DDX5

This gene encodes a member of the DEAD box family of RNA helicases that are involved in a variety of cellular processes as a result of its role as an adaptor molecule, promoting interactions with a large number of other factors. This protein is involved in pathways that include the alteration of RNA structures, plays a role as a coregulator of transcription, a regulator of splicing, and in the processing of small noncoding RNAs. Members of this family contain nine conserved motifs, including the conserved Asp-Glu-Ala-Asp (DEAD) motif, important to ATP binding and hydrolysis as well as RNA binding and unwinding activities. Dysregulation of this gene may play a role in cancer development. Alternative splicing results in multiple transcript variants. [provided by RefSeq, Sep 2017]

DEAD-Box Helicase 5

Involved in the alternative regulation of pre-mRNA splicing; its RNA helicase activity is necessary for increasing tau exon 10 inclusion and occurs in a RBM4-dependent manner. Binds to the tau pre-mRNA in the stem-loop region downstream of exon 10. The rate of ATP hydrolysis is highly stimulated by single-stranded RNA. Involved in transcriptional regulation; the function is independent of the RNA helicase activity. Transcriptional coactivator for androgen receptor AR but probably not ESR1. Synergizes with DDX17 and SRA1 RNA to activate MYOD1 transcriptional activity and involved in skeletal muscle differentiation. Transcriptional coactivator for p53/TP53 and involved in p53/TP53 transcriptional response to DNA damage and p53/TP53-dependent apoptosis. Transcriptional coactivator for RUNX2 and involved in regulation of osteoblast differentiation. Acts as transcriptional repressor in a promoter-specific manner; the function probably involves association with histone deacetylases, such as HDAC1. As component of a large PER complex is involved in the inhibition of 3' transcriptional termination of circadian target genes such as PER1 and NR1D1 and the control of the circadian rhythms.

Alternative mRNA splicing, via spliceosome Source: UniProtKB
Androgen receptor signaling pathway Source: UniProtKB
BMP signaling pathway Source: BHF-UCL
Epithelial to mesenchymal transition Source: UniProtKB
Intracellular estrogen receptor signaling pathway Source: UniProtKB
Intrinsic apoptotic signaling pathway by p53 class mediator Source: UniProtKB
mRNA splicing, via spliceosome Source: Reactome
mRNA transcription Source: CACAO
Myoblast differentiation Source: UniProtKB
Negative regulation of transcription by RNA polymerase II Source: UniProtKB
Nuclear-transcribed mRNA catabolic process Source: UniProtKB
Positive regulation of DNA damage response, signal transduction by p53 class mediator Source: UniProtKB
Positive regulation of production of miRNAs involved in gene silencing by miRNA Source: BHF-UCL
Pri-miRNA transcription by RNA polymerase II Source: UniProtKB
Regulation of alternative mRNA splicing, via spliceosome Source: UniProtKB
Regulation of androgen receptor signaling pathway Source: UniProtKB
Regulation of osteoblast differentiation Source: UniProtKB
Regulation of skeletal muscle cell differentiation Source: UniProtKB
Regulation of transcription by RNA polymerase II Source: UniProtKB
Rhythmic process Source: UniProtKB-KW

Cytoplasm; Nucleus; Nucleolus. During the G0 phase, predominantly located in the nucleus. Cytoplasmic levels increase during the G1/S phase. During the M phase, located at the vicinity of the condensed chromosomes. At G1, localizes in the cytoplasm.

Arg-502 is dimethylated, probably to asymmetric dimethylarginine.
Sumoylated; sumoylation, promoted by PIAS1, promotes interaction with HDAC1 and transcriptional repression activity. Sumoylation also significantly increases stability, and reduces polyubiquitination.
Polyubiquitinated, leading to proteasomal degradation.
Weakly phosphorylated in the G1/S phase of the cell cycle and much more at G2/M, especially at Thr and Tyr residues.