EC Number   |
General Information |
Reference |
|---|
   2.4.1.198 | evolution |
the enzyme belongs to the acyl coenzyme A dehydrogenase (ACAD) family member, thus the enzyme protein folds into a beta-sheet flanked by two alpha-helical domains |
759061 |
| 2.4.1.198 | malfunction |
depletingCaGpi19p, an accessory subunit of the enzyme complex that initiates GPI biosynthesis, specifically down-regulates ERG11, altering ergosterol levels and drug response. ERG11 down-regulation is not due to general cell wall defects or GPI deficiency. CaGPI19 mutants show increased cAMP/PKA signalling |
-, 721539 |
| 2.4.1.198 | malfunction |
GPI19 mutants show up-regulation of GPI2, whereas GPI2 mutants show upregulation of GPI19. GPI2 disruption leads to defective hyphal morphogenesis due to altered Ras signaling. Reintroduction of GPI2 into the GPI2 heterozygous strain can reverse the phenotypes |
736462 |
| 2.4.1.198 | malfunction |
in the CaGPI19 conditional null strain, isozyme CaGpi2 is overexpressed |
-, 759489 |
| 2.4.1.198 | malfunction |
knockdown of dscr5 disrupts Knypek membrane localization and causes an enhanced Frizzled 7 receptor endocytosis in a caveolin-dependent manner, dscr5 knockdown promotes specific Dishevelled degradation by the ubiquitin-proteosome pathway, knockdown of dscr5 disrupts convergence of lateral cells and extension of dorsal cells, knockdown of dscr5 does not affect embryonic patterning |
703374 |
| 2.4.1.198 | malfunction |
mutations in Pig-a prevent GPI-anchor synthesis resulting in loss of cell-surface GPI-linked proteins |
758711 |
| 2.4.1.198 | malfunction |
piga-1-knockout worms show 100% lethality, with decreased mitotic germline cells and abnormal eggshell formation. Cell-specific rescue of the null allele, expression of piga-1 in somatic gonads and/or in germline is sufficient for normal embryonic development and the maintenance of the germline mitotic cells. The RNAi phenotypes of each gene, including larval arrest, scrawny larvae, and germline defects, may result from N-/O-glycosylation inhibition as well as GPI-anchor inhibition |
723140 |
| 2.4.1.198 | malfunction |
recombinant expression of Candida albicans GPI2 subunit in a Scaccharomyces cerevisiae GPI2 subunit conditional lethal mutant cannot restore its growth defects |
736210 |
| 2.4.1.198 | malfunction |
Saccharomyces cerevisiae Gpi2, an accessory subunit of the enzyme catalyzing the first step of glycosylphosphatidylinositol (GPI) anchor biosynthesis, selectively complements some of the functions of its homologue in Candida albicans |
736210 |
| 2.4.1.198 | malfunction |
targeted deletion of the gene encoding GntA in A. fumigatus results in complete absence of zwitterionic glycoinositolphosphoceramide, a phenotype that can be reverted by episomal expression of GntA in the mutant |
736199 |
