Browse our DDX17 Proteins (DDX17)

Human DEAD (Asp-Glu-Ala-Asp) Box Polypeptide 17 (DDX17) interaction partners

1. Data indicate a central role for DEAD-box helicase 17 (DDX17) in the pathway involving transcription factor REST (REST) and miRNAs that allows neuronal gene repression.

2. The results of qRT-PCR for circDDX17 in 60 paired CRC tissues showed that circDDX17 was significantly down-regulated in CRC tissues and associated with unfavorable clinicopathological parameters. In vitro experiments showed that silencing of circDDX17 promoted CRC cell proliferation, migration, invasion, and inhibited apoptosis.

3. This study demonstrated that the association of DDX17delG in the treatment-resistant ophthalmoplegic subphenotype of myasthenia gravis.

4. Mutant p53 protein (Mutp53) binds and sequesters RNA helicases p72/82 from microprocessor causing an attenuation of microRNAs (miRNAs) maturation.

5. DDX17 contributes to acquired gefitinib resistance through exportin/importin-dependent cytoplasmic shuttling and activation of beta-catenin in non-small lung cancer cells.

6. The miRNA biogenesis factors, DDX17 and KHSRP, regulate the protein level of Ago2 in human cells.

7. DDX17 is a Sox2-binding protein in estrogen receptor-positive breast cancer; in reporter responsive (RR) cells but not reporter unresponsive (RU) cells, DDX17 enhances the tumorigenic and stem-like features of Sox2 by promoting its binding to its target genes

8. Overexpression of p72 decreased Beclin1 expression partially by increasing miR-34-5p and miR-5195-3p expression in glioma cells.

9. Systematic Determination of Human Cyclin Dependent Kinase (CDK)-9 Interactome Identifies Novel Functions in RNA Splicing Mediated by the DDX5 and DDX17 RNA Helicases

10. Downregulation of DDX5 and DDX17 protein expression during myogenesis and epithelial-to-mesenchymal transdifferentiation contributes to the switching of splicing programs during these processes.

11. Depletion of DDX17 but not the related helicase DDX5 increased Rift Valley fever virus replication in human cells.

12. DDX17 promotes the production of HIV-1 infectious particles by modulating HIV-1 RNA metabolism.

13. Data indicate that transcriptional coregulator ddx5/ddx17 RNA helicases can simultaneously regulate the transcriptional activity and alternative splicing of NFAT5 transcription factor.

14. 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.

15. Pleiotropic effects of p300-mediated acetylation on p68 and p72 RNA helicase.

16. Short-term exercise resulted in a significant increase of mRNA expression of genes encoding proteins involved in the formation of precatalytic splisosome: DDX17.

17. Results show that the abundant DEAD-box RNA helicase p72, but not its close relative p68, affects the splicing of alternative exons containing AC-rich exon enhancer elements.

18. has a role in pre-mRNA splicing, in particular, at the early stages of the splicing reaction involving U1snRNP

19. p72 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 1-474 of p72 can repress transcription as well as the full-length protein.

20. p72 RNA helicase may not only be involved in the p53-Mdm2 regulatory loop, but also profoundly impact on the transcriptome through various CBP/p300 and P/CAF interacting proteins.

Mouse (Murine) DEAD (Asp-Glu-Ala-Asp) Box Polypeptide 17 (DDX17) interaction partners

1. Mechanistic studies reveal that MeXis interacts with and guides promoter binding of the transcriptional coactivator DDX17. The identification of MeXis as a lncRNA modulator of LXR-dependent gene expression expands understanding of the mechanisms underlying cell type-selective actions of nuclear receptors in physiology and disease.

2. Data show that p72/DDX17 specifically interacts with the miR-132 loop sequence and influences the relative ratio of the mature mice miR-212/132 miRNAs.

3. Downregulation of DDX5 and DDX17 protein expression during myogenesis and epithelial-to-mesenchymal transdifferentiation contributes to the switching of splicing programs during these processes.

4. Data indicate that transcriptional coregulator ddx5/ddx17 RNA helicases can simultaneously regulate the transcriptional activity and alternative splicing of NFAT5 transcription factor.