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Literature summary for 3.4.22.28 extracted from

  • Fernandes, M.H.V.; Maggioli, M.F.; Otta, J.; Joshi, L.R.; Lawson, S.; Diel, D.G.
    Senecavirus A 3C protease mediates host cell apoptosis late in infection (2019), Front. Immunol., 10, 363 .
    View publication on PubMedView publication on EuropePMC
Search for more literature for 3.4.22.28

Protein Variants

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

Localization Comment Organism GeneOntology No. Textmining

Natural Substrates/ Products (Substrates)

Natural Substrates Organism Comment (Nat. Sub.) Natural Products Comment (Nat. Pro.) Rev. Reac.
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

Organism UniProt Comment Textmining
Senecavirus A
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 SVA
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Substrates and Products (Substrate)

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

Synonyms Comment Organism
Senecavirus A 3C protease
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 Senecavirus A
SVA 3Cpro
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 Senecavirus A

General Information

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