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DELTAFgGCS1
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a null mutation of the FgGCS1 gene becomes resistant to antifungal defensins MsDef1, but not to MtDef4 from Medicago. It shows a significant change in the conidial morphology and displays dramatic polar growth defect, and its mycelia are resistant to cell wall degrading enzymes.GCS1 is not required for pathogenicity of Fusarium graminearum
C143A
site-directed mutagenesis, increased activity, reduced expression level compared to wild-type
C207A
site-directed mutagenesis, reduced activity, reduced inhibitory effect of N-ethylmaleimide, reduced expression level compared to wild-type
C213A
site-directed mutagenesis, reduced activity, reduced expression level compared to wild-type
C232A
site-directed mutagenesis, reduced expresssion level compared to wild-type
C290A
site-directed mutagenesis, reduced expression level compared to wild-type
C296A
site-directed mutagenesis, reduced activity, reduced expression level compared to wild-type
C321A
site-directed mutagenesis, reduced activity
C321A/C323A
site-directed mutagenesis, reduced activity
C343A
site-directed mutagenesis, enhanced activity, slightly reduced expression level compared to wild-type
C384A
site-directed mutagenesis, enhanced activity
C86A
site-directed mutagenesis, reduced activity, reduced expression level compared to wild-type
C98A
site-directed mutagenesis, reduced activity, reduced expression level compared to wild-type
H169A
26.4% activity compared to wild-type, reduced inhibition by diethyldicarbonate and increased protection by UDP-glucose
H193A
33.0% activity compared to wild-type, reduced inhibition by diethyldicarbonate and reduced protection by UDP-glucose
H193N
23.0% activity compared to wild-type, reduced inhibition by diethyldicarbonate and reduced protection by UDP-glucose
H26A
5.2% activity compared to wild-type
H26D
10.5% activity compared to wild-type
H26N
44.5% activity compared to wild-type
H26R
118.5% activity compared to wild-type, slightly enhanced inhibition by diethyldicarbonate and slightly reduced protection by UDP-glucose
H308A
35.2% activity compared to wild-type, slightly reduced inhibition by diethyldicarbonate and slightly reduced protection by UDP-glucose
H308A/H309A
10.8% activity compared to wild-type
H309A
69.1% activity compared to wild-type
H322A
3.8% activity compared to wild-type
H322D
2.6% activity compared to wild-type
H322N
49.8% activity compared to wild-type, slightly enhanced inhibition by diethyldicarbonate and slightly reduced protection by UDP-glucose
H36A
103.2% activity compared to wild-type, slightly enhanced inhibition by diethyldicarbonate and slightly reduced protection by UDP-glucose
H90A
119.3% activity compared to wild-type
additional information
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animals lacking CGT do not synthesize glycosphingolipids, arrest growth at the first larval stage, and display defects in a subset of cells in their digestive tract, restoring CGT function in these digestive tract cells but not in a variety of other tissues is sufficient to rescue the phenotypes associated with loss of CGT function
additional information
animals lacking CGT do not synthesize glycosphingolipids, arrest growth at the first larval stage, and display defects in a subset of cells in their digestive tract, restoring CGT function in these digestive tract cells but not in a variety of other tissues is sufficient to rescue the phenotypes associated with loss of CGT function
additional information
animals lacking CGT do not synthesize glycosphingolipids, arrest growth at the first larval stage, and display defects in a subset of cells in their digestive tract, restoring CGT function in these digestive tract cells but not in a variety of other tissues is sufficient to rescue the phenotypes associated with loss of CGT function
additional information
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loss of enzyme function by RNA interference leads to increased apoptotic cell death, conversely targeted expression of the enzyme can rescue cell death, overview
additional information
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antisense expression inhibits enzyme activity
additional information
Ugcg flox/flox, mice that lack oligodendroglial expression of Ugcg, no influence on glycosphingolipid content in brain and myelin extracts
additional information
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deletion mutants, lacking the first 10 or the last 8 amino acid residues, show only 4% of the wild-type activity