EC Number   |
Application |
Reference |
|---|
   3.4.21.108 | medicine |
involvement of HtrA2 in the etiology of Alzheimer's disease |
670224 |
| 3.4.21.108 | medicine |
link between HtrA2/Omi and Parkinsons disease or Alzheimers disease |
686002 |
| 3.4.21.108 | medicine |
loss of HtrA2 function might contribute to the activation of a stress response of mitochondrial origin in the brain that promotes neurodegeneration |
697178 |
| 3.4.21.108 | medicine |
mutations in the OMI/HTRA2 gene are linked to Parkinsons disease |
699689 |
| 3.4.21.108 | medicine |
mutations of the OMI/HTRA2 gene are linked to Parkinsons disease |
698176, 698185 |
| 3.4.21.108 | medicine |
myocardial ischemia/reperfusion significantly increases cytosolic Omi/HtrA2 content and markedly increases apoptosis, ucf-101 can inhibit apoptosis |
668267 |
| 3.4.21.108 | medicine |
Omi/HtrA2 is involved in neuronal cell death following focal cerebral ischemia/reperfusion. Blocking the proteolytic activity of Omi/HtrA2 with specific inhibitors, such as the ucf-101, may be a way to afford neuroprotection and minimize cellular damage in cerebral ischemia/reperfusion |
689170 |
| 3.4.21.108 | medicine |
protease activity of HtrA2 is essential for the production of C161. Processing of amyloid precursor protein into C161 by HtrA2 is a natural event occurring under normal physiological conditions. Direct cleavage of mitochondrial beta-amyloid precursor protein by HtrA2 may prevent mitochondrial dysfunction caused by accumulation of amyloid precursor protein. Regulation of HtrA2 protease activity may be a therapeutic target in Alzheimer disease |
687526 |
| 3.4.21.108 | medicine |
role for HtrA2/Omi in apoptosis |
686002 |
| 3.4.21.108 | medicine |
the function of Omi/HtrA2 is linked to selective vulnerability of striatal neurons in Huntingtons disease |
697749 |
