Browse our anti-HTRA2 (HTRA2) Antibodies

Fruit Fly (Drosophila melanogaster) HtrA Serine Peptidase 2 (HTRA2) interaction partners

1. Mitochondrial serine protease HtrA2/Omi is an important mediator of germ cell death.

2. Data show the presence of apoptosis at the cellular level in both ade2 and Prat mutants, and the upregulated gene HtrA2, which encodes an apoptosis effector and is thus a candidate for initiating apoptosis in response to purine depletion.

3. Drosophila Omi (dOmi), a fly homologue of the serine protease Omi/HtrA2, alleviates th/DIAP1 inhibition of all caspases by proteolytically degrading th/DIAP1 and induces apoptosis both in cultured cells and in the developing fly eye.

4. The binding of DIAP1 to dOmi resulted in DIAP1-mediated polyubiquitination of dOmi, suggesting that DIAP1 could target dOmi for proteasomal degradation.

5. found that Rhomboid-7, a mitochondrial protease not previously implicated in PD, acts as an upstream component of this pathway, and showed that it is required to cleave the precursor forms of both Pink1 and Omi

6. HtrA2 was shown to be phosphorylated in a PINK1-dependent manner, suggesting it might act in the PINK1 pathway.

Human HtrA Serine Peptidase 2 (HTRA2) interaction partners

1. The association between the change in HtrA2 and proteins associated with LATS1 in ovarian serous cancer cell lines after repeated treatment with cisplatin was evaluated in vitro. In immunohistochemical analysis, repeated cisplatin treatment induced downregulation of HtrA2 protein expression, before and after cisplatin-based chemotherapy in SAC.

2. STEMI patients with elevated circulating HtrA2 levels were identified as having ischemia-reperfusion injury.

3. The important functions for HTRA2 in programmed cell death.

4. A pathogenic role of serine protease HtrA2 in Parkinson's and Alzheimer's diseases has been described. (Review)

5. The first report of recessive deleterious mutations in HTRA2 in human. Absence of HTRA2/Omi is associated with severe neurodegenerative disorder of infancy, abnormal mitochondria, 3-methylglutaconic aciduria and increased sensitivity to apoptosis.

6. HTRA2 and ANO3 mutations are not common causes of essential tremor

7. HtrA2 under stress conditions induces vimentin cleavage in wild-type and SH-SY5Y cells transfected with ABP with the Alzheimer disease-associated Swedish mutation. Interplay between Omi/HtrA2 and vimentin affects mitochondrial distribution in neurons.

8. The a5 helix of PDZ was involved in both, the intra- and intersubunit changes of interactions and thus seems to play an important role in HtrA2 activation.

9. study examined the association of HTRA2 p.G399S mutation with essential tremor(ET) and Parkinson disease (PD) in Asians and found that HTRA2 p.G399S is rare and does not appear to play a major role in subjects with coexistent ET and PD nor in those with pure ET or PD phenotype

10. The NG2 proteoglycan protects oligodendrocyte precursor cells against oxidative stress via interaction with OMI/HtrA2.

11. Omi/HtrA2 overexpression promotes hepatocellular carcinoma cell apoptosis and the ped/pea-15 expression level causes this difference of the Omi/HtrA2 pro-apoptotic marker in the various hepatocellular carcinoma cell lines

12. HtrA2 might promote the apoptosis of non-small cell lung cancer cells, and serve as a target for NSCLC's treatment.

13. 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.

14. HtrA2 expression was a predictor for sensitivity to chemotherapy, and could be a candidate of molecular target in the treatment of high-grade serous ovarian cancers.

15. results suggest that in some families, HTRA2 p.G399S is responsible for hereditary essential tremor and that homozygotes for this allele develop Parkinson disease

16. This study shows that PARK13 and PINK1 are subcellular-specific, but dynamic, proteins with a reciprocal molecular relationship.

17. Rate of HTRA2 sequence variants in Taiwanese Parkinson's disease (PD) is very low; although the HTRA2 R36W variant may contribute to the PD risk in some cases, HTRA2 is not playing a major role in PD pathogenicity

18. demonstrate a novel N-terminal ligand-mediated triggering of an allosteric switch essential for transforming HtrA2 to a proteolytically competent state in a PDZ-independent yet synergistic activation process

19. downregulation of Omi/HtrA2 may contribute to the potent anti-atherosclerotic effect of shear stress by preventing endothelial cells from entering apoptosis.

20. The proteases HtrA2 and UCHL1 regulate TNF-induced necroptosis.

Mouse (Murine) HtrA Serine Peptidase 2 (HTRA2) interaction partners

1. The therapeutic function of HtrA2 in inflammatory diseases is linked with Th17 development and the STAT3 pathway in splenocytes.

2. Study show that overexpression of mitochondrial Omi/HtrA2 induces cardiac apoptosis and dysfunction.

3. Omi/HtrA2-HAX-1 chain played a significant role in mitochondrial homeostasis.

4. Mice overexpressing wild-type or G399S mutant HtrA2 have mitochondrial defects resulting in neurodegeneration.

5. Protease Omi facilitates neurite outgrowth by cleaving the transcription factor E2F1 in differentiated neuroblastoma cells; E2F1 is a substrate of Omi.

6. Protease Omi impairs mitochondrial function by cleaving Hax-1, which induces apoptosis in oxygen-glucose deprivation and reoxygenation -treated N2a cells and causes reperfusion injury in middle cerebral artery occlusion mice.

7. The NG2 proteoglycan protects oligodendrocyte precursor cells against oxidative stress via interaction with OMI/HtrA2.

8. 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.

9. Neural-specific deletion of Htra2 causes cerebellar neurodegeneration and defective processing of mitochondrial OPA1.

10. 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.

11. Inactivation of Omi/HtrA2 protease leads to the deregulation of mitochondrial Mulan E3 ubiquitin ligase and increased mitophagy.

12. Phosphorylated HtrA2/Omi cleaves beta-actin and decreases the amount of filamentous actin (F-actin) in the cytosol.

13. The proteases HtrA2/Omi and UCH-L1 regulate TNF-induced necroptosis.

14. Downregulation of PARL after ischemia is a key step in ischemic neuronal injury, and that it decreases HtrA2 processing and increases neuronal vulnerability.

15. increased expression and leakage of Omi/HtrA2 enhanced MI/R injury in aging hearts via degrading XIAP and promoting myocardial apoptosis.

16. 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.

17. 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.

18. Identification of a novel anti-apoptotic E3 ubiquitin ligase that ubiquitinates antagonists of inhibitor of apoptosis proteins SMAC, HtrA2, and ARTS.

19. Data show that Omi plays an important role in suppressing the microglial inflammatory reaction by inhibiting the ERK1/2-mediated NF-kappaB pathway.

20. Focal cerebral ischemia significantly decreased cytosolic accumulation of HAX-1, induced an upregulation of HtrA2, an upregulation of AIF and activation of caspase-3