2.4.1.198: phosphatidylinositol N-acetylglucosaminyltransferase
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For detailed information about phosphatidylinositol N-acetylglucosaminyltransferase, go to the full flat file.
Word Map on EC 2.4.1.198
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2.4.1.198
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paroxysmal
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nocturnal
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hemoglobinuria
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gpi-anchored
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hematopoietic
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genotoxicity
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marrow
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x-linked
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anemia
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aplastic
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micronucleus
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hemolysis
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cytometric
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granulocytes
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micronucleated
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intravascular
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analysis
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n-ethyl-n-nitrosourea
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comet
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gpi-linked
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glycosylphosphatidylinositol-anchored
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complement-mediated
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pigret
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clastogenic
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gpi-deficient
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mn-rets
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gpi-aps
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eculizumab
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myelodysplastic
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procarbazine
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enu-treated
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4-nitroquinoline-1-oxide
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haemopoietic
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immunomagnetic
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genotoxicants
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repeat-dose
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enu-induced
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proaerolysin
- 2.4.1.198
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paroxysmal
-
nocturnal
- hemoglobinuria
-
gpi-anchored
-
hematopoietic
-
genotoxicity
- marrow
-
x-linked
- anemia
-
aplastic
- micronucleus
-
hemolysis
-
cytometric
- granulocytes
-
micronucleated
-
intravascular
- analysis
-
n-ethyl-n-nitrosourea
- comet
-
gpi-linked
-
glycosylphosphatidylinositol-anchored
-
complement-mediated
-
pigret
-
clastogenic
-
gpi-deficient
-
mn-rets
-
gpi-aps
- eculizumab
-
myelodysplastic
- procarbazine
-
enu-treated
- 4-nitroquinoline-1-oxide
-
haemopoietic
-
immunomagnetic
-
genotoxicants
-
repeat-dose
-
enu-induced
- proaerolysin
Reaction
Synonyms
acetyl-D-glucosaminyltransferase, uridine diphosphoacetylglucosamine alpha1,6-, afpig-a, Down syndrome critical region protein 5, DR437w, Dscr5, glycosylphosphatidylinositol N-acetylglucosaminyltransferase complex, glycosylphosphatidylinositol-N-acetylglucosaminyltransferase, GntA, GPI-GlcNAc transferase, GPI-GnT, GPI-N-acetylglucosaminyltransferase, GPI-N-acetylglucosaminyltransferase complex, GPI1, GPI15, GPI19, GPI2, GPI3, phosphatidylinositol N-acetylglucosaminyltransferase subunit A, phosphatidylinositol/UDP-GlcNAc:GlcNAc transferase, PIG-A, PigA, UDP-N-acetyl-D-glucosamine:phosphatidylinositol N-acetyl-D-glucosaminyltransferase, uridine diphosphoacetylglucosamine alpha1,6-acetyl-D-glucosaminyltransferase
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General Information on EC 2.4.1.198 - phosphatidylinositol N-acetylglucosaminyltransferase
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GENERAL INFORMATION 
ORGANISM
UNIPROT
COMMENTARY 
LITERATURE
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
malfunction
metabolism
physiological function
additional information
modeling with PigG, the acyl carrier protein, suggests a reasonable mode of interaction with PigA. The structure helps to explain the proline oxidation mechanism, in which Glu244 plays a central role by abstracting the substrate protons. It also reveals a plausible pocket for oxygen binding to the Si side of FAD
malfunction
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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
malfunction
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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
malfunction
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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
malfunction
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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
