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Literature summary extracted from
- Functions of DEAD box RNA helicases DDX5 and DDX17 in chromatin organization and transcriptional regulation (2018), BMB Rep., 51, 613-622 .
Localization
| EC Number | Localization | Comment | Organism | GeneOntology No. | Textmining |
|---|---|---|---|---|---|
| 3.6.4.13 | chromatin | - |
Mus musculus | 785 | - |
| 3.6.4.13 | chromatin | - |
Homo sapiens | 785 | - |
Metals/Ions
| EC Number | Metals/Ions | Comment | Organism | Structure |
|---|---|---|---|---|
| 3.6.4.13 | Mg2+ | required | Drosophila melanogaster |  |
| 3.6.4.13 | Mg2+ | required | Mus musculus | |
| 3.6.4.13 | Mg2+ | required | Homo sapiens | |
Natural Substrates/ Products (Substrates)
| EC Number | Natural Substrates | Organism | Comment (Nat. Sub.) | Natural Products | Comment (Nat. Pro.) | Rev. | Reac. |
|---|---|---|---|---|---|---|---|
| 3.6.4.13 | ATP + H2O | Drosophila melanogaster | - |
ADP + phosphate | - |
? | |
| 3.6.4.13 | ATP + H2O | Mus musculus | - |
ADP + phosphate | - |
? | |
| 3.6.4.13 | ATP + H2O | Homo sapiens | - |
ADP + phosphate | - |
? | |
Organism
| EC Number | Organism | UniProt | Comment | Textmining |
|---|---|---|---|---|
| 3.6.4.13 | Drosophila melanogaster | - |
- |
- |
| 3.6.4.13 | Drosophila melanogaster | P19109 | - |
- |
| 3.6.4.13 | Homo sapiens | P17844 | - |
- |
| 3.6.4.13 | Homo sapiens | Q92841 | - |
- |
| 3.6.4.13 | Mus musculus | Q501J6 | - |
- |
| 3.6.4.13 | Mus musculus | Q61656 | - |
- |
Source Tissue
| EC Number | Source Tissue | Comment | Organism | Textmining |
|---|---|---|---|---|
| 3.6.4.13 | breast cancer cell | - |
Homo sapiens | - |
| 3.6.4.13 | colorectal cancer cell | - |
Homo sapiens | - |
| 3.6.4.13 | muscle fibre | - |
Mus musculus | - |
| 3.6.4.13 | muscle fibre | - |
Homo sapiens | - |
| 3.6.4.13 | myoblast | - |
Mus musculus | - |
| 3.6.4.13 | neuroblastoma cell | - |
Mus musculus | - |
| 3.6.4.13 | neuroblastoma cell | - |
Homo sapiens | - |
| 3.6.4.13 | non-small cell lung cancer cell | - |
Homo sapiens | - |
| 3.6.4.13 | osteoblast | - |
Mus musculus | - |
Substrates and Products (Substrate)
| EC Number | Substrates | Comment Substrates | Organism | Products | Comment (Products) | Rev. | Reac. |
|---|---|---|---|---|---|---|---|
| 3.6.4.13 | ATP + H2O | - |
Drosophila melanogaster | ADP + phosphate | - |
? | |
| 3.6.4.13 | ATP + H2O | - |
Mus musculus | ADP + phosphate | - |
? | |
| 3.6.4.13 | ATP + H2O | - |
Homo sapiens | ADP + phosphate | - |
? | |
Synonyms
| EC Number | Synonyms | Comment | Organism |
|---|---|---|---|
| 3.6.4.13 | DDX17 | - |
Mus musculus |
| 3.6.4.13 | DDX17 | - |
Homo sapiens |
| 3.6.4.13 | DDX17 | - |
Drosophila melanogaster |
| 3.6.4.13 | DDX5 | - |
Mus musculus |
| 3.6.4.13 | DDX5 | - |
Homo sapiens |
| 3.6.4.13 | DEAD box RNA helicase | - |
Drosophila melanogaster |
| 3.6.4.13 | DEAD box RNA helicase | - |
Mus musculus |
| 3.6.4.13 | DEAD box RNA helicase | - |
Homo sapiens |
| 3.6.4.13 | p68 | - |
Drosophila melanogaster |
| 3.6.4.13 | p68 | - |
Mus musculus |
| 3.6.4.13 | p68 | - |
Homo sapiens |
| 3.6.4.13 | P72 | - |
Mus musculus |
| 3.6.4.13 | P72 | - |
Homo sapiens |
| 3.6.4.13 | P72 | - |
Drosophila melanogaster |
| 3.6.4.13 | Rm62 | - |
Drosophila melanogaster |
| 3.6.4.13 | RNA helicase DDX17 | - |
Mus musculus |
| 3.6.4.13 | RNA helicase DDX17 | - |
Homo sapiens |
| 3.6.4.13 | RNA helicase DDX17 | - |
Drosophila melanogaster |
| 3.6.4.13 | RNA helicase DDX5 | - |
Drosophila melanogaster |
| 3.6.4.13 | RNA helicase DDX5 | - |
Mus musculus |
| 3.6.4.13 | RNA helicase DDX5 | - |
Homo sapiens |
General Information
| EC Number | General Information | Comment | Organism |
|---|---|---|---|
| 3.6.4.13 | evolution | DDX5 (p68) and DDX17 (p72) belong to the large family of evolutionarily conserved DEAD box RNA helicases. The regulatory activity of DDX5 and DDX17 in transcription is conserved throughout evolution. Possible evolutionary divergence of the insulation process between drosophila and mammals | Drosophila melanogaster |
| 3.6.4.13 | evolution | DDX5 (p68) and DDX17 (p72) belong to the large family of evolutionarily conserved DEAD box RNA helicases. The regulatory activity of DDX5 and DDX17 in transcription is conserved throughout evolution. Possible evolutionary divergence of the insulation process between drosophila and mammals | Mus musculus |
