Recombinant Mouse Serine protease HTRA2, mitochondrial (Htra2)

1. Study show that overexpression of mitochondrial Omi/HtrA2 induces cardiac apoptosis and dysfunction. PMID:27924873
2. Mice overexpressing wild-type or G399S mutant HtrA2 have mitochondrial defects resulting in neurodegeneration. PMID:26604148
3. Protease Omi facilitates neurite outgrowth by cleaving the transcription factor E2F1 in differentiated neuroblastoma cells; E2F1 is a substrate of Omi. PMID:26238290
4. The NG2 proteoglycan protects oligodendrocyte precursor cells against oxidative stress via interaction with OMI/HtrA2. PMID:26340347
5. Loss of Omi protease activity results in an abnormal increase of GSK3b, leading to the degradation of PGC-1a, which causes an impairment of mitochondrial biogenesis and induces neurodegeneration. PMID:25118933
6. Neural-specific deletion of Htra2 causes cerebellar neurodegeneration and defective processing of mitochondrial OPA1. PMID:25531304
7. Our findings indicate that radiation-inducible gene therapy may have potential to be a more effective and specific therapy for uveal melanoma because the therapeutic gene can be spatially or temporally controlled by exogenous radiation. PMID:24606398
8. Inactivation of Omi/HtrA2 protease leads to the deregulation of mitochondrial Mulan E3 ubiquitin ligase and increased mitophagy. PMID:24709290
9. Phosphorylated HtrA2/Omi cleaves beta-actin and decreases the amount of filamentous actin (F-actin) in the cytosol. PMID:24662565
10. Downregulation of PARL after ischemia is a key step in ischemic neuronal injury, and that it decreases HtrA2 processing and increases neuronal vulnerability. PMID:23921894
11. increased expression and leakage of Omi/HtrA2 enhanced MI/R injury in aging hearts via degrading XIAP and promoting myocardial apoptosis. PMID:22535253
12. Results demonstrate that HtrA2 deficiency causes mtDNA damage through ROS generation and mutation, which may lead to mitochondrial dysfunction and consequent triggering of cell death in aging cells. PMID:23542127
13. HtrA2-knockout cells exhibit increased proton translocation through the ATP synthase, in combination with decreased ATP production and truncation of the F1 alpha-subunit, suggesting the ATP synthase as the source of the proton leak. PMID:22739987
14. Identification of a novel anti-apoptotic E3 ubiquitin ligase that ubiquitinates antagonists of inhibitor of apoptosis proteins SMAC, HtrA2, and ARTS. PMID:23479728
15. HtrA2 and Cdk5 interact in human and mouse cell lines and brain. PMID:21701498
16. HtrA2/Omi deletion leads to functional reduction in the activity of small-conductance Ca(2+)-activated potassium channels, causing substantia nigra compacta dopamine neurons to fire action potentials in an irregular pattern & enhancing burst firing. PMID:20926611
17. results identify Omi as a novel regulator of autophagy and suggest that Omi might be important in the cellular quality control of proteins involved in neurodegenerative diseases PMID:20467442
18. found reduced AICD production in mitochondria isolated from Omi/HtrA2 knockout mouse embryonic fibroblasts, indicating a significant role of Omi/HtrA2 on gamma-secretase activity PMID:20705111
19. Omi/HtrA2 is associated with apoptotic signaling pathways in tubular epithelial cells activated by unilateral ureteral obstruction, thereby resulting in kidney fibrosis. PMID:20219823
20. A direct effect of loss of Omi/HtrA2 on mitochondrial morphology and a novel role of this mitochondrial serine protease in the modulation of OPA1. PMID:20064504
21. Omi interacts with caspase-inhibitor XIAP and induces enhanced caspase activity. PMID:11803371
22. The neurodegeneration and juvenile lethality in mnd2 mice result from a defect in mitochondrial Omi protease PMID:14534547
23. mice entirely lacking expression of HtrA2/Omi suffer loss of a population of neurons in the striatum, resulting in a neurodegenerative disorder with a parkinsonian phenotype PMID:15509788
24. Ischemia/reperfusion results in Omi/HtrA2 translocation from the mitochondria to the cytosol, where it promotes cardiomyocyte apoptosis via a protease activity-dependent, caspase-mediated pathway. PMID:15611365
25. Omi/HtrA2 is an inducer of anoikis and an important regulator of ras-induced transformation PMID:16461771
26. HtrA2 has a role as a regulator of APP metabolism through endoplasmic reticulum-associated degradation PMID:17684015
27. Results suggest that the primary function of neuronal HtrA2/Omi might be to protect neurons against stress in contrast to its role in the somatic system. PMID:17707776
28. Hax1, is required to suppress apoptosis in lymphocytes and neurons; suppression requires the interaction of Hax1 with the mitochondrial proteases Parl and HtrA2 PMID:18288109
29. HtrA2 molecules are occupied by autoproteolytic peptide products and reveal clues for an autoregulatory mechanism that might have significant importance in HtrA-associated virulence of ycobatc tuberculosis. PMID:18479146
30. These results collectively suggest that the homeostatic but not proapoptotic function of Omi/HtrA2 is linked to selective vulnerability of striatal neurons in HD pathology. PMID:18662332
31. identify Mpv17l as a unique interacting protein and regulator of HtrA2 protease mediating antioxidant and antiapoptotic function in mitochondria PMID:18772386
32. Data show that loss of HtrA2 results in upregulation of integrated stress response genes in the brain, and accumulation of unfolded proteins in mitochondria, defective mitochondrial respiration and enhanced production of reactive oxygen species. PMID:19023330
33. Data show that the amyloid beta-binding serine protease Omi is a stress-relieving heat-shock protein that protects neurons against neurotoxic oligomeric amyloid beta. PMID:19435805

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UNIGENE: Mm.21880

KEGG: mmu:64704

STRING: 10090.ENSMUSP00000087073