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
malfunction
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recombinant expression of Candida albicans GPI2 subunit in a Scaccharomyces cerevisiae GPI2 subunit conditional lethal mutant cannot restore its growth defects
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
malfunction
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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
malfunction
in the CaGPI19 conditional null strain, isozyme CaGpi2 is overexpressed
malfunction
mutations in Pig-a prevent GPI-anchor synthesis resulting in loss of cell-surface GPI-linked proteins
malfunction
the strain overexpressing CaGpi2 is hyperfilamentous and also heat-shock-sensitive, a phenotype typical of hyperactive Ras mutants. When Hsp90 levels are downregulated, due to CaGpi2 overexpression, the interaction of CaRas1 with Cyr1 is promoted at the cost of its interaction with Ira2. Thus, the filamentation pathway remains turned on even at 30°C, resulting in a hyperfilamentous phenotype
malfunction
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in the CaGPI19 conditional null strain, isozyme CaGpi2 is overexpressed
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malfunction
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the strain overexpressing CaGpi2 is hyperfilamentous and also heat-shock-sensitive, a phenotype typical of hyperactive Ras mutants. When Hsp90 levels are downregulated, due to CaGpi2 overexpression, the interaction of CaRas1 with Cyr1 is promoted at the cost of its interaction with Ira2. Thus, the filamentation pathway remains turned on even at 30°C, resulting in a hyperfilamentous phenotype
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malfunction
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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
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metabolism
analysis of the regulatory function of the enzyme, overview
metabolism
the ability of Candida albicans to switch between yeast to hyphal form is a property that is primarily associated with the invasion and virulence of this human pathogenic fungus. Several glycosylphosphatidylinositol (GPI)-anchored proteins are expressed only during hyphal morphogenesis. One of the major pathways that controls hyphal morphogenesis is the Ras signaling pathway. Cross-talk between GPI anchor biosynthesis and Ras signaling occurs in Candida albicans. The first step of GPI biosynthesis is activated by Ras in Candida albicans. Activation of Ras signaling is independent of the catalytic competence of GPI-GnT
metabolism
the ability of Candida albicans to switch between yeast to hyphal form is a property that is primarily associated with the invasion and virulence of this human pathogenic fungus. Several glycosylphosphatidylinositol (GPI)-anchored proteins are expressed only during hyphal morphogenesis. One of the major pathways that controls hyphal morphogenesis is the Ras signaling pathway. Cross-talk between GPI anchor biosynthesis and Ras signaling occurs in Candida albicans. The first step of GPI biosynthesis is activated by Ras in Candida albicans. Activation of Ras signaling is independent of the catalytic competence of GPI-GnT. Possible interaction between Ras signaling and GPI-GnT in Candida albicans, detailed overview
metabolism
the enzyme is involved in the glycophosphatidylinositol (GPI) anchor synthesis pathway which is highly conserved between species
metabolism
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the ability of Candida albicans to switch between yeast to hyphal form is a property that is primarily associated with the invasion and virulence of this human pathogenic fungus. Several glycosylphosphatidylinositol (GPI)-anchored proteins are expressed only during hyphal morphogenesis. One of the major pathways that controls hyphal morphogenesis is the Ras signaling pathway. Cross-talk between GPI anchor biosynthesis and Ras signaling occurs in Candida albicans. The first step of GPI biosynthesis is activated by Ras in Candida albicans. Activation of Ras signaling is independent of the catalytic competence of GPI-GnT. Possible interaction between Ras signaling and GPI-GnT in Candida albicans, detailed overview
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metabolism
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the ability of Candida albicans to switch between yeast to hyphal form is a property that is primarily associated with the invasion and virulence of this human pathogenic fungus. Several glycosylphosphatidylinositol (GPI)-anchored proteins are expressed only during hyphal morphogenesis. One of the major pathways that controls hyphal morphogenesis is the Ras signaling pathway. Cross-talk between GPI anchor biosynthesis and Ras signaling occurs in Candida albicans. The first step of GPI biosynthesis is activated by Ras in Candida albicans. Activation of Ras signaling is independent of the catalytic competence of GPI-GnT
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physiological function
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Dscr5 functionally interacts with Knypek/Glypican 4 and is required for its localization at the cell surface, Dscr5 interacts with the planar cell polarity pathway in convergent extension movements
