DDX5 — DEAD-box helicase 5
DDX5 belongs to a gene co-expression module in 9 of 28 SCUBA cell types. Each module groups genes that rise and fall together in that cell type; the genes it shares a module with are its closest co-expression partners there.
DDX5's module in each cell type
About the gene
| Synonyms | G17P1, HLR1, p68 |
|---|---|
| Chromosome | 17: 64498254-64508199 |
| Predicted location | Intracellular |
| Essential gene | Yes |
| Protein class | Cancer-related genes, Enzymes, Essential proteins, Plasma proteins, Predicted intracellular proteins |
| Molecular function | Helicase, Hydrolase, RNA-binding |
| Biological process | Biological rhythms, mRNA processing, mRNA splicing, Transcription, Transcription regulation |
Function
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 a 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.
Human Protein Atlas · Open Targets · UniProt
Gene annotation from the Human Protein Atlas and UniProt; see sources & licences.