Ddx20 Antibody - middle region (ARP36400_P050)
- Known as:
- Ddx20 Antibody - middle region (ARP36400_P050)
- Catalog number:
- arp36400_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- Ddx20 Antibody - middle region (ARP36400_P050)
Related genes to: Ddx20 Antibody - middle region (ARP36400_P050)
- Gene:
- DDX20 NIH gene
- Name:
- DEAD-box helicase 20
- Previous symbol:
- -
- Synonyms:
- DP103, GEMIN3
- Chromosome:
- 1p13.2
- Locus Type:
- gene with protein product
- Date approved:
- 1999-12-14
- Date modifiied:
- 2016-10-05
Related products to: Ddx20 Antibody - middle region (ARP36400_P050)
Related articles to: Ddx20 Antibody - middle region (ARP36400_P050)
- - Source: PubMed
Publication date: 2026/03/24
He LuFan XuxuZhu ZhaoyuPei DanshiWang YizhuoLi XizhongRen QingfengZheng HaixueLi WeiweiZhu Zixiang - The properties of central nervous system microglia adjust dynamically in response to various environmental signals, under both normal and disease conditions. However, the regulation of microglia homeostasis is not well understood. We hypothesize that the DEAD-box RNA helicase Ddx20 plays a key role in maintaining microglial homeostasis. To test this hypothesis, we generated mice with conditional deletion of Ddx20 in microglia using Iba1-iCre knock-in mice, and analyzed the effects of spinal cord injury and aging. Ddx20 ablation led to a drastic alteration of microglial morphology and a marked downregulation of gene networks involved in maintaining microglial identity, immune surveillance, and homeostatic functions; these effects become more prominent with spinal cord injury and aging. Our findings provide novel insights into the role of Ddx20 as a molecular regulator of microglial homeostasis and response to central nervous system injury. - Source: PubMed
Publication date: 2026/03/19
Kawai YosukeBizen NorihisaNishiyama KeiTakebayashi Hirohide - Oligodendrocyte abnormalities disrupt the integrity of myelin and axons, ultimately leading to neuronal loss; however, the pathogenesis of this condition remains unclear, necessitating the development of new animal models. Ddx20 is an RNA-binding factor essential for oligodendrocyte development. To investigate the function of Ddx20 in mature oligodendrocytes, we generated tamoxifen-inducible Ddx20 knockout mice. Systemic deterioration occurred around 4 weeks after tamoxifen administration, characterized by rapid oligodendrocyte loss, massive microglial activation, and subsequent neuronal loss, particularly in the ventral gray matter of the spinal cord. Microglial depletion experiments using PLX3397 administration worsened the phenotype at around 4 weeks, suggesting that microglia play a neuroprotective role up to that point. RNA-seq analysis revealed a significant shift in gene expression after 4 weeks, indicating a change in microglial characteristics at the terminal stage. These results demonstrate that Ddx20 is crucial for maintaining oligodendrocytes, and this novel mouse offers valuable insights how oligodendrocyte abnormalities and subsequent involvement of microglial activation can contribute to neuronal cell death. - Source: PubMed
Publication date: 2025/10/16
Ise MasatakaBizen NorihisaSimankova AnnaOkuyama KentaroShibata ShinsukeTada MariTakebayashi Hirohide - African swine fever (ASF) is an acute, hemorrhagic, and highly contagious disease in pigs caused by the African swine fever virus (ASFV). Our previous studies have demonstrated that deletion of the MGF360-9L gene weakens ASFV virulence in pigs, yet the underlying mechanism remains unclear. To investigate the mechanism of MGF360-9L regulating ASFV pathogenicity, the relationship between MGF360-9L and host proteins was identified by mass spectrometry. We found that host protein DEAD-box helicase 20 (DDX20) interacted with and colocalized with MGF360-9L. Overexpression of DDX20 inhibited ASFV replication, whereas knockdown of DDX20 had the opposite effects. Moreover, DDX20 inhibited ASFV replication by promoting the activation of type I interferon signaling. Surprisingly, DDX20 was gradually degraded following ASFV infection. Mechanistically, MGF360-9L promoted the autophagic degradation of DDX20 by recruiting autophagy-related protein Ras-related protein Rab-1A (Rab1A). Silencing Rab1A suppressed ASFV replication, while overexpression of Rab1A exhibited the opposite effects. Furthermore, Rab1A, MGF360-9L and DDX20 could form a complex to facilitate the degradation of DDX20. Knockdown of Rab1A impaired MGF360-9L-mediated degradation of DDX20 during ASFV infection. In summary, our study demonstrates that MGF360-9L targets DDX20 for autophagy degradation to antagonize its antiviral function and facilitate ASFV replication. This finding broadens our understanding of the regulatory network between ASFV and its host, and provides new insights into the pathogenesis and immune evasion mechanisms of ASFV. - Source: PubMed
Publication date: 2025/10/14
He LuFan XuxuZhu ZhaoyuPei DanshiWang YizhuoLi XizhongRen QingfengZheng HaixueLi WeiweiZhu Zixiang - Gemin3 (Gem3) or DEAD-box RNA helicase 20 (Ddx20) has been mostly implicated in the assembly of spliceosomal small nuclear ribonucleoproteins (snRNPs) as part of the SMN-Gemins complex. Nonetheless, several studies have hinted at its participation in diverse snRNP-independent activities. Here, we utilised a narrow unbiased genetic screen to discover novel Gem3 interactors in Drosophila with the aim of gaining better insights on its function in vivo. Through this approach, we identified a novel genetic interaction between Gem3 and NAT1, which encodes the Drosophila orthologue of translational regulator eIF4G2. Despite lack of a physical association, loss of NAT1 function was found to downregulate Gem3 mRNA levels. Extensive convergence in transcriptome alterations downstream of Gem3 and NAT1 silencing further supports a functional relationship between these factors in addition to showing a requirement for both in actin cytoskeleton organisation and organism development, particularly neurodevelopment. In confirmation, flies with either Gem3 or NAT1 depletion exhibited brain growth defects and reduced muscle contraction. Severe delays in developmental progression were also observed in a newly generated Gem3 hypomorphic mutant. Our data linking Gemin3 to a key component of the translational machinery support an emerging role for Gemin3 in translation that is also critical during organism development. - Source: PubMed
Publication date: 2025/02/07
Cacciottolo RebeccaCauchi Ruben J