| 3.6.4.13 | evolution | DDX5 (p68) and DDX17 (p72) belong to the large family of evolutionarily conserved DEAD box RNA helicases. The regulatory activity of DDX5 and DDX17 in transcription is conserved throughout evolution. Possible evolutionary divergence of the insulation process between drosophila and mammals | Homo sapiens |
| 3.6.4.13 | evolution | DDX5 (p68) and DDX17 (p72) belong to the large family of evolutionarily conserved DEAD box RNA helicases.The regulatory activity of DDX5 and DDX17 in transcription is conserved throughout evolution. Possible evolutionary divergence of the insulation process between drosophila and mammals | Mus musculus |
| 3.6.4.13 | malfunction | the aberrant expression of DDX5 and/or DDX17 contributes to pathologies such as cancer | Drosophila melanogaster |
| 3.6.4.13 | malfunction | the aberrant expression of DDX5 and/or DDX17 contributes to pathologies such as cancer | Mus musculus |
| 3.6.4.13 | malfunction | the aberrant expression of DDX5 and/or DDX17 contributes to pathologies such as cancer | Homo sapiens |
| 3.6.4.13 | malfunction | the aberrant expression of DDX5 and/or DDX17 contributes to pathologies such as cancer. DDX17 depletion is associated with a decrease of breast cancer tumor characteristics (e.g. colony formation), highlighting its importance in breast tumorigenesis | Homo sapiens |
| 3.6.4.13 | metabolism | protein and noncoding RNA partners of DDX5 and DDX17, DDX5/DDX17 and the regulation of gene insulation, overview. DDX5 and DDX17 can regulate alternative splicing through other mechanisms, via a direct effect on the local folding of their targeted transcripts or via the recruitment of RNA binding cofactors | Mus musculus |
| 3.6.4.13 | metabolism | protein and noncoding RNA partners of DDX5 and DDX17, DDX5/DDX17 and the regulation of gene insulation, overview. DDX5 and DDX17 can regulate alternative splicing through other mechanisms, via a direct effect on the local folding of their targeted transcripts or via the recruitment of RNA binding cofactors | Homo sapiens |
| 3.6.4.13 | metabolism | protein and noncoding RNA partners of DDX5 and DDX17, overview. DDX5 and DDX17 can regulate alternative splicing through other mechanisms, via a direct effect on the local folding of their targeted transcripts or via the recruitment of RNA binding cofactors | Drosophila melanogaster |
| 3.6.4.13 | physiological function | RNA helicases DDX5 and DDX17 are multitasking proteins that regulate gene expression in different biological contexts through diverse activities. The enzymes are associated with long noncoding RNAs that are key epigenetic regulators, DDX5 and DDX17 may act through modulating the activity of various ribonucleoprotein complexes that could ensure their targeting to specific chromatin loci. Potential roles of DDX5 and DDX17 in the 3D chromatin organization with impact on gene expression at the transcriptional and post-transcriptional levels | Drosophila melanogaster |
| 3.6.4.13 | physiological function | RNA helicases DDX5 and DDX17 are multitasking proteins that regulate gene expression in different biological contexts through diverse activities. The enzymes are associated with long noncoding RNAs that are key epigenetic regulators, DDX5 and DDX17 may act through modulating the activity of various ribonucleoprotein complexes that could ensure their targeting to specific chromatin loci. Potential roles of DDX5 and DDX17 in the 3D chromatin organization with impact on gene expression at the transcriptional and post-transcriptional levels. Both RNA helicases are identified as SOX2 binding proteins in glioblastoma cells, suggesting that DDX5 may also be involved in SOX2 transcriptional activity. DDX17 contributes to the activation of SOX2-responsive genes by stabilizing SOX2 binding to its target promoters in ERalpha-positive breast cancer cells. DDX5 and DDX17 directly control the SMAD4-dependent expression of master EMT factors SNAI1 and SNAI2 upon TGF-beta treatment. DDX17 and DDX5 are necessary for repressing the expression of a large subset of neuronal genes in undifferentiated neuroblastoma cells, in cooperation with the REST transcription factor. DDX5 and DDX17 interact and synergize with acetyltransferases CBP (CREB-binding protein) and p300 to activate transcription, such as in the context of SMAD3-mediated transcriptional activation. DDX5 and DDX17 interact with the BRG1 chromatin remodeler. In muscle cells, DDX5 and DDX17 recruit BRG1 to MYOD target genes, increasing the chromatin accessibility for the transcription machinery, which helps coactivate MYOD-dependent transcription | Homo sapiens |
