Database for Annotation, Visualization and Integrated Discovery 2.1
National Institute of Allergy and Infectious Disease
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DEAD-box helicase 5(DDX5) DEAD-box helicase 5(DDX5) Related Genes Homo sapiens
GENERIF_SUMMARY Essential for pre-mrna splicing in vitro; may function in destabilizing the U1-5'ss interaction. Depletion of p68 RNA helicase arrested spliceosome assembly at the prespliceosome stage, synergism with transcriptional coactivators CBP and p300, role in c-H-ras alternative splicing regulation, p68 is an important transcriptional regulator, functioning as a co-activator and/or co-repressor depending on the context of the promoter & the transcriptional complex. AA 1-478 of p68 can repress transcription as well as the full-length protein., there is a tightly controlled expression and nucleolar localization of p68 in keratinocytes in vitro and during skin repair in vivo that functionally contributes to keratinocyte proliferation and gene expression, mechanism by which p68 may act as a tumour cosuppressor in governing p53 transcriptional activity, data suggest that function(s) of p68 RNA helicase may be subjected to the regulation of multiple cell signal pathways, In addition, it could be demonstrated that increasing the Tlk1 activity in HT1080 cells by forced Tlk1 overexpression leads to an increased phosphorylation of endogenous p68., Patient with chronic hepatitis C carrying DDX5 haplotypes are at an increased risk of developing advanced liver fibrosis., Data show that P68 RNA helicase mediates platelet-derived growth factor-induced epithelial mesenchymal transition by displacing Axin from beta-catenin., SUMO modification of the DEAD box protein p68 modulates its transcriptional activity and promotes its interaction with HDAC1, A mutant that carries mutations at the phosphorylation sites (Y593/595F) dramatically sensitizes TRAIL-resistant cells to TRAIL-induced apoptosis, suggesting a potential therapeutic strategy to overcome TRAIL resistance., The percentage correlation between Q-RT-PCR and microarray were 70% and 48% by using DDX5 and GAPDH as internal controls, respectively., p68/p72 may contribute to colon cancer formation by directly up-regulating proto-oncogenes and indirectly by down-regulating the growth suppressor p21(WAF1/CIP1)., P68 RNA helicase is an essential component of the let-7 microRNA pathway, The DEAD-box proteins p68(Ddx5) and p72(Ddx17) were used as models for this coexpression frequency analysis as there are defined functions for these proteins in splicing and transcription., DEAD-box RNA helicase p68 is not required for nuclear translocation of beta-catenin in colon cancer cells., A ubiquitously expressed, androgen-insensitive gene, DDX5, fused in frame with ETV4, leading to the expression of a DDX5-ETV4 fusion protein was identified in prostate cancer., p68 is a novel AR transcriptional coactivator that is significantly overexpressed in PCa with a possible role in progression to hormone-refractory disease., Upregulated in at least 50% of multiple myeloma cases tested., the Ddx5 (Asp-Glu-Ala-Asp box polypeptide 5) protein showed specific interaction with SARS-CoV helicase., Distinct but important roles for both p68 and p72 in regulating ERalpha activity in breast cancer., DDX5 is a repressor of fibrogenic genes in HSCs through interaction with transcriptional complexes., crystallization and preliminary diffraction analysis of N-terminal region of DDX5 is reported.X-ray diffraction data were processed to a resolution of 2.7 A., Pleiotropic effects of p300-mediated acetylation on p68 and p72 RNA helicase., a striking inverse association of p68 and delta133p53 expression in primary breast cancers was identified., DEAD-box RNA helicase p68 (DDX5) and its associated noncoding RNA, steroid receptor RNA activator (SRA), form a complex with CTCF that is essential for insulator function, Using an RNA affinity pulldown-coupled mass spectrometry approach the study identified DDX5/RNA helicase p68 as an activator of TAU exon 10 splicing., High DDX5 is associated with basal breast cancer cells., Data indicate that transcriptional coregulator ddx5/ddx17 RNA helicases can simultaneously regulate the transcriptional activity and