Ask about this productRelated genes to: DDX50 antibody
- Gene:
- DDX50 NIH gene
- Name:
- DExD-box helicase 50
- Previous symbol:
- -
- Synonyms:
- GU2, MGC3199, GUB, RH-II/GuB
- Chromosome:
- 10q22.1
- Locus Type:
- gene with protein product
- Date approved:
- 2003-06-13
- Date modifiied:
- 2016-10-05
Related products to: DDX50 antibody
Related articles to: DDX50 antibody
- Homocysteine (Hcy) is an independent risk factor for atherosclerosis (AS). Hcy induces the transformation of vascular smooth muscle cells (VSMCs) into foam cells, which play a crucial role in this process. However, the detailed mechanism is still unclear. To identify the key regulatory proteins during this process and clarify the possible mechanism of Hcy-induced foam cell formation in VSMCs, thereby providing theoretical support for the intervention of AS. VSMCs were allocated into two groups: a control cohort and a group exposed to Hcy to simulate an AS-like state. Quantitative proteomic profiling was performed using the label-free quantitative DIA (LFQ-DIA) approach to detect differentially expressed proteins between these groups. To explore functional implications, enrichment analyses involving Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways were conducted. Protein-protein interaction networks were constructed using the STRING database to identify central interactors. Target proteins were subsequently validated through parallel reaction monitoring (PRM). Furthermore, histological analyses (hematoxylin and eosin (HE) staining, Oil Red O staining), biochemical assays of lipid content (total cholesterol (TC) and triglycerides (TG)), and Western blot analysis were utilized to confirm the role and mechanism of identified proteins in the context of Hcy-driven foam cell conversion. The results showed that proteomic analysis identified 4804 proteins in total, of which 4799 passed missing-value filtering and were retained for downstream quantitative analysis. A total of 54 proteins were identified as differentially expressed using thresholds of adjusted p-value < 0.05 and fold change > 1.5. Among them, 13 proteins were upregulated, while 41 were downregulated in response to Hcy treatment. For PRM validation, 20 candidate proteins were selected according to proteomic evidence, biological relevance, and technical feasibility. Among them, 16 proteins (COX7C, STX5, UBQLN2, DDX50, TBCB, GSR, PCNP, CDV3, PEBP1, PPIA, S100A6, EIF4E2, UBQLN1, ARMC1, NUDCD2, and H1-2) showed the same direction of fold-change values as in the LFQ-DIA dataset, thereby underscoring the reliability of the proteomic analysis. Data are available via ProteomeXchange with identifier PXD064315. Histological staining demonstrated enhanced lipid accumulation, and the protein expression of the contraction phenotype marker a-SMA decreased, while the protein expression of the synthesis phenotype marker OPN increased. This indicates that Hcy induces VSMCs to transform from a contraction phenotype to a synthesis phenotype, resulting in the formation of foam cells. The protein levels of COX7C and sterol regulatory element-binding proteins (SREBP1C and SREBP2) were elevated upon Hcy exposure. Overexpression of COX7C further augmented the expression of SREBP1C and SREBP2, exacerbated lipid accumulation, and promoted foam cell transformation in Hcy-treated VSMCs. On the other hand, knockdown of COX7C had the opposite effect. Overall, the results of the present study suggest that COX7C plays a crucial regulatory role in Hcy-induced transformation of VSMCs into foam cells. Its pathogenic role is likely mediated through the upregulation of SREBP1C and SREBP2, thereby promoting lipid accumulation. These findings provide new insights into AS pathogenesis and identify COX7C maybe a potential therapeutic target. - Source: PubMed
Publication date: 2026/02/05
Wang XiuyuMa XinpengZhang XiangMa XingZhang Minghao - R-loops consist of an RNA-DNA hybrid and a displaced single-stranded DNA strand that play a central role in several biological processes. However, as the presence of aberrant R-loops forms a significant threat to genome stability, R-loop formation and resolution is strictly controlled by RNAse H and helicases. In a screening for RNA helicases, previously described as RNA-DNA hybrid interactors, that control genome integrity, we identified for the first time DDX37 and DDX50. Depletion of DDX37 and DDX50 promotes DNA damage, as demonstrated by H2AX phosphorylation and increased comet tail length. In addition, knock down of these RNA helicases decreases the DNA replication track length and leads to RPA focus formation, results that are indicative of replication stress. Downregulation of DDX37 and DDX50 triggers an increase in RNA-DNA hybrids, that can be reverted by the overexpression of RNase H1. Interestingly, inhibition of transcription prevented the increased RNA-DNA hybrid formation and DNA damage upon DDX37 or DDX50 depletion. Together these results demonstrate that DDX37 and DDX50 are important for resolving RNA-DNA hybrids appearing during transcription and thereby preventing DNA damage by replication stress. - Source: PubMed
