Ask about this productRelated genes to: DDX39B antibody
- Gene:
- DDX39B NIH gene
- Name:
- DExD-box helicase 39B
- Previous symbol:
- BAT1
- Synonyms:
- D6S81E, UAP56
- Chromosome:
- 6p21.33
- Locus Type:
- gene with protein product
- Date approved:
- 2001-07-13
- Date modifiied:
- 2016-09-27
Related products to: DDX39B antibody
Related articles to: DDX39B antibody
- The recent study aims to analyze the role of non-coding RNAs, particularly circRNAs, in HIV pathogenesis using construction of immune-related regulatory networks. In compliance with ethical standards and institutional guidelines, publicly available HIV-related mRNA and microRNA expression datasets were systematically retrieved from the Gene Expression Omnibus repository. These datasets underwent rigorous bioinformatics analysis employing the "limma" package in R to identify differentially expressed genes (DEGs) and microRNAs (DEmiRNAs). Validated interaction data from miRBase and ENCORI databases facilitated the construction of circRNA-DEmiRNA and DEmiRNA-DEG regulatory networks. Protein-protein interaction networks were generated through STRING database analysis, with hub genes defined as those within the highest 5% of interaction degrees. Furthermore, single-cell RNA sequencing (scRNA-seq) datasets from HIV-infected individuals were analyzed using the "Seurat" package to identify DEGs in CD4+ and CD8+ T cell subsets. Cross-validation between microarray and scRNA-seq data ensured robustness of identified hub genes. Our results revealed substantial alterations in RNA expression associated with both high viral load and low viral load HIV infections. Single-cell analyses indicated significant gene expression shifts in T cell populations: 194 upregulated and 813 downregulated genes in CD4+ T cells, and 244 upregulated and 567 downregulated genes in CD8+ T cells. Integrated analysis delineated five hub genes consistently dysregulated across T cell subsets. STAT1 and DDX39B were upregulated, whereas CXCL8, CXCL12, and PTGS2 were downregulated. The pathway enrichment analysis indicated that these genes are implicated in key regulatory pathways relevant to infectious disease mechanisms. Alongside of DEGs, our studies indicated that multiple miRNAs, such as hsa-miR-21-5p, hsa-miR-146a-5p and hsa-let-7b-5p are differentially expressed in HIV-infected samples in comparison to the normal samples. Afterward, DEmiRNA-DEGs network studies demonstrated different axes between significantly up- and down-regulated DEGs with down- and up-regulated miRNAs, respectively. Following, ceRNA regulatory network revealed circRNAs, which can interact with DEmiRNA-DEGs networks, like hsa_circ_0089761-hsa-miR-21-5p-CXCL12, hsa_circ_0003812-hsa-miR-146a-5p-PTGS2, and has_circ_0007185-has_let-7b-5p-DDX39B. Overall, this integrative analysis suggests potential circRNA-mediated regulatory mechanisms in HIV infection and highlights potential candidate circRNAs that may serve as biomarkers or therapeutic targets for further investigation. - Source: PubMed
Publication date: 2026/08/14
Faraji NeginRouhi LeilaBolhassani AzamHasannejad-Asl BehnamBaesi KazemAbbasian Ladan - Preeclampsia (PE), a hypertensive disorder unique to pregnancy, is linked to impaired trophoblast function. DEAD-box helicase 39B (DDX39B) plays key roles in embryonic development. This study investigated its role in regulating trophoblast biology during PE progression. We conducted functional assays using CCK-8, clone formation, EdU, Transwell, Wound healing and TUNEL in the HTR-8/SVneo trophoblast cells. The interaction between Wilms tumor 1-associating protein (WTAP) and DDX39B was analyzed by Co-IP assay. RIP assay or RNA pull down were used to assess the association between the ELAV-like RNA-binding protein 1 (ELAVL1)/WTAP and L-lactate dehydrogenase A (LDHA) mRNA. Additionally, MeRIP assay was employed to evaluate m6A levels on LDHA transcripts. Overexpression of DDX39B promoted the proliferation and migration of trophoblast cells and suppressed cells apoptosis, while DDX39B knockdown had the opposite result. In addition, WTAP knockdown reversed the promoting effects of DDX39B overexpression on trophoblast proliferation and migration. Mechanistically, DDX39B promoted post-translational stabilization of WTAP by directly interacting with WTAP protein. WTAP enhanced the m6A methylation of LDHA mRNA by recruiting ELAVL1. As expected, LDHA knockdown abrogated the pro-proliferative and anti-apoptotic effects of WTAP overexpression on trophoblasts. Our findings established a novel DDX39B/WTAP/m6A/LDHA regulatory axis, wherein DDX39B acted as an RNA-binding protein to stabilize WTAP, enhancing LDHA expression and promoting trophoblast proliferation, migration, and survival. Dysregulation of this pathway might contribute to PE pathogenesis, offering new avenues for targeted therapies. - Source: PubMed
Publication date: 2026/06/19
