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抗Human DDX17 抗体:
抗Rat (Rattus) DDX17 抗体:
抗Mouse (Murine) DDX17 抗体:
Human Polyclonal DDX17 Primary Antibody for ICC, IF - ABIN152386
Jin, Chen, Di, Miron, Hou, Gao, Shao: Estrogen receptor (ER) beta or p53 attenuates ERalpha-mediated transcriptional activation on the BRCA2 promoter. in The Journal of biological chemistry 2008
Show all 3 Pubmed References
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.
This study demonstrated that the association of DDX17delG in the treatment-resistant ophthalmoplegic subphenotype of myasthenia gravis.
Mutant p53 protein (Mutp53) binds and sequesters RNA helicases p72/82 from microprocessor causing an attenuation of microRNAs (miRNAs) maturation.
DDX17 contributes to acquired gefitinib resistance through exportin/importin-dependent cytoplasmic shuttling and activation of beta-catenin in non-small lung cancer cells.
The miRNA biogenesis factors, DDX17 and KHSRP, regulate the protein level of Ago2 in human cells.
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
Overexpression of p72 decreased Beclin1 expression partially by increasing miR-34-5p and miR-5195-3p expression in glioma cells.
Systematic Determination of Human Cyclin Dependent Kinase (CDK)-9 Interactome Identifies Novel Functions in RNA Splicing Mediated by the DDX5 and DDX17 RNA Helicases
Downregulation of DDX5 and DDX17 protein expression during myogenesis and epithelial-to-mesenchymal transdifferentiation contributes to the switching of splicing programs during these processes.
Depletion of DDX17 but not the related helicase DDX5 increased Rift Valley fever virus replication in human cells.
DDX17 promotes the production of HIV-1 infectious particles by modulating HIV-1 RNA metabolism.
Data indicate that transcriptional coregulator ddx5/ddx17 RNA helicases can simultaneously regulate the transcriptional activity and alternative splicing of NFAT5 transcription factor.
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.
Pleiotropic effects of p300-mediated acetylation on p68 and p72 RNA helicase.
Short-term exercise resulted in a significant increase of mRNA expression of genes encoding proteins involved in the formation of precatalytic splisosome: DDX17.
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.
has a role in pre-mRNA splicing, in particular, at the early stages of the splicing reaction involving U1snRNP
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.
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.
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).
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.
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.
DEAD box proteins, characterized by the conserved motif Asp-Glu-Ala-Asp (DEAD), are putative RNA helicases. They are implicated in a number of cellular processes involving alteration of RNA secondary structure, such as translation initiation, nuclear and mitochondrial splicing, and ribosome and splicesosome assembly. Based on their distribution patterns, some members of this family are believed to be involved in embryogenesis, spermatogenesis, and cellular growth and division. This gene encodes a DEAD box protein, which is an ATPase activated by a variety of RNA species, but not by dsDNA. This protein, and that encoded by DDX5 gene, are more closely related to each other than to any other member of the DEAD box family. This gene can encode multiple isoforms due to both alternative splicing and the use of alternative translation initiation codons, including a non-AUG (CUG) start codon.
DEAD (Asp-Glu-Ala-Asp) box polypeptide 17
, DEAD box polypeptide 17
, DEAD box protein p72
, DEAD/H (Asp-Glu-Ala-Asp/His) box polypeptide 17 (72kD)
, RNA-dependent helicase p72
, probable ATP-dependent RNA helicase DDX17
, DEAD (Asp-Glu-Ala-Asp) box polypeptide 46
, DEAD box protein 17