Publication date: 2025/03/04
Hernández-Reyes YerayFonseca-Rodríguez CintiaFreire RaimundoSmits Veronique A J - Optic disc drusen (ODD) are believed to have a genetic predisposition, with autosomal dominant inheritance pattern with incomplete penetrance suggested through family pedigree analysis. ODD prevalence is higher in certain genetic disorders, such as pseudoxanthoma elasticum and retinitis pigmentosa. This study aimed to identify candidate genes potentially involved in the development of ODD. - Source: PubMed
Publication date: 2025/01/26
Steensberg Alvilda HOvens ChrisFraser Clare LMalmqvist LasseBertelsen MetteGrønskov KarenHamann Steffen - Glucose binding can alter protein oligomerization to enable differentiation. Here, we demonstrate that glucose binding is a general capacity of DExD/H-box RNA helicases, including DDX50, which was found to be essential for the differentiation of diverse cell types. Glucose binding to conserved DDX50 ATP binding sequences altered protein conformation and dissociated DDX50 dimers. DDX50 monomers bound STAU1 to redirect STAU1 from an RNA-decay-promoting complex with UPF1 to a DDX50-STAU1 ribonuclear complex. DDX50 and STAU1 bound and stabilized a common set of essential pro-differentiation RNAs, including JUN, OVOL1, CEBPB, PRDM1, and TINCR, whose structures they also modified. These findings uncover a DDX50-mediated mechanism of reprograming STAU1 from its canonical role in Staufen-mediated mRNA decay to an opposite role stabilizing pro-differentiation RNAs and establish an activity for glucose in controlling RNA structure and stability. - Source: PubMed
Publication date: 2025/01/06
Miao WeiliPorter Douglas FSiprashvili ZurabFerguson Ian DDucoli LucaNguyen Duy TKo Lisa ALopez-Pajares VanessaSrinivasan SuhasHong Audrey WYang Yen-YuCao ZhongwenMeyers Robin MMeyers Jordan MTao ShiyingWang YinshengKhavari Paul A - The study aimed to investigate prevalent chromosomal breakpoints identified in balanced structural chromosomal anomalies and to pinpoint potential candidate genes linked with male infertility. This was acchieved through a comprehensive approach combining RNA-seq and microarray data analysis, enabling precise identification of candidate genes. The Cytogenetics data from 2,500 infertile males referred to Royan Research Institute between 2009 and 2022 were analyzed, with 391 cases meeting the inclusion criteria of balanced chromosomal rearrangement. Of these, 193 cases exhibited normal variations and were excluded from the analysis. By examining the breakpoints, potential candidate genes were suggested. Among the remaining 198 cases, reciprocal translocations were the most frequent anomaly (129 cases), followed by Robertsonian translocations (43 cases), inversions (34 cases), and insertions (3 cases).Some patients had more than one chromosomal abnormality. Chromosomal anomalies were most frequently observed in chromosomes 13 (21.1%), 14 (20.1%), and 1 (16.3%) with 13q12, 14q12, and 1p36.3 being the most prevalent breakpoints, respectively. Chromosome 1 contributed the most to reciprocal translocations (20.2%) and inversions (17.6%), while chromosome 14 was the most involved in the Robertsonian translocations (82.2%). The findings suggested that breakpoints at 1p36.3 and 14q12 might be associated with pregestational infertility, whereas breakpoints at 13q12 could be linked to both gestational and pregestational infertility. Several candidate genes located on common breakpoints were proposed as potentially involved in male infertility. Bioinformatics analyses utilizing three databases were conducted to examine the expression patterns of 78 candidate genes implicated in various causes of infertility. In azoospermic individuals, significant differential expression was observed in 19 genes: 15 were downregulated (TSSK2, SPINK2, TSSK4, CDY1, CFAP70, BPY2, BTG4, FKBP6, PPP2R1B, SPECC1L, CENPJ, SKA3, FGF9, NODAL, CLOCK), while four genes were upregulated (HSPB1, MIF, PRF1, ENTPD6). In the case of Asthenozoospermia, seven genes showed significant upregulation (PRF1, DDX21, KIT, SRD5A3, MTCH1, DDX50, NODAL). Though RNA-seq data for Teratozoospermia were unavailable, microarray data revealed differential expression insix genes: three downregulated (BUB1, KLK4, PIWIL2) and three upregulated (AURKC, NPM2, RANBP2). These findings enhance our understanding of the molecular basis of male infertility and could provide valuable insights for future diagnostic and therapeutic strategies. - Source: PubMed
Publication date: 2024/10/02
Hossein Garakani MelikaKakavand KianoushSabbaghian MarjanGhaheri AzadehMasoudi Najmeh SadatShahhoseini MaryamHassanzadeh VahidehZamanian MohammadrezaMeybodi Anahita MohseniMoradi Shabnam Zarei