| 3.6.4.13 | physiological function | RNA helicases DDX5 and DDX17 are multitasking proteins that regulate gene expression in different biological contexts through diverse activities. The enzymes are associated with long noncoding RNAs that are key epigenetic regulators, DDX5 and DDX17 may act through modulating the activity of various ribonucleoprotein complexes that could ensure their targeting to specific chromatin loci. Potential roles of DDX5 and DDX17 in the 3D chromatin organization with impact on gene expression at the transcriptional and post-transcriptional levels. Both RNA helicases are identified as SOX2 binding proteins in glioblastoma cells, suggesting that DDX5 may also be involved in SOX2 transcriptional activity. DDX5 may also contribute to cancer development by modulating various signaling pathways. DDX5 interacts with beta-catenin in non-small-cell lung cancer cells as well as colorectal cancer cells, and it also promotes its nuclear translocation, which is associated with the coactivation of Wnt-responsive genes such as MYC or CCND1. DDX5 and beta-catenin are also involved together in the regulation of androgen receptor (AR) transcriptional activity in prostate cancer cells, where DDX5 promotes the recruitment of both transcription factors to AR target genes. Finally, the interaction between DDX5 and beta-catenin contributes to the epithelial to mesenchymal transition (EMT), a process involved in the formation of metastases. DDX5 has been shown to enhance SMAD3 transcriptional activity in response to TGF-beta. DDX5 and DDX17 directly control the SMAD4-dependent expression of master EMT factors SNAI1 and SNAI2 upon TGF-beta treatment. DDX17 and DDX5 are necessary for repressing the expression of a large subset of neuronal genes in undifferentiated neuroblastoma cells, in cooperation with the REST transcription factor. DDX5 and DDX17 interact and synergize with acetyltransferases CBP (CREB-binding protein) and p300 to activate transcription, such as in the context of SMAD3-mediated transcriptional activation. DDX5 and DDX17 interact with the BRG1 chromatin remodeler. In muscle cells, DDX5 and DDX17 recruit BRG1 to MYOD target genes, increasing the chromatin accessibility for the transcription machinery, which helps coactivate MYOD-dependent transcription. DDX5 may be involved in the control of DNA methylation and/or demethylation of CpG dinucleotides, as it interacts with DNA methyltransferase 3 proteins (DNMT3A and B) as well as with thymine DNA glycosylase (TDG). DDX5 is recruited to chromatin along with both DNMT3A/B and TDG proteins at the beginning of each transcription cycle of an ERalpha-responsive promoter | Homo sapiens |
| 3.6.4.13 | physiological function | RNA helicases DDX5 and DDX17 are multitasking proteins that regulate gene expression in different biological contexts through diverse activities. The enzymes are associated with long noncoding RNAs that are key epigenetic regulators, DDX5 and DDX17 may act through modulating the activity of various ribonucleoprotein complexes that could ensure their targeting to specific chromatin loci. Potential roles of DDX5 and DDX17 in the 3D chromatin organization with impact on gene expression at the transcriptional and post-transcriptional levels. DDX5 may also contribute to cancer development by modulating various signaling pathways | Drosophila melanogaster |
