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Human DDX5 Protein expressed in HEK-293 Cells - ABIN2719286
Kost, Yang, Li, Zhang, Liu, Kim, Ahn, Lee, Liu: A Novel Anti-Cancer Agent, 1-(3,5-Dimethoxyphenyl)-4-[(6-Fluoro-2-Methoxyquinoxalin-3-yl)Aminocarbonyl] Piperazine (RX-5902), Interferes With β-Catenin Function Through Y593 Phospho-p68 RNA Helicase. in Journal of cellular biochemistry 2015
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The role of DDX5 in regulating esophageal cancer cell proliferation and tumorigenesis.DDX5 is highly expressed in esophageal cancer.
Downregulation of p68 RNA Helicase (DDX5) Activates a Survival Pathway Involving mTOR (zeige FRAP1 Proteine) and MDM2 (zeige MDM2 Proteine) Signals.(
Results show refined biochemical and biological comparison of yeast Dbp2 (zeige DHX16 Proteine)and human DDX5 enzymes. Human DDX5 possesses a 10-fold higher unwinding activity than Dbp2, partially due to the presence of a mammalian/avian specific C-terminal extension. Also, ectopic expression of DDX5 rescues the cold sensitivity, cryptic initiation defects, and impaired glucose import in dbp2Delta cells, suggesting functional conservation.
p53 (zeige TP53 Proteine) gain-of-function mutations accelerate endometrial carcinoma progression and metastasis by interfering with Drosha (zeige DROSHA Proteine) and p68 (zeige ANXA6 Proteine) binding and pri-miR (zeige MLXIP Proteine)-26a-1 processing, resulting in reduced miR (zeige MLXIP Proteine)-26a expression and EZH2 (zeige EZH2 Proteine) overexpression.
Cervical cancer cell DDX5 gene is transcriptionally upregulated by calcitriol through a VDRE located in its proximal promoter.
Systematic Determination of Human Cyclin Dependent Kinase (zeige CDK1 Proteine) (CDK)-9 (zeige CDK9 Proteine) Interactome Identifies Novel Functions in RNA Splicing Mediated by the DEAD Box DDX5 and DDX17 (zeige DDX17 Proteine) RNA Helicases
LMTK3 escapes tumour suppressor miRNAs via sequestration of DDX5.
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.
Results show that a new mechanism of oncogenesis is attributed to p68 (zeige ANXA6 Proteine) by upregulation of AKT (zeige AKT1 Proteine) and consequent nuclear exclusion and degradation of tumor suppressor FOXO3a (zeige FOXO3 Proteine).
DDX5 played an important role in the proliferation and tumorigenesis of non-small-cell lung cancer cells by activating the beta-catenin (zeige CTNNB1 Proteine) signaling pathway.
The results highlight a novel molecular mechanism underlying stability of neurogenesis-associated mRNAs controlled by the Klf4 (zeige KLF4 Proteine)/Ddx5/Stau1 (zeige STAU1 Proteine) axis during mammalian corticogenesis.
Study provided strong evidence that mammalian DDX5 and S. cerevisiae Dbp2 (zeige DHX16 Proteine) are functionally conserved especially in cellular metabolism, despite enzymatic differences.
these results reveal important functions of DDX5 in regulating reprogramming and highlight the importance of a Ddx5-miR125b-Rybp (zeige RYBP Proteine) axis in controlling cell fate.
DDX5 is a crucial factor involved in the complex transcriptional cascade of events that regulate adipogenesis and is essential for the initiation of adipogenesis.
Data indicate that Arf tumor suppressor blocks the functional interaction between c-Myc (zeige MYC Proteine) and p68 (zeige ANXA6 Proteine) DEAD-box protein (zeige INTS6 Proteine) (DDX5).
Downregulation of DDX5 and DDX17 (zeige DDX17 Proteine) protein expression during myogenesis and epithelial-to-mesenchymal transdifferentiation contributes to the switching of splicing programs during these processes.
p68 (zeige ANXA6 Proteine) levels may have an important role in influencing the decision between cell-cycle arrest and apoptosis in response to DNA damage.
our data demonstrate that Ddx5 and SRA (zeige MSR1 Proteine) function as coactivators of Notch (zeige NOTCH1 Proteine) signaling.
Data indicate that transcriptional coregulator ddx5/ddx17 (zeige DDX17 Proteine) RNA helicases can simultaneously regulate the transcriptional activity and alternative splicing of NFAT5 (zeige NFAT5 Proteine) transcription factor.
Solution structures of the double-stranded RNA-binding domains from RNA helicase A.
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 spliceosome 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 a RNA-dependent ATPase, and also a proliferation-associated nuclear antigen, specifically reacting with the simian virus 40 tumor antigen. This gene consists of 13 exons, and alternatively spliced transcripts containing several intron sequences have been detected, but no isoforms encoded by these transcripts have been identified.
ATP-dependent RNA helicase DDX5
, DEAD (Asp-Glu-Ala-Asp) box polypeptide 5
, DEAD box protein 5
, DEAD box-5
, DEAD/H (Asp-Glu-Ala-Asp/His) box polypeptide 5 (RNA helicase, 68kD)
, RNA helicase p68
, probable ATP-dependent RNA helicase DDX5
, D-E-A-D (aspartate-glutamate-alanine-aspartate) box polypeptide 5
, DEAD (aspartate-glutamate-alanine-aspartate) box polypeptide 5
, DEAD box RNA helicase DEAD1
, DEAD/H (Asp-Glu-Ala-Asp/His) box polypeptide 5
, p68 RNA helicase
, ddx5 gene protein
, PCR product with interspecies-compatible primers
, putative ATP-dependent RNA helicase DDX5
, DEAD (Asp-Glu-Ala-Asp) box helicase 5
, DEAD-box helicase 5 L homeolog