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
- Non-small cell lung cancer (NSCLC) remains a significant global health challenge, making the exploration of potential therapeutic targets critically important. In this study, we discovered that ZNF200 is highly expressed in NSCLC tissues and plays an oncogenic role by promoting cell proliferation and metastasis both in vitro and in vivo. Mechanistically, ZNF200 recruits DDX17 to the promoter region of RBPJ to upregulate the expression of RBPJ and activate the Notch signaling pathway. ZNF200 and DDX17 increase H3K4me3 enrichment at the RBPJ promoter. Furthermore, ZNF200 interacts with SETD1A to regulate H3K4me3 deposition, sustaining the transcriptional activity of the RBPJ promoter. Interestingly, DDX17 could maintain the protein stability of ZNF200 by inhibiting the ubiquitin-proteasome degradation pathway, which further increased the expression level of ZNF200 in the nucleus. Additionally, we revealed that miR-139 inhibits ZNF200 expression and that the introduction of miR-139 abrogates the increased cell proliferation and metastasis caused by ZNF200 over-expression. Overall, our work demonstrates the critical role and molecular mechanism of ZNF200 in regulating NSCLC development, highlighting the potential of targeting ZNF200 as an effective strategy in NSCLC treatment. - Source: PubMed
Publication date: 2026/06/24
Zhang YankeZhu HongbinWang XueqinDong WeiZhang MaoyuSong XinyueHan DanyeChai QianFeng XueyiWei XiaozhengChen HongyuLi YonghuaiZhao LeiDai Qian - Lenvatinib, a first-line therapy for hepatocellular carcinoma (HCC), is frequently compromised by the development of acquired resistance. Although aberrant protein ubiquitination contributes to drug resistance, the underlying mechanisms remain incompletely understood. In this study, we identify ubiquitin-specific protease 32 (USP32) as a clinically significant oncogene that is overexpressed in HCC and closely associated with aggressive tumor progression and lenvatinib resistance. USP32 knockdown markedly inhibits tumor growth, metastasis, and restores lenvatinib sensitivity both in vitro and in vivo, whereas USP32 overexpression aggravates malignant behaviors. Mechanistically, USP32 directly interacts with and deubiquitinates DEAD-box helicase 17 (DDX17) by cleaving K48-linked polyubiquitin chains, thereby stabilizing DDX17. Furthermore, DDX17 transcriptionally represses the tumor-suppressive microRNA miR-3163, leading to hyperactivation of the MAPK signaling pathway involved in lenvatinib resistance. Notably, combined treatment with the MAPK inhibitor selumetinib and lenvatinib synergistically overcomes drug resistance in lenvatinib-resistant xenograft models. Collectively, our findings identify USP32 as an important regulator of HCC malignancy and lenvatinib resistance via the DDX17/miR-3163/MAPK axis, highlighting its potential as a therapeutic target in refractory HCC. - Source: PubMed
Publication date: 2026/06/25
Yu YangXu Bo-RuiHuang Hao-RanNong Zi-WenWu Fei-FengZhang Guo-PeiLi Shao-Qiang - People with HIV exhibit elevated inflammation and cardiovascular risk despite antiretroviral therapy. To define the genetic architecture of inflammasome-associated inflammation, we performed whole-genome sequencing and quantified plasma IL-6, IL-1β, and IL-18 in 1,000 ART-suppressed PWH from the U.S. Military HIV Natural History Study. Genome-wide analyses identified 14 loci implicating antiviral defense (), lipid metabolism (), and vascular remodeling (). Transcriptome-wide analyses across cardiovascular and immune tissues identified regulatory programs linking interferon signaling, immune activation, and vascular biology to circulating cytokine levels. Mendelian randomization analyses supported causal relationships between inflammasome-associated cytokines and vascular events. Functional integration with genome-wide CRISPR perturbation datasets in primary CD4 T cells linked cytokine-associated loci to HIV antiviral pathways and cytokine regulatory networks. External validation in cohorts without HIV demonstrated pathway-level convergence despite limited variant-level overlap. These findings define genetic mechanisms linking inflammasome signaling, antiviral defense, and cardiovascular risk. - Source: PubMed
Publication date: 2026/06/10
Chung RyanChalasani Namratha ShivaniBarbehenn Alton SLundgren ErikSavur SoniaShome SayaneSheikhzadeh Caroline HSarvadhavabhatla SannidhiDonaire Maria SophiaPae VivianChu XiupingWinder DanielMaguire Colin TTopal SenayGanesan AnuradhaYabes Joseph MLarson Derek TLalani TahaniyatEwers Evan CColombo Rhonda EDugan EliRathore UjjwalMarson AlexanderAgan Brian KTomalka Jeffrey ASekaly Rafick PIoannidis Nilah MLee Sulggi A - 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