Protein Variants | Comment | Organism |
---|---|---|
C159R | site-directed mutagenesis, inactive mutant | Senecavirus A |
H47D | site-directed mutagenesis, inactive mutant | Senecavirus A |
additional information | while expression of wild-type SVA 3Cpro results in activation of Casp-3 and cleavage of NF-kappaB-p65, expression of the 3Cpro catalytic-dead mutants H47D or C159R does not lead to Casp-3 activation nor to NF-kappaB-p65 cleavage | Senecavirus A |
Localization | Comment | Organism | GeneOntology No. | Textmining |
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Natural Substrates | Organism | Comment (Nat. Sub.) | Natural Products | Comment (Nat. Pro.) | Rev. | Reac. |
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additional information | Senecavirus A | NF-kappaB-p65 activation by SVA 3Cpro. NF-kappaB-p65 cleavage occurs at the caspase cleavage site (444LQFDTDED), suggesting that cleavage of NF-kappaB-p65 is mediated by caspases and not by the direct action of SVA 3Cpro. While expression of wild-type SVA 3Cpro results in activation of Casp-3 and cleavage of NF-kappaB-p65, expression of the 3Cpro catalytic-dead mutants H47D or C159R does not lead to Casp-3 activation nor to NF-kappaB-p65 cleavage | ? | - |
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Organism | UniProt | Comment | Textmining |
---|---|---|---|
Senecavirus A | - |
SVA | - |
Substrates | Comment Substrates | Organism | Products | Comment (Products) | Rev. | Reac. |
---|---|---|---|---|---|---|
additional information | NF-kappaB-p65 activation by SVA 3Cpro. NF-kappaB-p65 cleavage occurs at the caspase cleavage site (444LQFDTDED), suggesting that cleavage of NF-kappaB-p65 is mediated by caspases and not by the direct action of SVA 3Cpro. While expression of wild-type SVA 3Cpro results in activation of Casp-3 and cleavage of NF-kappaB-p65, expression of the 3Cpro catalytic-dead mutants H47D or C159R does not lead to Casp-3 activation nor to NF-kappaB-p65 cleavage | Senecavirus A | ? | - |
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Synonyms | Comment | Organism |
---|---|---|
Senecavirus A 3C protease | - |
Senecavirus A |
SVA 3Cpro | - |
Senecavirus A |
General Information | Comment | Organism |
---|---|---|
metabolism | while cleavage of NF-kB-p65 is secondary to caspase activation, the proteolytic activity of SVA 3Cpro is essential for induction of apoptosis. Expression of SVA 3Cpro is associated with apoptosis and cleavage of NF-kappaB-p65. While expression of 3Cpro does not affect expression levels of the upstream NF-kappaB kinases (IKKalpha, IKKbeta), a marked decrease in the levels of IkappaB-alpha and NF-kappaB-p65 are observed in 3Cpro expressing cells | Senecavirus A |
physiological function | activity of SVA 3Cpro is essential for induction of apoptosis. SVA induces apoptosis, presumably, as a mechanism to facilitate virus release and/or spread from infected cells. During infection SVA induces activation of NF-kappaB, as evidenced by nuclear translocation of NF-kappaB-p65 and NF-kappaB-mediated transcription, late in infection a cleaved product corresponding to the C-terminus of NF-kappaB-p65 is detected in infected cells, resulting in lower NF-kappaB transcriptional activity. NF-kappaB seems to play an essential role in protecting host cells from picornavirus-induced apoptosis. Late induction of apoptosis seems essential for SVA infection cycle. While expression of wild-type SVA 3Cpro results in activation of Casp-3 and cleavage of NF-kappaB-p65, expression of the 3Cpro catalytic-dead mutants H47D or C159R does not lead to Casp-3 activation nor to NF-kappaB-p65 cleavage. But NF-kappaB-p65 cleavage occurs at the caspase cleavage site (444LQFDTDED), suggesting that cleavage of NF-kappaB-p65 is mediated by caspases and not by the direct action of SVA 3Cpro | Senecavirus A |