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5-[5-(2-nitrophenyl)furfuryliodine]1,3-diphenyl-2-thiobarbituric acid
antisense HtrA2
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significantly inhibits IFN/all-trans retinoic acid-induced degradation of X-linked inhibitor of apoptosis protein
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diisopropylfluorophosphate
complete inhibition at 4 mM
DPMFKL
peptide DPMFKL which inhibits protease HtrA1, EC 3.4.21.107, is not inhibitory to enzyme HtrA2 up to 0.1 mM. For protease HtrA2 mutant lacking the regulatory domain, the peptide acts as a competitive inhibitor, displaying a IC50 value of 0.33 mM
etoposide
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ratio of C161M/APP decreases 66% during 0.0040 mM etoposide-induced apoptosis compared with the non-apoptotic condition
N-tosyllysine chloromethyl ketone
phenylmethanesulfonyl fluoride
51% inhibition at 5 mM
staurosporine
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after transiently expressing HtrA2 and APP695M in HEK-293 cells for 24 h, the cells are induced by 0.0001 mM staurosporine, resulting in decreased rather than an increased production level of C161M during apoptosis
ucf-102
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inhibits, but to a lesser extent than ucf-101
ucf-103
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inhibits, but to a lesser extent than ucf-101
ucf-104
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58% inhibition at 0.02 mM
viral mitochondrial inhibitor of apoptosis
vMIA
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vIRF1
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human herpes virus-8 (HHV-8)-coded oncoprotein, disrupts interactions of GRIM-19 with HtrA2
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5-[5-(2-nitrophenyl)furfuryliodine]1,3-diphenyl-2-thiobarbituric acid
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UCF-101
5-[5-(2-nitrophenyl)furfuryliodine]1,3-diphenyl-2-thiobarbituric acid
UCF-101
N-tosyllysine chloromethyl ketone
51% inhibition at 5 mM
N-tosyllysine chloromethyl ketone
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N-tosyllysine chloromethyl ketone
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blocks ability of wild-type Omi to proteolyse WTS
siRNA
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suppresses endogenous HtrA2, which results in almost 2030% reduction of C161 production
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siRNA
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reduces endogenous Omi expression in HeLa cells
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ucf-101
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blocks protease activity of Omi, protects renal cells from cisplatin-induced cell death, together with 0.05 mM cisplatin, 0.07 mM ucf-101 can block X-linked inhibitor of apoptosis protein degradation
ucf-101
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0.02 mM abrogates the death effect of the TNF-alpha + zVAD combination
ucf-101
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inhibits degradation of endogenous ped/pea-15 by Omi/HtrA2
ucf-101
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treatment of lung epithelial adenocarcinoma cell A549 decreases the cleavage of annexin A2 under both serum withdrawal and cisplatin treatment
ucf-101
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proteolysis of Wilms'tumor suppressor protein WT1 is prevented
ucf-101
specific inhibitor
ucf-101
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78% inhibition at 0.02 mM, complete inhibition at 0.08 mM
ucf-101
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blocks protease activity of Omi, protects renal cells from cisplatin-induced cell death, mice treated with cisplatin and ucf-101 were more resistant to nephrotoxicy than animals treated with ciplatin alone
ucf-101
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blocks HtrA2 protease activity, inhibition of apoptosis
ucf-101
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treatment of retinal epithelial cells with UCF-101 reduces the cytosolic translocation of HtrA2/Omi, attenuates caspase-3 activation, and decreases apoptosis
ucf-101
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specific inhibitor of Omi/HtrA2. Reduces the number of TUNEL-positive cells, attenuates the X-linked inhibitor of apoptosis protein-breakdown and reduces the infarct size
ucf-101
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specific inhibitor for Omi/HtrA2 protects against cerebral ischemia
additional information
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Akt abrogates HtrA2/Omi pro-apoptotic function through phosphorylation of serine 212 in cytoplasm and inhibition of its release from the mitochondria in response to cisplatin treatment. Caspase inhibitor z-VAD-FMK reduces the mature HtrA2/Omi-induced cell death by ca. 45%
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additional information
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HtrA2 phosphorylation is decreased in brains of patients with Parkinson's disease carrying mutations in PINK1 (Y431H and C575R)
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additional information
halogen substitutions at peptide inhibitor's Trp1 residue are most effective in improving peptide selectivity
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additional information
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ucf-101 fails to exert any additional protective effect in transfected cells
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3.4.21.108 HtrA2 peptidase
results (
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