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
- DEAD box helicases DDX17 and DDX5 control transcription termination and the associated processing of the 3' end of pre-messenger RNAs. Here, we demonstrate that the transcriptional readthrough induced by DDX17 depletion, either alone or in combination with DDX5, leads to an increased production of chimeric transcripts from tandemly oriented gene, or tracRNAs, in neuroblastoma cells. Analysis of neuroblastoma tumours in which tracRNAs are abundant revealed that low expression of DDX17 and DDX5 genes is associated with high-risk tumours and poor overall patient survival, and inversely linked with MYCN oncogene amplification. We demonstrate that changes in MYCN expression do not affect the expression of either helicase, but alter transcription termination leading to the production of tracRNAs. MYCN acts on termination through its direct binding to the 3' region of genes and it interacts with DDX17, suggesting that it may interfere with the activity of the helicase. Collectively, our work reveals a novel function of MYCN in transcription termination and suggests that the deregulation of MYCN and DDX17/DDX5 expression in neuroblastoma may lead to the expression of non-canonical and potentially harmful RNA molecules. - Source: PubMed
Publication date: 2026/05/28
Clerc ValentineAouadi KhouailaValat JessicaGrand XavierKhourab Lou-SahraDuquet AlizéeFontrodona NicolasBazire MatéoRama NicolasAuboeuf DidierGibert BenjaminMortreux FranckBourgeois Cyril F - Sepsis mortality stems from infection-triggered immune dysregulation, causing multiple organ dysfunction. B cells, key to adaptive immunity, protect against infection and regulate inflammation through antibodies, cytokines, and cell signaling. Their dysfunction is linked to sepsis outcomes, but their dynamic differentiation and underlying mechanisms remain poorly understood. - Source: PubMed
Publication date: 2026/05/16
Zhuo XiumingJian GangrenChen Hongyi - Colorectal cancer (CRC) progression is critically associated with metastasis, yet the molecular drivers remain incompletely characterized. Here, we identify circFAT1, a circular RNA derived from exon 2 of the tumor suppressor gene FAT1, as a metastasis-promoting factor in CRC. Through polysome profiling and RNA sequencing, we demonstrate that circFAT1 is upregulated in CRC tissues and exhibits translational activity. Functional assays reveal that circFAT1 encodes a novel 1057-amino acid protein that enhances CRC cell migration, invasion, and metastatic dissemination in vivo, independent of proliferation. Mechanistically, the circFAT1-encoded protein interacts with DDX17 to facilitate β-catenin nuclear translocation, forming a ternary complex that binds promoter regions of RHOA and FRAT1 to activate their transcription. This axis drives epithelial-mesenchymal transition (EMT), as evidenced by downregulation of E-cadherin and upregulation of N-cadherin, vimentin, ZEB1 and Snail. Strikingly, linear FAT1 inversely suppresses CRC cell motility, highlighting the functional dichotomy between circular and linear isoforms. Our findings establish circFAT1 as a pro-metastatic driver in CRC and provide a mechanistic framework for targeting the circFAT1/DDX17/β-catenin signaling axis in therapeutic strategies. - Source: PubMed
Publication date: 2026/05/16
Xu JieyingChen BingZhao JingjingZhang HenaWang ZhenHuang ShenglinLi Yan - Hepatocellular carcinoma (HCC) is a highly heterogeneous malignancy with an increasing global incidence and mortality. Dysregulated gene expression drives uncontrolled proliferation and metastasis, contributing to poor patient survival despite therapeutic advances. The DEAD-box RNA helicase DDX17 has been implicated in tumorigenesis, but its functional role and underlying mechanisms in HCC remain incompletely defined. Here, we found that DDX17 drives HCC tumorigenesis via a novel mechanism involving direct binding to Raptor, a core component of the mTORC1 complex, thereby activating mTORC1 signaling and inhibiting autophagy, as evidenced by reduced autophagosome formation and a decreased LC3-II/LC3-I ratio. Moreover, DDX17 unwinds the RNA G-quadruplex (rG4) structure in the Raptor 3′ untranslated region (3′ UTR), enhancing its translation and establishing Raptor as an rG4-dependent oncogenic target. Combined DDX17 knockdown and rapamycin treatment synergistically suppressed proliferation and induced autophagy. Additionally, DDX17 inhibition reshaped tumor cell metabolism by decreasing extracellular acidification and promoting lipid droplet accumulation following autophagy induction, highlighting its role in metabolic adaptation. These findings suggest that DDX17 promotes HCC progression by unwinding the rG4 motif in Raptor mRNA to enhance translation, activating mTORC1 signaling, and suppressing autophagy. Hence, co-targeting DDX17 and mTORC1 produces strong synergistic antitumor effects, revealing a promising therapeutic strategy for HCC. - 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