EC Number   |
Protein Variants |
Reference |
|---|
   2.4.1.198 | E244A |
site-directed mutagenesis |
759061 |
| 2.4.1.198 | more |
a gpi19 deletion allele that lacks nearly the entire coding sequence in the EG123 strain background confirmed the lethality of this mutation |
673403 |
| 2.4.1.198 | more |
a set of temperature-sensitive gpi19 allels is created using error-prone PCR. All of the gpi19 alleles, with the exception of gpi19-4, are osmotically remedial. The gpi19 mutants are hypersensitive to zymolyase treatment. The least severely impaired alleles of gpi19 (gpi19-1 and gpi19-2) are suppressed for their growth defects at restrictive temperature by either GFA1 overexpression or exogenous glucosamine. The gpi19 mutants display weak filamentation phenotypes and invasive growth, which is enhanced by the inclusion of sorbitol in the medium to suppress their growth defects. |
673403 |
| 2.4.1.198 | more |
afpig-a null mutant, strain CEA17 (pyrG-). This mutant shows a complete loss in glycosylphosphatidylinositol-N-acetylglucoaminyltransferase activity. None of the membrane bound glycosylphosphatidylinositol-anchored phospholipases, phosphatase, eCM33por Gl1p is found in the membrane preparation of the mutant. The mutant can grow at temperatures from 30°C to 50°C, but the growth rates are greatly inhibited. When the mutant is grown in the presence of various cell wall-disrupting agents, it is more sensitive to Calcofluor white, Congo-red, Nikkomycin Z and SDS, than the wild type. The mannoproteins and beta-glucans in mycelial cell wall of the mutant is 2.5fold and 2fold of the wild type or revertant respectively. The deletion of the afpig-a gene leads to earlier polarity, germ tube emergence and septation of mutant conidiospores in the early duplication cycles and to significant changes in developmental events and morphogenesis during conidiation. Two virulence factors, mycelial catalase Cat1 and Asp-haemolysin, are missing in the mutant, but the chitinase ChiB is found remarkably increased. After the inoculation of wild-type and mutant conidia into immunocompromised mice, early mortality is nearly identical among all groups. The remaining mice receiving the deletion mutant survived significantly longer. |
-, 676082 |
| 2.4.1.198 | more |
analysis of enzyme-deficient WY-ZY4 strain (BWP17- Caras1/Caras2 mutant). CaGpi2 overexpression results in Hsp90 down-regulation, which is reflected in a decrease in transcript levels as well as in Hsp90 activity. Depletion of CaGpi2 can perhaps reduce the levels of CaRas1 available at the PM for signaling in the cAMP/PKA pathway for hyphal morphogenesis. Generation of revertant strains for all GPI-GnT subunits are created in their respective heterozygous strains |
-, 759489 |
| 2.4.1.198 | more |
analysis of enzyme-deficient WY-ZY4 strain (BWP17- Caras1/Caras2 mutant). Depletion of CaGpi2 can perhaps reduce the levels of CaRas1 available at the PM for signaling in the cAMP/PKA pathway for hyphal morphogenesis. Generation of revertant strains for all GPI-GnT subunits are created in their respective heterozygous strains |
-, 759489 |
| 2.4.1.198 | more |
analysis of enzyme-deficient WY-ZY4 strain (BWP17- Caras1/Caras2 mutant). Generation of revertant strains for all GPI-GnT subunits are created in their respective heterozygous strains |
-, 759489 |
| 2.4.1.198 | more |
disruption of the genes in F9 cells via homologous recombination, causing a severe but not complete defect in the generation of glycosylphosphatidylinositol-anchored proteins, highly reduced activity in vivo, no activity in vitro, decrease in GPI1 also caused decrease of PIG-C and PIG-H |
638132 |
| 2.4.1.198 | more |
generation of single knock-out of gene GPI2 and double knockout mutants of genes GPI1 and GPI119 from Cancdida albicans strain BWP17, microsomes generated from GPI2 mutants exhibited lower GPI-GnT activity as compared with CAI4, phenotypes, overview |
736462 |
| 2.4.1.198 | more |
GPI anchor deficiency is most often caused by mutation in the Pig-a gene, thus measuring GPI anchor deficiency is considered to be almost equivalent to measuring Pig-a mutation. Development and validation of an in vitro Pig-a assay in L5178Y mouse lymphoma cells, method optimization, overview. Antibodies against GPI-linked CD90.2 and stably expressed CD45 are used to determine GPI-status by flow cytometry, antibody concentration and incubation times are optimized. The optimum phenotypic expression period is 8 days. Application of the in vitro Pig-a assay to a selection of well-validated genotoxic and non-genotoxic compounds. EMS, N-ethyl-N-nitrosourea, and 4-nitroquinoline-N-oxide dose dependently increase the numbers of GPI(-) cells, while etoposide, mitomycin C, and a bacterial-specific mutagen do not dependently increase the numbers of GPI(-) cells |
758711 |
