Ask about this productRelated genes to: DDX17 antibody
- Gene:
- DDX17 NIH gene
- Name:
- DEAD-box helicase 17
- Previous symbol:
- -
- Synonyms:
- P72
- Chromosome:
- 22q13.1
- Locus Type:
- gene with protein product
- Date approved:
- 1999-08-20
- Date modifiied:
- 2016-01-07
Related products to: DDX17 antibody
Related articles to: DDX17 antibody
- - Source: PubMed
Publication date: 2026/04/22
Lv ChaoxiangLuo NaWei ChunliZhang QiqiGuo KanJiang XiaCao XiuhuaMazaher MaghsoudlooElFar AliFu Junjiang - RNA helicases are fundamental ATP-dependent enzymes that remodel RNA structures and ribonucleoprotein complexes. Recent studies reveal that RNA helicases are critical regulators of circular RNA networks, where circRNAs function as stable regulators of gene expression with important implications in disease. This study integrates structural, mechanistic, and functional insights into how RNA helicase families regulate circRNA biogenesis, stability, and function. Accumulating evidence demonstrates that RNA helicases can suppress circRNA biogenesis by remodeling intronic structures, such as DHX9 suppression, or promote biogenesis through DDX5/DDX17, which resolve inhibitory intronic structures by recruiting splicing factors (QKI, SRSF1) and stabilizing spliceosome assembly. We also highlight helicase-mediated control of circRNA stability and decay, such as EIF4A3, DDX5, and DDX17 protecting circRNAs from degradation by blocking decay factors, as well as reciprocal regulation in which circRNAs scaffold to modulate translation. In this review, we summarize RNA helicase families structures and circRNA biogenesis mechanisms, explore their extensive roles in circRNA regulation, and propose RNA helicases as central regulators and promising therapeutic targets, offering new avenues for biomarker development and RNA-based therapies. - Source: PubMed
Publication date: 2026/03/18
Al-Subari Musaed HamoodXiao YugangZhu Qubo - Acute kidney injury (AKI) is a severe clinical syndrome with high morbidity and mortality, yet its pathogenesis remains incompletely understood, and effective therapeutic strategies are still lacking. In this study, we observed significant upregulation of N-acetyltransferase 10 (NAT10) in the tubular epithelial cells of Cisplatin-induced AKI. Lentivirus-mediated knockdown of NAT10 or treatment with NAT10 inhibitor Remodelin, ameliorated Cisplatin-induced renal dysfunction and tubular injury. Importantly, NAT10 inhibition markedly attenuated cellular senescence in Cisplatin-induced AKI, as evidenced by reduced senescence-associated β-galactosidase (SA-β-gal) activity, downregulation of senescence markers (p53, p21 and γ-H2A.X) and decreased levels of senescence-associated secretory phenotype (SASP) factors (IL-1β, IL-6 and TNF-α). Mechanistically, co-immunoprecipitation assay suggested that NAT10 interacted with DDX17 to regulate its expression. Knockdown or inhibition of NAT10 reduced the protein expression of DDX17 in Cisplatin-injured kidneys. While silencing DDX17 could inhibit Cisplatin-induced senescence in HK-2 cells. Furthermore, we demonstrated that the effects of NAT10 on Cisplatin-induced tubular injury and senescence was dependent on DDX17. Our study revealed a novel mechanism by which NAT10 promoted Cisplatin-induced renal tubular cell senescence via DDX17 upregulation, suggesting that targeting the NAT10/DDX17 signaling axis may offer a potential therapeutic strategy for AKI. - Source: PubMed
Publication date: 2026/01/30
Zhu YutingXu WenchaoWan ChengDeng BowenXie YaruYang BinJiang HongyangZhang Chun - Identifying novel targets that ameliorating dopaminergic neuron iron metabolism dysregulation may provide potential therapeutic strategies for Parkinson's disease (PD). Buddlejasaponin IVb (BJP-IVb) is the first natural product that can ameliorate iron regulatory protein 2 (IRP2)-mediated iron metabolism dysregulation in dopaminergic neuron to suppress PD. BJP-IVb may exert this bioactivity through novel target. However, the pharmacological target of BJP-IVb is unclear. - Source: PubMed
Publication date: 2026/02/07
Li Qiang-MingZhu Man-LeiLi XiangHe Jing-XingZha Xue-QiangLuo Jian-PingZhang Feng-Yun - Sepsis-induced cardiomyopathy (SICM) is a severe complication of sepsis, in which mitochondrial dysfunction contributes to poor outcomes. DEAD-box helicase 17 (Ddx17), a member of the DEAD-box RNA helicase family, is known to regulate mitochondrial function, but its role in SICM remains unclear. In this study, mice with cardiomyocyte-specific Ddx17 knockdown (Ddx17-cKD) and overexpression (Ddx17-OE) were generated, and sepsis models were established using cecal ligation and puncture. Mechanistic findings were further validated in vitro using immunoprecipitation and dual-luciferase assays. Ddx17 expression was markedly reduced in the cardiac tissues of septic mice and in lipopolysaccharide-treated cardiomyocytes. Knockdown of Ddx17 increased mitochondrial reactive oxygen species accumulation, enhanced cell death and decreased superoxide dismutase activity. In contrast, Ddx17 overexpression attenuated mitochondrial apoptosis and oxidative stress, restored adenosine triphosphate production and mitochondrial membrane potential and improved cardiac function in septic mice. Mechanistically, Ddx17 interacted with signal transducer and activator of transcription 3 (STAT3) to suppress transcription of the mitochondrial fission protein dynamin-related protein 1 while maintaining the level of the fusion protein mitofusin 1, thereby preserving mitochondrial integrity and cardiomyocyte homeostasis. These findings demonstrate that Ddx17 protects against sepsis-induced cardiomyopathy by regulating mitochondrial dynamics, reducing oxidative stress and preventing apoptosis, thereby highlighting Ddx17 as a potential therapeutic target for septic cardiac dysfunction. - Source: PubMed
Jiang Ya-TingSu Li-RanNi Fang-JingLu Luo-YeGong Yu-QiangLuo JunShen Chen-XiCao Yang