Ask about this productRelated genes to: DDX59 antibody
- Gene:
- DDX59 NIH gene
- Name:
- DEAD-box helicase 59
- Previous symbol:
- -
- Synonyms:
- DKFZP564B1023, ZNHIT5
- Chromosome:
- 1q32.1
- Locus Type:
- gene with protein product
- Date approved:
- 2005-02-22
- Date modifiied:
- 2016-01-07
Related products to: DDX59 antibody
Related articles to: DDX59 antibody
- Kawasaki disease (KD) is a systemic vasculitis. Mitochondria was found to promote the activation of NLRP3 inflammatory vesicles, which have been shown to be a key driver of vascular disease. And there are few relevant reports of mitochondrial dynamic (MD) in KD. This study aimed to distinguish the potential biomarkers related to MD in KD and supply ideas for the intervention and treatment of KD. Currently, functional experimental verification in this field is lacking, and this study preliminarily explores their potential correlations through bioinformatics analysis. - Source: PubMed
Publication date: 2026/07/28
Hu TingtingLin ShaoyongYang RongrongGuo Xiaofeng - Despite critical roles in diseases, human pathways acting on strictly nuclear non-coding RNAs have been refractory to forward genetics. To enable their forward genetic discovery, we developed a single-cell approach that "Mirrors" activities of nuclear pathways with cytoplasmic fluorescence. Application of Mirror to two nuclear pathways targeting MALAT1's 3' end, the pathway of its maturation and the other, the degradation pathway blocked by the triple-helical Element for Nuclear Expression (ENE), identified nearly all components of three complexes: Ribonuclease P and the RNA Exosome, including nuclear DIS3, EXOSC10, and C1D, as well as the Nuclear Exosome Targeting (NEXT) complex. Additionally, Mirror identified DEAD-box helicase DDX59 associated with the genetic disorder Oral-Facial-Digital syndrome (OFD), yet lacking known substrates or roles in nuclear RNA degradation. Knockout of DDX59 exhibits stabilization of the full-length MALAT1 with a stability-compromised ENE and increases levels of 3'-extended forms of small nuclear RNAs. It also exhibits extensive retention of minor introns, including in OFD-associated genes, suggesting a mechanism for DDX59 association with OFD. Mirror efficiently identifies pathways acting on strictly nuclear non-coding RNAs, including essential and indirectly-acting components, and as a result can uncover unexpected links to human disease. - Source: PubMed
Publication date: 2025/05/22
Che RuiPanah MonirehMirani BhoomiKnowles KristaOstapovich AnastaciaMajumdar DebaratiChen XiaotongDeSimone JosephWhite WilliamNoonan MeganLuo HongAlexandrov Andrei - The precise function of DDX59 Antisense RNA 1 (DDX59- AS1) in lung adenocarcinoma (LUAD) has yet to be fully elucidated. - Source: PubMed
Wang YanliLi WeiWei SuZhang LixiLi DongbingQi Xu - Despite critical roles in diseases, human pathways acting on strictly nuclear non-coding RNAs have been refractory to forward genetics. To enable their forward genetic discovery, we developed a single-cell approach that "Mirrors" activities of nuclear pathways with cytoplasmic fluorescence. Application of Mirror to two nuclear pathways targeting MALAT1's 3' end, the pathway of its maturation and the other, the degradation pathway blocked by the triple-helical Element for Nuclear Expression (ENE), identified nearly all components of three complexes: Ribonuclease P and the RNA Exosome, including nuclear DIS3, EXOSC10, and C1D, as well as the Nuclear Exosome Targeting (NEXT) complex. Additionally, Mirror identified DEAD-box helicase DDX59 associated with the genetic disorder Oral-Facial-Digital syndrome (OFD), yet lacking known substrates or roles in nuclear RNA degradation. Knockout of DDX59 exhibits stabilization of the full-length MALAT1 with a stability-compromised ENE and increases levels of 3'-extended forms of small nuclear RNAs. It also exhibits extensive retention of minor introns, including in OFD-associated genes, suggesting a mechanism for DDX59 association with OFD. Mirror efficiently identifies pathways acting on strictly nuclear non-coding RNAs, including essential and indirectly-acting components, and, as a result, uncovers unexpected links to human disease. - Source: PubMed
Publication date: 2025/01/19
Che RuiPanah MonirehMirani BhoomiKnowles KristaOstapovich AnastaciaMajumdar DebaratiChen XiaotongDeSimone JosephWhite WilliamNoonan MeganLuo HongAlexandrov Andrei - lncRNAs play a critical role in multiple steps of gene regulation associated with tumor progression. However, the engagement of DDX59-AS1, a lncRNA, remains equivocal, particularly in oral squamous cell carcinoma (OSCC). In this study, the expression of DDX59-AS1 and its association with immune infiltration were investigated, and its prognostic value in OSSC was evaluated. OSCC patients were collected from The Cancer Genome Atlas (TCGA) database. The expression of DDX59-AS1 in OSCC and healthy tissue was compared using Wilcoxon rank sum test. The relationship between DDX59-AS1 and clinicopathological features was analyzed using Logistic regression. Gene ontology (GO) terminology analysis, gene set enrichment analysis (GSEA), and single sample GSEA (ssGSEA) were utilized to interpret the enrichment pathway and functionality and to quantify the immune cell infiltration of DDX59-AS1. The correlation between survival and DDA59-AS1 was evaluated by Kaplan-Meier analysis and Cox regression. The prognostic impact of DDX59-AS1 was predicted by the nomogram based on Cox multivariate analysis. High expression of DDX59-AS1 was significantly correlated with T stage, clinical stage, race, and age ( < 0.05). Multivariate survival analysis demonstrated that the high expression of DDX59-AS1 was associated with lower overall and specific survival rates. The prognosis prediction was validated by the nomogram and calibration curves. The expression of DDX59-AS1 was negatively correlated with Mast cells, Tfh, T cells, Treg, and B cells, and positively related with the Tgd infiltration level. DDX59-AS1 played a crucial role in the progression and prognosis of OSCC and was potentially a predictive biomarker for OSCC. - Source: PubMed
Publication date: 2022/08/23
Sun YangZhou QianrongSun JianBi WeiLi RuixueWu XingwenLi NiSong LiangYang FeiYu Youcheng