EC Number   |
Disease |
PubMed ID |
Title of Publication |
Category |
Confidence Level |
|---|
   3.4.21.108 | Acute Kidney Injury |
20219823 |
Omi/HtrA2 protease is associated with tubular cell apoptosis and fibrosis induced by unilateral ureteral obstruction. |
causal interaction |
4 |
| 3.4.21.108 | Acute Kidney Injury |
20219823 |
Omi/HtrA2 protease is associated with tubular cell apoptosis and fibrosis induced by unilateral ureteral obstruction. |
unassigned |
0 |
| 3.4.21.108 | Adenocarcinoma |
12887511 |
Immunohistochemical analysis of Omi/HtrA2 expression in stomach cancer. |
causal interaction |
3 |
| 3.4.21.108 | Adenocarcinoma |
12887511 |
Immunohistochemical analysis of Omi/HtrA2 expression in stomach cancer. |
diagnostic usage |
4 |
| 3.4.21.108 | Adenocarcinoma |
12887511 |
Immunohistochemical analysis of Omi/HtrA2 expression in stomach cancer. |
therapeutic application |
2 |
| 3.4.21.108 | Adenocarcinoma |
12887511 |
Immunohistochemical analysis of Omi/HtrA2 expression in stomach cancer. |
ongoing research |
4 |
| 3.4.21.108 | aldehyde dehydrogenase (nad+) deficiency |
32048867 |
Acetaldehyde dehydrogenase 2 deficiency increases mitochondrial reactive oxygen species emission and induces mitochondrial protease Omi/HtrA2 in skeletal muscle. |
causal interaction |
4 |
| 3.4.21.108 | aldehyde dehydrogenase (nad+) deficiency |
32048867 |
Acetaldehyde dehydrogenase 2 deficiency increases mitochondrial reactive oxygen species emission and induces mitochondrial protease Omi/HtrA2 in skeletal muscle. |
diagnostic usage |
3 |
| 3.4.21.108 | aldehyde dehydrogenase (nad+) deficiency |
32048867 |
Acetaldehyde dehydrogenase 2 deficiency increases mitochondrial reactive oxygen species emission and induces mitochondrial protease Omi/HtrA2 in skeletal muscle. |
ongoing research |
1 |
| 3.4.21.108 | aldehyde dehydrogenase (nad+) deficiency |
32048867 |
Acetaldehyde dehydrogenase 2 deficiency increases mitochondrial reactive oxygen species emission and induces mitochondrial protease Omi/HtrA2 in skeletal muscle. |
unassigned |
0 |
