockdown, RNA-seq transcriptome analysis, brain morphology and muscle contraction assays Developmental biology Medium 39924071

Source papers

Stage 0 corpus · 43 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
1999 Gemin3: A novel DEAD box protein that interacts with SMN, the spinal muscular atrophy gene product, and is a component of gems. The Journal of cell biology 235 10601333
2014 DEAD-box helicase DP103 defines metastatic potential of human breast cancers. The Journal of clinical investigation 119 25083991
2005 The DEAD-box protein DP103 (Ddx20 or Gemin-3) represses orphan nuclear receptor activity via SUMO modification. Molecular and cellular biology 109 15713642
1999 Characterization of DP103, a novel DEAD box protein that binds to the Epstein-Barr virus nuclear proteins EBNA2 and EBNA3C. The Journal of biological chemistry 95 10383418
2000 Direct interaction of Smn with dp103, a putative RNA helicase: a role for Smn in transcription regulation? Human molecular genetics 82 10767334
2001 The DEAD box protein DP103 is a regulator of steroidogenic factor-1. Molecular endocrinology (Baltimore, Md.) 74 11145740
2003 A novel domain within the DEAD-box protein DP103 is essential for transcriptional repression and helicase activity. Molecular and cellular biology 70 12482992
2021 Human bone mesenchymal stem cells-derived exosomal miRNA-361-5p alleviates osteoarthritis by downregulating DDX20 and inactivating the NF-κB signaling pathway. Bioorganic chemistry 68 34052737
2005 Transcriptional factor FOXL2 interacts with DP103 and induces apoptosis. Biochemical and biophysical research communications 58 16153597
2003 The Ddx20/DP103 dead box protein represses transcriptional activation by Egr2/Krox-20. The Journal of biological chemistry 58 14699164
2011 Epstein-Barr virus nuclear antigen 3C stabilizes Gemin3 to block p53-mediated apoptosis. PLoS pathogens 55 22174681
2008 DEAD-box protein-103 (DP103, Ddx20) is essential for early embryonic development and modulates ovarian morphology and function. Endocrinology 53 18258677
2008 A motor function for the DEAD-box RNA helicase, Gemin3, in Drosophila. PLoS genetics 47 19023405
2008 Gemin3 is an essential gene required for larval motor function and pupation in Drosophila. Molecular biology of the cell 45 18923150
2010 Drosophila SMN complex proteins Gemin2, Gemin3, and Gemin5 are components of U bodies. Experimental cell research 37 20452345
2011 NANOS1 and PUMILIO2 bind microRNA biogenesis factor GEMIN3, within chromatoid body in human germ cells. Histochemistry and cell biology 34 21800163
2010 Abnormal interaction of motor neuropathy-associated mutant HspB8 (Hsp22) forms with the RNA helicase Ddx20 (gemin3). Cell stress & chaperones 34 20157854
2018 The multiple lives of DEAD-box RNA helicase DP103/DDX20/Gemin3. Biochemical Society transactions 33 29523774
2012 A miRNA machinery component DDX20 controls NF-κB via microRNA-140 function. Biochemical and biophysical research communications 29 22445758
2010 SMN, Gemin2 and Gemin3 associate with beta-actin mRNA in the cytoplasm of neuronal cells in vitro. Journal of molecular biology 28 20620147
2022 Ddx20, an Olig2 binding factor, governs the survival of neural and oligodendrocyte progenitor cells via proper Mdm2 splicing and p53 suppression. Cell death and differentiation 22 34974536
2019 SMN complex member Gemin3 self-interacts and has a functional relationship with ALS-linked proteins TDP-43, FUS and Sod1. Scientific reports 21 31822699
2011 Gem formation upon constitutive Gemin3 overexpression in Drosophila. Cell biology international 20 21627586
2016 High expression of DDX20 enhances the proliferation and metastatic potential of prostate cancer cells through the NF-κB pathway. International journal of molecular medicine 19 27121695
2021 The combined detection of Amphiregulin, Cyclin A1 and DDX20/Gemin3 expression predicts aggressive forms of oral squamous cell carcinoma. British journal of cancer 18 34290392
2024 DDX20 is required for cell-cycle reentry of prospermatogonia and establishment of spermatogonial stem cell pool during testicular development in mice. Developmental cell 17 38657611
2023 DDX20: A Multifunctional Complex Protein. Molecules (Basel, Switzerland) 14 37894677
2012 Conserved requirement for DEAD-box RNA helicase Gemin3 in Drosophila oogenesis. BMC research notes 13 22361416
2007 Modulation of transcriptional activity of the DEAD-box family of RNA helicases, p68 (Ddx5) and DP103 (Ddx20), by SUMO modification. Biochemical Society transactions 13 18031238
2024 DDX20 positively regulates the interferon pathway to inhibit viral infection. Antiviral research 10 38552910
2016 Genetic variants in the MicroRNA biosynthetic pathway Gemin3 and Gemin4 are associated with a risk of cancer: a meta-analysis. PeerJ 10 27019773
2022 Survival motor neuron protein and neurite degeneration are regulated by Gemin3 in spinal muscular atrophy motoneurons. Frontiers in cellular neuroscience 8 36619669
2022 A Macrophage Differentiation-Mediated Gene: DDX20 as a Molecular Biomarker Encompassing the Tumor Microenvironment, Disease Staging, and Prognoses in Hepatocellular Carcinoma. Oxidative medicine and cellular longevity 5 36246406
2024 DAPK enhances DDX20 protein stability via suppression of TRIM25-mediated ubiquitination-based DDX20 degradation. Cancer cell international 3 39558224
2022 Integration of RNAi and RNA-seq uncovers the regulation mechanism of DDX20 on vitellogenin expression in Scylla paramamosain. Comparative biochemistry and physiology. Part D, Genomics & proteomics 2 36244220
2017 Analysis of the polymorphic variants of RAN and GEMIN3 genes and risk of Primary Open-Angle Glaucoma in the Polish population. Ophthalmic genetics 2 29095070
2025 Envafolimab Inhibits the Growth of Gastric Cancer Cells with Low PD-L1 Expression through the DDX20/NF-κB/TNF-α Signaling Pathway. Current cancer drug targets 1 39021191
2025 A critical genetic interaction between Gemin3/Ddx20 and translation initiation factor NAT1/eIF4G2 drives development. Developmental biology 1 39924071
2026 Ddx20, DEAD-box helicase 20 is essential for maintaining microglial homeostasis. Experimental neurology 0 41864319
2026 DP103 as a critical modulator of Wnt signaling and cancer stemness: implications for precision treatment in triple negative breast cancer. Cell death & disease 0 42248871
2025 African swine fever virus MGF360-9L degrades DDX20 through the Rab1A-dependent autophagy pathway to antagonize its antiviral effect. Virologica Sinica 0 41101506
2024 Single nucleotide polymorphisms of GEMIN3 modify the risk of primary Sjögren's syndrome in female patients. The American journal of the medical sciences 0 38969288
2011 [Gemin3 inhibits cell apoptosis through suppression of p53 expression]. Zhonghua zhong liu za zhi [Chinese journal of oncology] 0 22335944

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