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Literature summary for 3.4.21.108 extracted from

  • Ding, X.; Patel, M.; Shen, D.; Herzlich, A.A.; Cao, X.; Villasmil, R.; Klupsch, K.; Tuo, J.; Downward, J.; Chan, C.C.
    Enhanced HtrA2/Omi expression in oxidative injury to retinal pigment epithelial cells and murine models of neurodegeneration (2009), Invest. Ophthalmol. Vis. Sci., 50, 4957-4966.
    View publication on PubMed
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Application

Application Comment Organism
medicine therapeutic interventions that inhibit HtrA2/Omi expression, translocation, or protease activity may represent novel therapeutic strategies for retinal pigment epithelial cells and retinal pigment epithelial cells-related diseases Mus musculus

Inhibitors

Inhibitors Comment Organism Structure
ucf-101 treatment of retinal epithelial cells with UCF-101 reduces the cytosolic translocation of HtrA2/Omi, attenuates caspase-3 activation, and decreases apoptosis Mus musculus

Localization

Localization Comment Organism GeneOntology No. Textmining
cytosol H2O2-induced oxidative damage of retinal pigment epithelial cells results in HtrA2/Omi translocation from mitochondria to cytosol, leading to RPE cell apoptosis via a caspase-mediated pathway Mus musculus 5829
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mitochondrion
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 Mus musculus 5739
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Organism

Organism UniProt Comment Textmining
Mus musculus
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-
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Source Tissue

Source Tissue Comment Organism Textmining

Synonyms

Synonyms Comment Organism
HtrA2/Omi
-
 Mus musculus

Expression

Organism Comment Expression
Mus musculus after specific HtrA2 downregulation using RNAi, increased cell viability is measured in H2O2-treated ARPE-19 cells down

General Information

General Information Comment Organism
malfunction fewer and abnormal mitochondria are found in HtrA2/Omi knockout mice photoreceptors and pigment epithelial cells Mus musculus