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Literature summary for 3.5.1.98 extracted from
- Temporal and spatial regulation of histone deacetylase-7 and beta-catenin in endothelial cells (2010), Circ. Res., 106, 1180-1183.
Organism
| Organism | UniProt | Comment | Textmining |
|---|---|---|---|
| Homo sapiens | - |
- |
- |
Source Tissue
| Source Tissue | Comment | Organism | Textmining |
|---|---|---|---|
| endothelial cell | - |
Homo sapiens | - |
Substrates and Products (Substrate)
| Substrates | Comment Substrates | Organism | Products | Comment (Products) | Rev. | Reac. |
|---|---|---|---|---|---|---|
| additional information | HDAC7 binds directly to beta-catenin in the cytoplasm of endothelial cells | Homo sapiens | ? | - |
? |  |
Synonyms
| Synonyms | Comment | Organism |
|---|---|---|
| HDAC7 | - |
Homo sapiens |
| histone deacetylase-7 | - |
Homo sapiens |
General Information
| General Information | Comment | Organism |
|---|---|---|
| malfunction | HDAC7 knockdown causes increased nuclear beta-catenin, decreased transcription of HDAC7, decreased expression of E2F2, cyclin-D1 and cyclin-E2, and increased retinoblastoma protein | Homo sapiens |
| physiological function | HDAC7 overexpression has the ability to trump vascular endothelial growth factor signaling to inhibit endothelial cell proliferation, overexpression of HDAC7 leads to decreased nuclear beta-catenin and decreased activity of beta-catenin-dependent effectors and an associated inhibition of endothelial cell proliferation | Homo sapiens |
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Release 2023.1 (January 2023)
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