EC Number   |
Protein Variants |
Reference |
|---|
   3.5.1.92 | E249Q |
site-directed mutagenesis |
733009 |
| 3.5.1.92 | E439Q |
site-directed mutagenesis |
733009 |
| 3.5.1.92 | E79A |
site-directed mutagenesis |
733009 |
| 3.5.1.92 | K178A |
site-directed mutagenesis |
733009 |
| 3.5.1.92 | more |
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 |
733009 |
| 3.5.1.92 | more |
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 |
757538 |
| 3.5.1.92 | more |
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 |
-, 733455 |
| 3.5.1.92 | more |
construction of Vnn1 knockout mice |
-, 756537 |
| 3.5.1.92 | more |
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 |
757002 |
| 3.5.1.92 | 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 |
734998 |