alternative splicing of NFAT5 transcription factor., The DEAD box RNA helicase p68, also referred to as DDX5, directly interacts with VDR., there is a direct interaction between DDX5 and NS5B and DDX5 has two independent NS5B-binding sites, Results show a novel role for DDX5 in cancer cell proliferation and suggest DDX5 as a therapeutic target in breast cancer treatment., High p68 RNA helicase expression is associated with glioma., RNA helicases Ddx17 and Ddx5 contribute to tumor-cell invasiveness by regulating alternative splicing of several DNA- and chromatin-binding factors, including the macroH2A1 histone., DDX5 might be critical for NOTCH1-mediated T-ALL pathogenesis and thus is a potential new target for modulating the Notch signaling in leukemia, p68, in the presence of Ca-calmodulin, can function as a microtubule motor., Data show that p68/DdX5 immunoprecipitated with RNA polymerase II (RNAP II) and suggest p68 is important in facilitating beta-catenin and androgen receptor (AR) transcriptional activity in prostate cancer cells., Results suggest that distinct DDX DEAD-box RNA helicases DDX3 and DDX5 cooperate to modulate the HIV-1 Rev function., DDX5 facilitates HIV-1 replication as a cellular co-factor of Rev., In conclusion, authors identified DDX5 as a positive regulator for Japanese encephalitis virus replication via its binding to viral 3' UTR., The data provide a model in which p68 and p53 interplay regulates PLK1 expression, and which describes the behavior of these molecules, and the outcome of their interaction, in human breast cancer., Data indicate that armadillo repeat protein ARVCF interacts with the splicing factors the splicing factor SRSF1 (SF2/ASF), the RNA helicase p68 (DDX5), and the heterogeneous nuclear ribonucleoprotein hnRNP H2., AML is dependent on DDX5 and that inhibiting DDX5 expression slows AML cell proliferation., Downregulation of DDX5 and DDX17 protein expression during myogenesis and epithelial-to-mesenchymal transdifferentiation contributes to the switching of splicing programs during these processes., Results show that a new mechanism of oncogenesis is attributed to p68 by upregulation of AKT and consequent nuclear exclusion and degradation of tumor suppressor FOXO3a., Data indicate that cyclooxygenase 2 (COX-2) correlates inversely to microRNA 183 (miR-183) and directly to DEAD-box helicase p68 (DDX5)., DDX5 protein is essential for normal cell proliferation; (2) the transition from G1 to S/G2 phase is accompanied by an increase of DDX5 protein concentration in the cells., study shows that correction of p68 may reduce toxicity of the mutant RNAs in DM1 and in DM2, Systematic Determination of Human Cyclin Dependent Kinase (CDK)-9 Interactome Identifies Novel Functions in RNA Splicing Mediated by the DEAD Box DDX5 and DDX17 RNA Helicases, DDX5 played an important role in the proliferation and tumorigenesis of non-small-cell lung cancer cells by activating the beta-catenin signaling pathway., Cervical cancer cell DDX5 gene is transcriptionally upregulated by calcitriol through a VDRE located in its proximal promoter., LMTK3 escapes tumour suppressor miRNAs via sequestration of DDX5.,
SP_COMMENT function:RNA-dependent ATPase activity. The rate of ATP hydrolysis is highly stimulated by single-stranded RNA. May be involved in pre-mRNA splicing., PTM:Arg-502 is dimethylated, probably to asymmetric dimethylarginine., similarity:Belongs to the DEAD box helicase family., similarity:Belongs to the DEAD box helicase family. DDX5/DBP2 subfamily., similarity:Contains 1 helicase ATP-binding domain., similarity:Contains 1 helicase C-terminal domain., subunit:Identified in the spliceosome C complex, at least composed of AQR, C19orf29, CDC40, CDC5L, CRNKL1, DDX23, DDX41, DDX48, DDX5, DGCR14, DHX35, DHX38, DHX8, EFTUD2, FRG1, GPATC1, HNRPA1, HNRPA2B1, HNRPA3, HNRPC, HNRPF, HNRPH1, HNRPK, HNRPM, HNRPR, HNRPU, KIAA1160, KIAA1604, LSM2, LSM3, MAGOH, MORG1, PABPC1, PLRG1, PNN, PPIE, PPIL1, PPIL3, PPWD1, PRPF19, PRPF4B, PRPF6, PRPF8, RALY, RBM22, RBM8A, RBMX, SART1, SF3A1, SF3A2, SF3A3, SF3B1, SF3B2, SF3B3, SFRS1, SKIV2L2, SNRNP200, SNRNP40, SNRPA1, SNRPB, SNRPB2, SNRPD1, SNRPD2, SNRPD3, SNRPE, SNRPF, SNRPG, SNW1, SRRM1, SRRM2, SYF2, SYNCRIP, TFIP11, THOC4, U2AF1, XAB2 and ZCCHC8.,