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Literature summary for 3.4.21.108 extracted from
- Omi/HtrA2 is a positive regulator of autophagy that facilitates the degradation of mutant proteins involved in neurodegenerative diseases (2010), Cell Death Differ., 17, 1773-1784.
Protein Variants
| Protein Variants | Comment | Organism |
|---|---|---|
| S276C | protease-defective mutant | Mus musculus |
Molecular Weight [Da]
| Molecular Weight [Da] | Molecular Weight Maximum [Da] | Comment | Organism |
|---|---|---|---|
| 35000 | - |
endogenous Omi, SDS-PAGE | Mus musculus |
Organism
| Organism | UniProt | Comment | Textmining |
|---|---|---|---|
| Mus musculus | - |
- |
- |
Substrates and Products (Substrate)
| Substrates | Comment Substrates | Organism | Products | Comment (Products) | Rev. | Reac. |
|---|---|---|---|---|---|---|
| beta-casein + H2O | - |
Mus musculus | ? | - |
? |  |
Synonyms
| Synonyms | Comment | Organism |
|---|---|---|
| high-temperature requirement factor A2 | - |
Mus musculus |
| HtrA2 | - |
Mus musculus |
| Omi | - |
Mus musculus |
General Information
| General Information | Comment | Organism |
|---|---|---|
| malfunction | knockdown of Omi decreases the basal level of autophagy and increases the level of neurodegenerative proteins such as pathogenic A53T alpha-synuclein and truncated polyglutamine-expanded huntingtin, as well as the endogenous autophagy substrate p62 | Mus musculus |
| physiological function | Omi activates autophagy in a dose-dependent manner through digestion of Hax-1, Omi-induced autophagy facilitates the degradation of neurodegenerative proteins such as pathogenic A53T alpha-synuclein and truncated polyglutamine-expanded huntingtin, as well as the endogenous autophagy substrate p62. Omi is important in the cellular quality control of proteins involved in neurodegenerative diseases | Mus musculus |
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Release 2023.1 (January 2023)
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