| + |
SOD3 | down-regulates quantity 
chemical modification
|
superoxide |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-272271 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 29301787 |
Oxidative stress contributes to diabetes mellitus (DM)–induced endothelial dysfunction, which is one of the most common causes of cardiovascular morbidity and mortality.1,2 The major cellular defense against superoxide (O2•−) is SODs (superoxide dismutases), which consists of the SOD1 (cytoplasmic copper zinc SOD [Cu/ZnSOD]), the SOD2 (mitochondrial MnSOD), and the SOD3 (extracellular Cu/ZnSOD). |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
ATP7A | up-regulates activity 
|
SOD3 |
0.684 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-272267 |
|
|
Mus musculus |
|
| pmid |
sentence |
| 29301787 |
Copper transporter ATP7A (copper-transporting/ATPase) is required for full activation of SOD3 (extracellular superoxide dismutase), which is secreted from vascular smooth muscle cells (VSMCs) and anchors to endothelial cell surface to preserve endothelial function by scavenging extracellular superoxide. |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| + |
superoxide | up-regulates activity
precursor of
|
SOD3 |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-272274 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 29301787 |
Oxidative stress contributes to diabetes mellitus (DM)–induced endothelial dysfunction, which is one of the most common causes of cardiovascular morbidity and mortality.1,2 The major cellular defense against superoxide (O2•−) is SODs (superoxide dismutases), which consists of the SOD1 (cytoplasmic copper zinc SOD [Cu/ZnSOD]), the SOD2 (mitochondrial MnSOD), and the SOD3 (extracellular Cu/ZnSOD). |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
copper(1+) | up-regulates activity
chemical activation
|
SOD3 |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-272301 |
|
|
|
|
| pmid |
sentence |
| 1542024 |
Copper as a cofactor and regulator of copper,zinc superoxide dismutase |
|
| Publications: |
1 |
| + |
SOD3 | up-regulates quantity
chemical modification
|
hydrogen peroxide |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-272273 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 29301787 |
Oxidative stress contributes to diabetes mellitus (DM)–induced endothelial dysfunction, which is one of the most common causes of cardiovascular morbidity and mortality.1,2 The major cellular defense against superoxide (O2•−) is SODs (superoxide dismutases), which consists of the SOD1 (cytoplasmic copper zinc SOD [Cu/ZnSOD]), the SOD2 (mitochondrial MnSOD), and the SOD3 (extracellular Cu/ZnSOD). |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
SOD3 | up-regulates quantity
chemical modification
|
dioxygen |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-272272 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 29301787 |
Oxidative stress contributes to diabetes mellitus (DM)–induced endothelial dysfunction, which is one of the most common causes of cardiovascular morbidity and mortality.1,2 The major cellular defense against superoxide (O2•−) is SODs (superoxide dismutases), which consists of the SOD1 (cytoplasmic copper zinc SOD [Cu/ZnSOD]), the SOD2 (mitochondrial MnSOD), and the SOD3 (extracellular Cu/ZnSOD). |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
3.0
SOD3
- 
- 