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anti-Human HTRA2 Antibodies:
anti-Mouse (Murine) HTRA2 Antibodies:
anti-Rat (Rattus) HTRA2 Antibodies:
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Human Monoclonal HTRA2 Primary Antibody for IHC (p), IHC - ABIN252514
Laforge, Bidère, Carmona, Devocelle, Charpentier, Senik: Apoptotic death concurrent with CD3 stimulation in primary human CD8+ T lymphocytes: a role for endogenous granzyme B. in Journal of immunology (Baltimore, Md. : 1950) 2006
Show all 3 Pubmed References
Human Polyclonal HTRA2 Primary Antibody for IF, WB - ABIN223216
Griparic, Kanazawa, van der Bliek: Regulation of the mitochondrial dynamin-like protein Opa1 by proteolytic cleavage. in The Journal of cell biology 2007
Show all 3 Pubmed References
Human Monoclonal HTRA2 Primary Antibody for IHC (p), WB - ABIN532000
Lee, Lee, Kim, Kim, Park, Kim, Lee, Yoo: Immunohistochemical analysis of Omi/HtrA2 expression in stomach cancer. in APMIS : acta pathologica, microbiologica, et immunologica Scandinavica 2003
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Mitochondrial serine protease HtrA2 (show F2 Antibodies)/Omi is an important mediator of germ cell death.
Data show the presence of apoptosis at the cellular level in both ade2 (show PAICS Antibodies) and Prat (show PPAT Antibodies) mutants, and the upregulated gene HtrA2, which encodes an apoptosis effector and is thus a candidate for initiating apoptosis in response to purine depletion.
Drosophila Omi (dOmi), a fly homologue of the serine protease Omi/HtrA2, alleviates th/DIAP1 (show DIAPH1 Antibodies) inhibition of all caspases by proteolytically degrading th/DIAP1 (show DIAPH1 Antibodies) and induces apoptosis both in cultured cells and in the developing fly eye.
The binding of DIAP1 (show DIAPH1 Antibodies) to dOmi resulted in DIAP1 (show DIAPH1 Antibodies)-mediated polyubiquitination of dOmi, suggesting that DIAP1 (show DIAPH1 Antibodies) could target dOmi for proteasomal degradation.
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 (show PINK1 Antibodies) and Omi
HtrA2 was shown to be phosphorylated in a PINK1 (show PINK1 Antibodies)-dependent manner, suggesting it might act in the PINK1 (show PINK1 Antibodies) pathway.
A pathogenic role of serine protease HtrA2 (show F2 Antibodies) in Parkinson's and Alzheimer's diseases has been described. (Review)
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.
HTRA2 and ANO3 (show ANO3 Antibodies) mutations are not common causes of essential tremor
HtrA2 under stress conditions induces vimentin (show VIM Antibodies) cleavage in wild-type and SH-SY5Y cells transfected with ABP (show ABP1 Antibodies) with the Alzheimer disease-associated Swedish mutation. Interplay between Omi/HtrA2 and vimentin (show VIM Antibodies) affects mitochondrial distribution in neurons.
The a5 helix of PDZ (show INADL Antibodies) was involved in both, the intra- and intersubunit changes of interactions and thus seems to play an important role in HtrA2 activation.
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
The NG2 (show MCSP Antibodies) proteoglycan (show Vcan Antibodies) protects oligodendrocyte precursor cells against oxidative stress via interaction with OMI/HtrA2.
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
HtrA2 might promote the apoptosis of non-small cell lung cancer cells, and serve as a target for NSCLC's treatment.
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.
Mice overexpressing wild-type or G399S mutant HtrA2 have mitochondrial defects resulting in neurodegeneration.
Protease Omi facilitates neurite outgrowth by cleaving the transcription factor E2F1 (show E2F1 Antibodies) in differentiated neuroblastoma (show ARHGEF16 Antibodies) cells; E2F1 (show E2F1 Antibodies) is a substrate of Omi.
Protease Omi impairs mitochondrial function by cleaving Hax-1 (show HAX1 Antibodies), which induces apoptosis in oxygen-glucose deprivation and reoxygenation -treated N2a cells and causes reperfusion injury in middle cerebral artery occlusion mice.
The NG2 (show Vcan Antibodies) proteoglycan (show Vcan Antibodies) protects oligodendrocyte precursor cells against oxidative stress via interaction with OMI/HtrA2.
Loss of Omi protease activity results in an abnormal increase of GSK3b (show GSK3b Antibodies), leading to the degradation of PGC (show PGC Antibodies)-1a, which causes an impairment of mitochondrial biogenesis and induces neurodegeneration.
Neural-specific deletion of Htra2 causes cerebellar neurodegeneration and defective processing of mitochondrial OPA1 (show MED12 Antibodies).
Inactivation of Omi/HtrA2 protease leads to the deregulation of mitochondrial Mulan E3 ubiquitin ligase (show MUL1 Antibodies) and increased mitophagy.
Phosphorylated HtrA2/Omi cleaves beta-actin and decreases the amount of filamentous actin (F-actin) in the cytosol.
The proteases HtrA2/Omi and UCH-L1 (show UCHL1 Antibodies) regulate TNF (show TNF Antibodies)-induced necroptosis.
Downregulation of PARL (show PARL Antibodies) after ischemia is a key step in ischemic neuronal injury, and that it decreases HtrA2 processing and increases neuronal vulnerability.
This gene encodes a serine protease. The protein has been localized in the endoplasmic reticulum and interacts with an alternatively spliced form of mitogen-activated protein kinase 14. The protein has also been localized to the mitochondria with release to the cytosol following apoptotic stimulus. The protein is thought to induce apoptosis by binding the apoptosis inhibitory protein baculoviral IAP repeat-containing 4. Nuclear localization of this protein has also been observed. Alternate splicing of this gene results in two transcript variants encoding different isoforms. Additional transcript variants have been described, but their full-length sequences have not been determined.
, HtrA serine peptidase 2
, protease, serine, 25
, serine protease HTRA2, mitochondrial-like
, HtrA-like serine protease
, Omi stress-regulated endoprotease
, high temperature requirement protein A2
, serine protease 25
, serine protease HTRA2, mitochondrial
, serine proteinase OMI
, motor neuron degeneration 2
, omi stress-regulated endoprotease
, serine protease OMI
, protease serine 25