EC Number   |
General Information |
Reference |
|---|
   2.1.1.41 | metabolism |
key enzyme in the biosynthesis of ergosterol |
702673 |
| 2.1.1.41 | physiological function |
deletion of both isoforms SMT80 and SMT90 leads to a complete loss of C24-methylated sterols, which are replaced by cholestane-based sterols. SMT-null mutants are fully viable and replicative in culture but show increased sensitivity to sphingolipid synthesis inhibition. They are not particularly vulnerable to heat, acidic pH, nitrosative or oxidative stress, yet exhibit high mitochondrial membrane potential and increased superoxide generation. Mutants possess high levels of GPI-anchored glycoconjugates, but show significantly attenuated virulence in mice |
757688 |
| 2.1.1.41 | physiological function |
enzyme transfers either one or two methyl groups to the C-24 position of the sterol side chain producing both C28 and C29 24-alkylsterols in approximately the same proportions. Expression of SAM:SMT in a Saccharomyces cerevisiae Erg6 mutant restores its ability to produce ergosterol as the major sterol, and also results in low levels of C29 sterols such as pneumocysterol |
-, 745462 |
| 2.1.1.41 | physiological function |
expression of the Pneumocystis carinii enzyme in a Saccharomyces cerevisiae erg6 knockout mutant restores its ability to produce the C28 sterol ergosterol as the major sterol, and also results in low levels of C29 sterols. In the yeast, the Pneumocystis carinii enzyme appears to be less able to add a second methyl group at the methylene function. In the transformed strain, ergosterol is the major sterol component comprising 75.2% of total sterols |
734382 |
