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
- Neuroendocrine prostate cancer (NEPC) is characterized by androgen receptor (AR) independence and poor response to conventional therapies, highlighting the need to unveil the molecular mechanisms behind NEPC. We previously showed that heme oxygenase 1 (HO-1, encoded by HMOX1) translocates to the nucleus exerting unexplored non-canonical functions. The present study delineates the nuclear interactome of HO-1, revealing a potential mechanism that impairs NEPC establishment. Through a proteomics approach integrated with bioinformatics analyses, we identified eleven novel nuclear interactors of HO-1. Unsupervised clustering analyses of RNA-seq data from prostate cancer (PCa) patient-derived xenografts (MDA PCa PDXs) and clinical cohorts demonstrated high expression of three HO-1 interactors (ILF3, SAFB, BCLAF1, and DDX17) in NEPC samples, with concomitant HMOX1 under-expression. Spatial transcriptomics in a mixed-histology tumor confirmed enrichment of the interactors in the NEPC foci. To better understand the link between HO-1 and NEPC, we established and characterized an in vitro model of NE transdifferentiation in PCa cell lines using forskolin to induce phenotypic reprogramming. HO-1 upregulation in transdifferentiated cells significantly attenuated the expression of NE markers and triggered a morphological shift, restoring epithelial phenotypes. This work identifies for the first time HO-1 nuclear interactome association with NEPC, where the HMOX1-ILF3-SAFB-BCLAF1-DDX17 print emerges as a useful marker for disease stratification. - Source: PubMed
Publication date: 2026/08/26
Seniuk RocioSanchis PabloSabater AgustinaPascual GastonBizzotto JuanLechuga JuliaDelfino MagdalenaShepherd Peter D ADong JiabinValacco María PiaCotignola JavierVazquez ElbaToro AyelenGueron GeraldineLabanca Estefania - [This corrects the article DOI: 10.21037/tau-2025-167.]. - Source: PubMed
Publication date: 2026/08/27
- HUWE1 (HECT, UBA, and WWE domain-containing protein 1) is an X-linked E3 ubiquitin ligase that regulates a broad range of substrates through both degradative and non-degradative ubiquitination. The essential role of HUWE1 is underscored by the neonatal lethality of Huwe1 knockout mice. Although HUWE1 has been extensively studied in cancer and neurodevelopment, its functions in brain aging and neurodegeneration remain poorly understood. Here, we used cross-linking-assisted immunoprecipitation coupled with mass spectrometry to characterize HUWE1 interactomes in 26-month-old wild-type and Tg-SwDI mouse brains. HUWE1 interactomes were enriched for proteins involved in gene expression, translation, synaptic signaling, and nucleic acid metabolism. HUWE1-associated protein complexes contained an extensive network of nucleic acid-binding proteins, including the G-quadruplex-associated helicases DDX5, DDX3X, DDX3Y, and DDX17, the nucleic acid-binding proteins nucleolin and FUS, and the DNA topology regulator TOP2B. These interactomes exhibited both disease- and sex-specific organization. Independent biochemical validation confirmed the association between HUWE1-containing complexes and the G-quadruplex helicase DDX5. In addition, APOE was uniquely detected in Tg-SwDI HUWE1 interactomes and was more abundant in females than in males, suggesting a disease- and sex-specific association between HUWE1-containing complexes and APOE. Taken together, these findings identify HUWE1 as a component of sex-specific nucleic acid-binding protein networks in the aging brain and provide new insights into its potential roles in neurodegeneration. - Source: PubMed
Publication date: 2026/09/05
Diaz Escarcega RocioM J Vijay KumarAbdul AzeezBommineni RiddhishManwani BhartiJung Sung YunTsvetkov Andrey S - Working memory refers to the multifaceted cognitive systems that are considered necessary for retaining information while performing complex tasks, such as reasoning and learning in humans. In vertebrates, working memory is evident as a conserved alternating searching strategy. We can use automated tracking tools to measure this search strategy in Xenopus tadpoles. The free-movement pattern Y-maze assay is validated for assessing spatial working memory and cognitive flexibility in Xenopus. Deviations from randomness in search strategies are quantified by comparing relative alternating and repeating Y-maze arm entry choices within a 60-min time period in the maze. Pharmacologically or genetically abolishing working memory in these tadpoles disrupts their search strategy and adaptive behavior in a Y-maze arena, providing a valuable model to investigate intellectual disabilities and the architecture of cognition. In this chapter, we present our protocol for measuring working memory and locomotive ability in Xenopus using automated behavioral tracking equipment along with our recommended sample collection procedure for genotyping. We routinely use this protocol to investigate neurodevelopmental phenotypes, providing in vivo functional evidence to support patient diagnoses for novel disorders such as those affecting GRIA1 and DDX17. - Source: PubMed
Powell SophieFletcher TiaBlythe AliceGodwin Annie - 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