Ask about this productRelated genes to: DDX59 Blocking Peptide
- 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 Blocking Peptide
Related articles to: DDX59 Blocking Peptide
- Coronary artery disease (CAD) is a leading cause of death and disability worldwide. Although genome-wide association studies (GWAS) have identified over 300 loci associated with CAD risk, the molecular mechanisms linking these variants to disease and subclinical atherosclerosis are not fully understood. - Source: PubMed
Publication date: 2026/08/03
Yang ChaojieAguet FrancoisAuguste GaelleArdlie KristinGerszten RobertPost Wendy SWheeler Heather ETaylor Kent DKasela SilvaLappalainen TuuliIm Hae KyungDurda PeterJohnson CraigGuo XiuqingLiu YongmeiPolak JosephHerrington DavidClish ClaryVan Den Berg DavidTracy Russell PCornell ElaineBlackwell TomPapanicolaou GeorgeVargas Jose DBekiranov StefanMcNamara Coleen AMiller Clint LRotter Jerome IRich Stephen SManichaikul Ani - 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