Ask about this productRelated genes to: DDX52 Blocking Peptide
- Gene:
- DDX52 NIH gene
- Name:
- DExD-box helicase 52
- Previous symbol:
- -
- Synonyms:
- ROK1
- Chromosome:
- 17q12
- Locus Type:
- gene with protein product
- Date approved:
- 2003-06-13
- Date modifiied:
- 2016-09-27
Related products to: DDX52 Blocking Peptide
Related articles to: DDX52 Blocking Peptide
- The DExD/H-box (DDX) helicase family plays critical roles in RNA metabolism and has been implicated in tumorigenesis. However, the pan-cancer activities and prognostic potential of DDX52, especially in liver hepatocellular carcinoma (LIHC), are largely unknown. - Source: PubMed
Publication date: 2026/08/06
Zhang ChongyuWang QiankunZhu MengchenLi XiaowenLi JiLiu XiYuan QinggongZhang YanZhang WunaiLi JunhuiYang WenbinLiu Nanbin - 17q12 microdeletion syndrome is a rare genetic disorder distinguished by diabetes, urogenital abnormalities, pancreatic hypoplasia, and neuropsychiatric developmental anomalies, with hyperuricemia being an infrequent occurrence. We present a unique case of 17q12 microdeletion, encompassing 17 protein-coding genes such as HNF1B, AATF, and DDX52 (3A:0), marking the first documented instance globally. - Source: PubMed
Publication date: 2026/03/25
Yang YueShen ZiyanZhang LiGuo WeiGong ShaominCai JieruWang JiayiYuan ShuangxinDing XiaoqiangZhang Xiaoyan - Targeted protein degradation, particularly through molecular glue degraders (MGDs), offers a promising strategy for targeting "undruggable" proteins. However, existing fluorescence-based screening approaches, such as time-resolved fluorescence resonance energy transfer, may be constrained by conformational changes or inefficient labeling of targets, necessitating more efficient screening approaches. Here, we present a MGDs screening approach based on surface plasmon resonance (SPR) coupled with degradomics and interactomics (SPR-DI). This approach leverages the high-throughput and label-free SPR for screening E3 ligands, followed by an unbiased "dual filter" of degradomics and interactomics to identify candidate proteins of interests (POIs). The feasibility of SPR-DI was validated using previously established MGD VH032, which can drive VHL to induce CDO1 degradation. Employing VHL and Keap1 as drivers E3, we then screened a natural product library and successfully identified triptolide and pycropodophyllin as potential MGDs. Subsequent investigations demonstrated that triptolide facilitates VHL-mediated degradation of IMP3, whereas picropodophyllin promotes Keap1-mediated degradation of DDX52 and LDHB. These degradation events were confirmed to depend on the respective E3 and ubiquitin-proteasome system, underscoring the capacity of these compounds to induce ternary complex formation. In conclusion, the establishment of SPR-DI provides a promising tool for the discovery of MGDs and their corresponding POIs, offering instructive insights to advance future MGD screening methodologies. - Source: PubMed
Publication date: 2026/01/08
Yang YueyingZhu RuiLiang JingYan HongweiZhang HuadongTian JundanZhang RuiLiu XiaofenLiu YangLi HuaChen Lixia - DExD-box (DDX) proteins are essential for RNA metabolism and are targets for treatment of cancers and neurodevelopmental disorders. The biochemical mechanisms of many DDX proteins remain unclear, including human DDX52. DDX52 is essential for cell survival and is an emerging biomarker for the onset of metastatic melanoma. In this work, we identified that human DDX52 is an ATP-dependent translocase with 3'-5' polarity, which can unwind DNA duplexes and DNA/RNA hybrids. Further, DDX52 is a nucleic acid annealase, an activity that requires an N-terminal intrinsically disordered protein region. DDX52 becomes hyperactive at DNA annealing if DDX52 helicase activity is inactivated by mutagenesis. Using CRISPR-Cas9 genetic editing, we generated U2OS cell lines heterozygous for DDX52 (DDX52+/-), which exhibit growth defects and impaired cell migration, providing direct support for previous suggestions that DDX52 may promote cancer cell metastasis and C-myc regulation. - Source: PubMed
Parkes Ashley JSpringer Philipp JBolt Edward - Primary liver cancer (PLC) and metformin are not well understood to be associated. We conducted a Mendelian randomization (MR) analysis using genetic data from IEU OpenGWAS and FinnGen R10, with metformin as the exposure and PLC as the outcome. The inverse variance weighting (IVW) method was the primary analytical approach, with heterogeneity assessed by Cochran's Q test, pleiotropy by MR-Egger intercept, and outliers by MR-PRESSO. Bioinformatics analyses further explored potential mechanisms, including differential gene expression, protein-protein interactions (PPI), Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses, immune cell infiltration analysis, and drug sensitivity analysis. MR results demonstrated a significant association between metformin use and reduced risk of PLC ( = -5.6046, OR = 0.0037, = 0.026), with a Benjamini-Hochberg false discovery rate (FDR) adjusted value of 0.13. However, no causal effect was observed for hepatocellular carcinoma (HCC) or intrahepatic cholangiocarcinoma (ICC). By cross-referencing transcriptome data from the GEO database GSE241466 with metformin-related gene loci, 34 overlapping genes were identified. Differentially expressed genes (DEGs) were filtered using |log2FC| > 0 and < 0.05, with five hub genes (DDX52, KIF11, GCDH, MRPL45, and TICRR) being particularly prominent. Functional enrichment analysis revealed involvement in cGMP-PKG signaling and fatty acid metabolism pathways. Further validation with GEPIA2, TIMER, and TISCH showed correlations between these genes and immune infiltration, while GSCA-based drug sensitivity analysis suggested therapeutic relevance. In summary, these findings indicate that metformin may reduce PLC risk by modulating metabolic and immune-related pathways, supporting its potential value as an adjunct therapeutic agent. However, further validation through large-scale clinical and basic research is warranted. - Source: PubMed
Publication date: 2025/11/02
Ma YongxinQi JiaojiaoChen ZhiqiangZhang YuboLiu KejunSuo JiaxinChen BendongBu Yang