3.5.1.92: pantetheine hydrolase
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For detailed information about pantetheine hydrolase, go to the full flat file.
Word Map on EC 3.5.1.92
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3.5.1.92
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cysteamine
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pantothen
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gpi-anchored
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ectoenzyme
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pantothenamides
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gelatinase-associated
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walter
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aminothiol
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pantethine
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biotinidase
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julius
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medicine
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diagnostics
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drug development
- 3.5.1.92
- cysteamine
-
pantothen
-
gpi-anchored
-
ectoenzyme
- pantothenamides
-
gelatinase-associated
-
walter
-
aminothiol
- pantethine
- biotinidase
-
julius
- medicine
- diagnostics
- drug development
Reaction
Synonyms
GPI-80, PAGEL, pantetheinase, pantetheinase-associated gene expressed in leukocytes, pantetheinases, pantetheine hydrolase, vanin, vanin 1, vanin gene family, vanin-1, vanin-1 pantetheinase, vanin-2, vanin-3, vascular non-inflammatory molecule-1, vascular noninflammatory molecule 1, VNN-1, VNN1, Vnn1 pantetheinase, VNN2, VNN3
ECTree
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Engineering
Engineering on EC 3.5.1.92 - pantetheine hydrolase
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N131S
naturally occuring mutation in both African Americans and Mexican Americans, the mutation is associated with significantly lower plasma vanin-1 protein levels, the N131S vanin-1 is subjected to rapid endoplasmic reticulum-associated degradation as the underlying mechanism for its reduction, N131S vanin-1 is degraded significantly faster than wild type vanin-1 greatly reducing vanin-1 present on the plasma membrane and pantetheinase activity, overview
T26I
additional information
naturally occuring mutation, similar vanin-1 protein levels are detected in cells expressing T26I vanin-1 compared to cells expressing wild-type vanin-1
construction of several VNN2 promoter-deletion mutants: deletion of the region between -1107 and -530 result in a marked and significant increase of basal and forskolin-stimulated promoter activities, suggesting factors repressing the promoter activity in this region. This region contains a number of consensus cis-acting elements of which COUP-TF, GATA, and Ebox appears to play a key role, as revealed by site-directed mutagenesis and promoter activity assays. Deletion between -530 and -262 markedly decreased basal and forskolin-stimulated promoter activities as compared to the-530VNN2.LUC construct. Further deletions do not change promoter activities, thus identifying the region -530/-262 as important in the regulation of the VNN2 promoter activity in bovine granulosa cells
additional information
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construction of several VNN2 promoter-deletion mutants: deletion of the region between -1107 and -530 result in a marked and significant increase of basal and forskolin-stimulated promoter activities, suggesting factors repressing the promoter activity in this region. This region contains a number of consensus cis-acting elements of which COUP-TF, GATA, and Ebox appears to play a key role, as revealed by site-directed mutagenesis and promoter activity assays. Deletion between -530 and -262 markedly decreased basal and forskolin-stimulated promoter activities as compared to the-530VNN2.LUC construct. Further deletions do not change promoter activities, thus identifying the region -530/-262 as important in the regulation of the VNN2 promoter activity in bovine granulosa cells
additional information
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construction of several VNN2 promoter-deletion mutants: deletion of the region between -1107 and -530 result in a marked and significant increase of basal and forskolin-stimulated promoter activities, suggesting factors repressing the promoter activity in this region. This region contains a number of consensus cis-acting elements of which COUP-TF, GATA, and Ebox appears to play a key role, as revealed by site-directed mutagenesis and promoter activity assays. Deletion between -530 and -262 markedly decreased basal and forskolin-stimulated promoter activities as compared to the-530VNN2.LUC construct. Further deletions do not change promoter activities, thus identifying the region -530/-262 as important in the regulation of the VNN2 promoter activity in bovine granulosa cells
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additional information
construction of a truncated mutant comprising amino acids 22-493, deleting the native signal sequence and the C-terminal GPI-anchor sequence, and cloning downstream of the mouse interleukin-3 signal peptide in the mammalian expression vector pAPEX-3P and a FLAG tag DYDDDDK
additional information
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construction of a truncated mutant comprising amino acids 22-493, deleting the native signal sequence and the C-terminal GPI-anchor sequence, and cloning downstream of the mouse interleukin-3 signal peptide in the mammalian expression vector pAPEX-3P and a FLAG tag DYDDDDK
additional information
construction of in p16/p19-/- mutant mice. Comparison of mouse survival and tumor incidence in three independent cohorts of p16/p19/Vnn1-/- versus p16/p19-/- mice, derived from two independently derived crosses between p16/p19-/- and Vnn1-/- mice. Whereas 35% p16p19-/- mice progressively develop lethal tumors within 220 days, 70% p16p19/Vnn1-/- die of aggressive tumors before 220 days. Whereas p16p19-/- mice develop various tumor types with a majority of lymphomas, p16/p19/Vnn1-/- mice predominantly develop skin STS typed as fibrosarcomas
additional information
development of vnn1 KO mice, which do not have an obvious spontaneous phenotype, they are resistant to inflammation and oxidative stress, thus indisputably proving a correlation between vanin 1, its pantetheinase activity and pro-inflammatory mediators