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Literature summary extracted from

  • Rasheed, M.; Battu, A.; Kaur, R.
    Aspartyl proteases in Candida glabrata are required for suppression of the host innate immune response (2018), J. Biol. Chem., 293, 6410-6433 .
    View publication on PubMedView publication on EuropePMC

Application

EC Number Application Comment Organism
3.4.23.41 medicine isoform YPS2 and YPS-C genes are required for survival in a murine model of systemic candidiasis. Lack of yapsins augments the inflammatory response of host macrophages during infection in an IL-1beta-dependent manner Nakaseomyces glabratus

Localization

EC Number Localization Comment Organism GeneOntology No. Textmining
3.4.23.24 cell surface
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Nakaseomyces glabratus 9986
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Organism

EC Number Organism UniProt Comment Textmining
3.4.23.24 Nakaseomyces glabratus
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-
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3.4.23.24 Nakaseomyces glabratus BG2
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-
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3.4.23.41 Nakaseomyces glabratus
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-
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Synonyms

EC Number Synonyms Comment Organism
3.4.23.24 aspartyl protease
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Nakaseomyces glabratus
3.4.23.24 yapsin
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Nakaseomyces glabratus
3.4.23.24 Yps
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Nakaseomyces glabratus
3.4.23.41 Yps
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Nakaseomyces glabratus

General Information

EC Number General Information Comment Organism
3.4.23.24 malfunction the Cgyps1-11 mutant lacking all 11 enzyme genes displays pleiotropic defects, including increased susceptibility to cell wall and osmotic stress, perturbed vacuole and pH homeostasis, and attenuated intracellular survival and pathogenesis Nakaseomyces glabratus
3.4.23.24 physiological function the enzyme is required for suppression of the host innate immune response by suppressing the interleukin-1production in macrophages. The enzyme genes are required for organ colonization and dissemination in a mouse model of systemic infection Nakaseomyces glabratus
3.4.23.41 physiological function in a mutant lacking aspartyl proteases Yps1 to Yps11, up-regulation of cell wall organization genes is found. The mutant contains lower beta-glucan and mannan levels and exhibits increased chitin content in the cell wall. Differential expression of genes implicated in inflammation, chemotaxis, ion transport, and the tumor necrosis factor signaling cascade is also observed. The mutant strain evokes a different immune response in the host, resulting in an enhanced release of the cytokine IL-1beta in THP-1 macrophages Nakaseomyces glabratus