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TRPV4 mediates Ca(2+) influx and nuclear accumulation of DDX3X in cells exposed to the Zika virus. Targeting of TRPV4 reduces infectivity of dengue, hepatitis C and Zika viruses. Our results highlight the role of TRPV4 in the regulation of DDX3X-dependent control of RNA metabolism and viral infectivity.
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DDX3 regulates MTP gene expression and lipid homeostasis through interplay with HNF4 and SHP.
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Through adopting the immunoprecipitation (IP), RNA immunoprecipitation (RIP), dual luciferase reporter assays, the authors illustrate that DDX3X could interact with Drosha/DGCR8 complex, elevate the processing activity of Drosha/DGCR8 complex on pri-miRNAs, and increase mature miRNA expression levels.
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our study suggested that DDX3 prevents generation of cancer stem cells through epigenetically regulating a subset of tumor-suppressive miRNAs expressions, which strengthens tumor suppressor role of DDX3 in hepatocellular carcinoma.
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this study shows that cancer-associated DDX3X mutations drive stress granule assembly and impair global translation
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we demonstrated that DDX3 modulated the activity of PP2A by controlling the phosphorylation of PP2A-C, which might enable PP2A-C to regulate NF-kappaB signal pathway by dephosphorylating IKK-beta.
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Data suggest that L protein from LCMV interactions with host proteome, specifically DDX3X, NKRF, and TRIM21. (LCMV = Lymphocytic choriomeningitis mammarenavirus; DDX3X = DEAD-box helicase 3; NKRF = NF-kappa-B-repressing factor; TRIM21 = tripartite motif-containing protein-21)
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DDX3 interacts extensively with RNA and ribosomal machinery to help remodel the translation landscape in response to stress, while cancer-related DDX3 variants adapt this response to selectively preserve translation
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Mechanistically, increased KRAS expression induced ROS production, which elevated HIF-1alpha and YAP1 expression. Increased HIF-1alpha persistently promoted DDX3 expression via a KRAS/ROS/HIF-1alpha feedback loop.
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Our study suggests that rottlerin exhibits its anti-cancer activity partly due to upregulation of DDX3 in hepatocellular carcinoma cells.
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DDX3 may play an oncogenic role to promote tumor growth and invasion in colon cancer cells
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data have demonstrated that Venezuelan equine encephalitis virus (VEEV)-nsP3 associates with DDX1 and DDX3 in infected cells to facilitate viral multiplication; determined that VEEV-nsP3 interacts with a pre-formed translational complex, comprising of DX3:eIF4A:eIF4G:PABP to potentially aid in translation of viral proteins.
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Data suggest that DEAD-box helicase 3 (DDX3X) physically interacts and co-localizes with poly(A)-binding cytoplasmic protein 1 (PABPC1) and caprin-1 in lamellipodia at the leading edge of spreading cells; these interactions are dependent on mRNA; depletion of DDX3X (via gene silencing with the CRISPR-Cas system) leads to decreased cell motility. These studies were conducted using MRC5 lung fibroblast cell line.
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The article describes RNA remodeling activity of human DDX3X and Caenorhabditis elegans LAF-1 tuned by protein concentration, RNA length, and ATP.
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the role of DDX3 in sarcomas
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DDX3 directly regulates TRAF3 ubiquitination and acts as a scaffold to co-ordinate assembly of signaling complexes downstream from MAVS.
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Here we identify the DEAD-box helicase 3 (DDX3) as a novel interaction partner of Y. enterocolitica YopM and present the three-dimensional structure of a YopM:DDX3 complex
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Here, the authors show that herpes simplex virus 1 gene expression, replication, and propagation depend on optimal DDX3X protein levels.
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de novo heterozygous DDX3X variants should be considered not only in females with unexplained ID, but also in individuals with a clinical diagnosis of T-CS.
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high metastatic DDX3 expression correlates with worse survival, implying that DDX3 is a potential therapeutic target in metastatic breast cancer, in particular in the clinically important group of TN patients.
