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Literature summary for 3.4.21.108 extracted from

  • Li, B.; Hu, Q.; Wang, H.; Man, N.; Ren, H.; Wen, L.; Nukina, N.; Fei, E.; Wang, G.
    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.
    View publication on PubMed
Search for more literature for 3.4.21.108

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