physiological function
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Dscr5 functionally interacts with Knypek/Glypican 4 and is required for its localization at the cell surface, Dscr5 interacts with the planar cell polarity pathway in convergent extension movements
physiological function
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the enzyme is part of the enzyme complex that initiates glycosylphosphatidylinositol, GPI, biosynthesis, it catalyzes the first step of GPI anchor biosynthesis. CaGPI19 appears to be mutually regulated with ERG11
physiological function
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the phosphatidylinositol N-acetylglucosaminyltransferase complex catalyzes the first step of GPI-anchor synthesis, which is indispensable for the germline development of the nematode Caenorhabditis elegans. GPI-anchor synthesis is indispensable for the maintenance of mitotic germline cell number
physiological function
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Saccharomyces cerevisiae enzyme subunit Gpi2 is an accessory subunit of the enzyme that catalyzes the first step of glycosylphosphatidylinositol (GPI) anchor biosynthesis. Saccharomyces cerevisiae enzyme subunit Gpi2 subunit physically interacts with and negatively modulates Ras signaling, while enzyme subunit Gpi2 from Candida albicans is a positive modulator of Ras signaling
physiological function
the enzyme complex, GPI-N-acetylglucosaminyltransferase (GPI-GnT), is involved in the first step of GPI anchor biosynthesis in eukaryotes. Candida albicans has several glycosylphosphatidylinositol (GPI)-anchored virulence factors. Inhibiting GPI biosynthesis attenuates its virulence. Enzyme complex subunit GPI2 is essential for growth and hyphal morphogenesis and is needed for filamentation. The GPI-GnT enzyme complex accessory subunits, GPI2 and GPI19, exhibit opposite effects on ergosterol biosynthesis and Ras signaling (which determines hyphal morphogenesis), because the two subunits negatively regulate one another. GPI19 controls ergosterol biosynthesis through ERG11 levels, whereas GPI2 determines the filamentation by cross-talk with Ras1 signaling. GPI2 affects GPI anchor biosynthesis and cell wall
physiological function
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the enzyme is involved in the initiation of zwitterionic glycoinositolphosphoceramide biosynthesis. Glycoinositolphosphoceramides (GIPCs) are complex sphingolipids that, in fungi, commonly contain an alpha-mannose residue linked at position 2 of the inositol. Several pathogenic fungi additionally synthesize zwitterionic GIPCs carrying an alpha-glucosamine residue at this position. In the human pathogen Aspergillus fumigatus, the alpha-N-acetylglucosaminyl-1,2-inositolphosphoceramide core is elongated to Manalpha1,3Manalpha1,6GlcNalpha1,2IPC, which is the most abundant glycoinositolphosphoceramide synthesized by this fungus. GntA uses UDP-N-acetylglucosamine as donor substrate to generate a glycolipid product resistant to saponification and to digestion by phosphatidylinositol-phospholipase C as expected for GlcNAcalpha1,2IPC
physiological function
the GPI-Nacetylglucosaminyltransferase (GPI-GnT) enzyme complex catalyzes the first and committing step of the pathway in Candida albicans involving transfer of N-acetylglucosamine from UDP-GlcNAc to phosphatidylinositol. Saccharomyces cerevisiae subunit Gpi2 enzyme subunit physically interacts with and negatively modulates Ras signaling, while enzyme subunit Gpi2 from Candida albicans is a positive modulator of Ras signaling. The effect of Candida albicans GPI2 subunit on sterol biosynthesis Candida albicans is independent of its interaction with the GPI-GnT enzyme complex and Ras signaling pathways
physiological function
hemizygous phosphatidylinositol class A (Pig-a) forms the catalytic subunit of N-acetylglucosaminyltransferase that is required for glycophosphatidylinositol (GPI) anchor biosynthesis
physiological function
of the two Candida albicans Ras proteins, CaRas1 alone activates GPI-GnT activity, and the activity is further stimulated by constitutively activated CaRas1. Of the six subunits of the GPI-N-acetylglucosaminyltransferase (GPI-GnT) that catalyze the first step of GPI biosynthesis, CaGpi2 is the key player involved in activating Ras signaling and hyphal morphogenesis. Activation of Ras signaling is independent of the catalytic competence of GPI-GnT
physiological function
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of the two Candida albicans Ras proteins, CaRas1 alone activates GPI-GnT activity, and the activity is further stimulated by constitutively activated CaRas1. Of the six subunits of the GPI-N-acetylglucosaminyltransferase (GPI-GnT) that catalyze the first step of GPI biosynthesis, CaGpi2 is the key player involved in activating Ras signaling and hyphal morphogenesis. Activation of Ras signaling is independent of the catalytic competence of GPI-GnT
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physiological function
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the enzyme is part of the enzyme complex that initiates glycosylphosphatidylinositol, GPI, biosynthesis, it catalyzes the first step of GPI anchor biosynthesis. CaGPI19 appears to be mutually regulated with ERG11
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