Li ChengZhou WenjunShen YuqinZhang JingJiang YanqiongLi Ruiman - Eukaryotic genomes generate a plethora of polyadenylated (pA) RNAs, which are packaged into ribonucleoprotein particles (RNPs). To ensure faithful gene expression, functional pA RNPs, including protein-coding RNPs, are exported to the cytoplasm, whereas transcripts within non-functional pA RNPs are degraded in the nucleus. How cells distinguish these opposing fates remains unknown. The DExD-box ATPase UAP56 (also known as DDX39B) is a central component of functional pA RNPs, and promotes their docking to the nuclear pore complex-anchored TREX-2, which triggers transcript release from UAP56 to facilitate export. Here we reveal that the poly(A) tail exosome targeting (PAXT) connection binds a TREX-2-like module, which releases pA RNAs from UAP56 for decay by the nuclear exosome. The core of this module consists of a LENG8-PCID2-SEM1 trimer, which we show is structurally and biochemically equivalent to the central GANP-PCID2-SEM1 trimer of TREX-2. Mutagenesis and transcriptomic data demonstrate that the nuclear fate of pA RNPs is governed by the contending actions of nucleoplasmic PAXT and nuclear pore complex-associated TREX-2, which interpret RNA-bound UAP56 as a signal for RNA decay or export, respectively. As RNA targets of PAXT are generally short and intron-poor, we propose an overall model for pA RNP fate determination whereby the distinct sub-nuclear localizations of PAXT and TREX-2 govern the degradation of short non-functional pA RNAs while allowing export of their longer and functional counterparts. - Source: PubMed
Publication date: 2026/06/17
Bugai AndriiHohmann UlrichLorenzo AnaGraf MaxFin LauraRouvière Jérôme OTirian LaszloDou YuhuiLe Rest MarionPolák PatrikJohnsen DennisJakobsen LisAndersen Jens SkorstengaardBrennecke JuliusPlaschka ClemensJensen Torben Heick - Premature ejaculation (PE) is a highly prevalent male sexual dysfunction with undefined etiopathogenesis and a lack of validated objective biomarkers. Lifelong premature ejaculation (LPE) represents a more severe and persistent form of the disorder. Noninvasive plasma protein biomarkers for LPE diagnosis and their association with dapoxetine treatment outcomes remain insufficiently investigated. - Source: PubMed
Publication date: 2026/06/05
Xu ChunluZhang QijieShen ZhiyiQian YichenDai YutianKan YiLuan Jiaochen - Interleukin-15 (IL-15) is expressed in various cancers, including melanoma, where it exists in distinct membrane-associated isoforms. Primary melanoma cells predominantly express the non-cleavable transmembrane form (tmbIL-15), while metastatic cells also express a cleavable membrane-bound form (mbIL-15) complexed with IL-15Rα. As tmbIL-15 is capable of reverse signaling upon IL-15Rα engagement, we investigated how this signaling axis modulates melanoma cell behavior across tumor stages. Transcriptomic analysis of melanoma patients revealed that high IL-15 expression correlates with immune activation, inflammation and epithelial-to-mesenchymal transition (EMT), along with coordinated upregulation of IL-15 receptor subunits. Proteomic profiling of melanoma cell lines stimulated with soluble IL-15Rα (sIL-15Rα) uncovered distinct, stage-specific responses. Although several proteins were commonly deregulated across cell lines, most showed opposite regulation in primary versus metastatic models, indicating that tmbIL-15 reverse signaling triggers context-dependent programs influenced by tumor progression. A stringent cross-comparison identified five proteins (PSAP, MARCKS, eEF1A1, DDX39B, and RACK1) as consistently and differentially regulated across tumor stages. Further comparison with published NK cell co-culture and EMT cytokine stimulation datasets revealed a subset of shared effectors, notably PSAP, TPM3 isoform 2 and MARCKS, suggesting that IL-15Rα-induced tmbIL-15 signaling is part of the immune editing phenomenon eliciting pro-tumoral activities complementary to the EMT process. Among these, PSAP emerged as the most robustly and consistently modulated effector, upregulated in primary melanoma cells and downregulated in metastatic ones upon sIL-15Rα stimulation. Its expression correlated positively with CD8+ T cell infiltration and negatively with NK cell infiltration, with distinct transcriptomic programs associated with high PSAP expression in primary versus metastatic settings. Altogether, these findings identify PSAP as a stage-specific mediator of tmbIL-15 reverse signaling in melanoma, integrating immune and EMT-related cues with potential implications for tumor progression and microenvironmental remodeling. - Source: PubMed
Publication date: 2026/04/15
Forcelloni SergioGiron-Michel JulienDel Boccio PieroCufaro Maria ConcettaDi Sebastiano AliceMariotti Francesca RomanaCiancaglini CeciliaChouaib SalemPadelli MaelVespa SimoneMac Giang DangEbert StefanBuart StéphanieMaggi EnricoMoretta LorenzoVacca PaolaTumino NicolaQuatrini LindaCaruana IgnazioAzzarone BrunoSantopolo Silvia