| 3.6.4.13 | physiological function | RNA helicases DDX5 and DDX17 are multitasking proteins that regulate gene expression in different biological contexts through diverse activities. The enzymes are associated with long noncoding RNAs that are key epigenetic regulators, DDX5 and DDX17 may act through modulating the activity of various ribonucleoprotein complexes that could ensure their targeting to specific chromatin loci. Potential roles of DDX5 and DDX17 in the 3D chromatin organization with impact on gene expression at the transcriptional and post-transcriptional levels. DDX5 may also contribute to cancer development by modulating various signaling pathways. Murine Ddx5 and Ddx17 are essential for the early stages of myoblast or osteoblast differentiation through their interaction with master transcription factors Myod or Runx2, respectively. In both cases, Ddx5 is recruited to Myod and Runx2 responsive promoters, and it enhances their transcriptional activity. During myogenesis, one consequence is the induced expression of myogenic microRNAs, myogenic transcription factors (Myog or Mef2c), as well as muscle specific genes. DDX17 and DDX5 are necessary for repressing the expression of a large subset of neuronal genes in undifferentiated neuroblastoma cells, in cooperation with the REST transcription factor. DDX5 and DDX17 interact and synergize with acetyltransferases CBP (CREB-binding protein) and p300 to activate transcription, such as in the context of SMAD3-mediated transcriptional activation. DDX5 and DDX17 interact with the BRG1 chromatin remodeler. In muscle cells, DDX5 and DDX17 recruit BRG1 to MYOD target genes, increasing the chromatin accessibility for the transcription machinery, which helps coactivate MYOD-dependent transcription. DDX5 may be involved in the control of DNA methylation and/or demethylation of CpG dinucleotides, as it interacts with DNA methyltransferase 3 proteins (DNMT3A and B) as well as with thymine DNA glycosylase (TDG). DDX5 is recruited to chromatin along with both DNMT3A/B and TDG proteins at the beginning of each transcription cycle of an ERalpha-responsive promoter. During myogenic differentiation of mouse C2C12 cells, both RNA helicases and steroid nuclear receptor activator RNA (SRA)coactivate the transcription factor MyoD, and the joint overexpression of SRA and Ddx5 stimulates the MyoD-induced conversion of mouse embryonic fibroblasts in skeletal muscle cells. The SRA lncRNA can act as a multimodal scaffold for several complexes, and it can be dynamically regulated by RNA helicases | Mus musculus |
| 3.6.4.13 | physiological function | RNA helicases DDX5 and DDX17 are multitasking proteins that regulate gene expression in different biological contexts through diverse activities. The enzymes are associated with long noncoding RNAs that are key epigenetic regulators, DDX5 and DDX17 may act through modulating the activity of various ribonucleoprotein complexes that could ensure their targeting to specific chromatin loci. Potential roles of DDX5 and DDX17 in the 3D chromatin organization with impact on gene expression at the transcriptional and post-transcriptional levels. Murine Ddx5 and Ddx17 are essential for the early stages of myoblast or osteoblast differentiation through their interaction with master transcription factors Myod or Runx2, respectively. In both cases, Ddx5 is recruited to Myod and Runx2 responsive promoters, and it enhances their transcriptional activity. During myogenesis, one consequence is the induced expression of myogenic microRNAs, myogenic transcription factors (Myog or Mef2c), as well as muscle specific genes. DDX17 and DDX5 are necessary for repressing the expression of a large subset of neuronal genes in undifferentiated neuroblastoma cells, in cooperation with the REST transcription factor. DDX5 and DDX17 interact and synergize with acetyltransferases CBP (CREB-binding protein) and p300 to activate transcription, such as in the context of SMAD3-mediated transcriptional activation. DDX5 and DDX17 interact with the BRG1 chromatin remodeler. In muscle cells, DDX5 and DDX17 recruit BRG1 to MYOD target genes, increasing the chromatin accessibility for the transcription machinery, which helps coactivate MYOD-dependent transcription. During myogenic differentiation of mouse C2C12 cells, both RNA helicases and steroid nuclear receptor activator RNA (SRA) coactivate the transcription factor MyoD, and the joint overexpression of SRA and Ddx5 stimulates the MyoD-induced conversion of mouse embryonic fibroblasts in skeletal muscle cells. The SRA lncRNA can act as a multimodal scaffold for several complexes, and it can be dynamically regulated by RNA helicases | Mus musculus |
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