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HTRA2 encodes a serine protease. Additionally we are shipping HTRA2 Proteins (12) and HTRA2 Kits (4) and many more products for this protein.
Showing 10 out of 138 products:
Human Polyclonal HTRA2 Primary Antibody for EIA, IHC (p) - ABIN500411
Crook, Clem, Miller: An apoptosis-inhibiting baculovirus gene with a zinc finger-like motif. in Journal of virology 1993
Show all 4 references for ABIN500411
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 references for ABIN223216
Human Polyclonal HTRA2 Primary Antibody for IHC, ELISA - ABIN1450773
Hillier, Graves, Fulton, Fulton, Pepin, Minx, Wagner-McPherson, Layman, Wylie, Sekhon, Becker, Fewell, Delehaunty, Miner, Nash, Kremitzki, Oddy, Du, Sun, Bradshaw-Cordum, Ali, Carter, Cordes, Harris et al.: Generation and annotation of the DNA sequences of human chromosomes 2 and 4. ... in Nature 2005
Human Polyclonal HTRA2 Primary Antibody for IHC (p), WB - ABIN657628
Hartkamp, Carpenter, Roberts: The Wilms' tumor suppressor protein WT1 is processed by the serine protease HtrA2/Omi. in Molecular cell 2010
Human Monoclonal HTRA2 Primary Antibody for EIA, WB - ABIN121159
Zumbrunn, Trueb: Primary structure of a putative serine protease specific for IGF-binding proteins. in FEBS letters 1997
Human Monoclonal HTRA2 Primary Antibody for IHC (p), IP - ABIN1107619
Seong, Choi, Park, Kim, Ahn, Seong, Kim, Kang, Rhim: Autocatalytic processing of HtrA2/Omi is essential for induction of caspase-dependent cell death through antagonizing XIAP. in The Journal of biological chemistry 2004
Human Polyclonal HTRA2 Primary Antibody for IHC, ELISA - ABIN1533174
Faccio, Fusco, Viel, Zervos: Tissue-specific splicing of Omi stress-regulated endoprotease leads to an inactive protease with a modified PDZ motif. in Genomics 2000
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.
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.
results suggest that in some families, HTRA2 p.G399S is responsible for hereditary essential tremor and that homozygotes for this allele develop Parkinson disease
This study shows that PARK13 and PINK1 (show PINK1 Antibodies) are subcellular-specific, but dynamic, proteins with a reciprocal molecular relationship.
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
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.
increased expression and leakage of Omi/HtrA2 enhanced MI/R injury in aging hearts via degrading XIAP (show XIAP Antibodies) and promoting myocardial apoptosis.
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