EC Number |
Protein Variants |
Reference |
---|
2.3.1.42 | DHAPATDELTA135 |
the mutant enzyme is completely inactive |
755947 |
2.3.1.42 | K852L |
mutant shows no activity and fails to support normal growth and survival during the stationary phase |
720841 |
2.3.1.42 | more |
construction of a DELTAmdat/DELTAlmdat null mutant results in complete abrogation of the parasite dihydroxyacetone phosphate acyltransferase activity, lack of LmDAT causes a major alteration in parasite division during the logarithmic phase of growth, an accelerated cell death during stationary phase, and loss of virulence in mice, phenotype, overview |
674766 |
2.3.1.42 | more |
deficient cell line caused by DNA 128 bp deletion leading to premature stop, strongly reduced activity |
486971 |
2.3.1.42 | more |
deletion analyses show that the large N-terminal extension of this initial acyltransferase may be important for its stability or activity. Abrogation of the C-terminal glycosomal targeting signal sequence of LmDAT lead to extraglycosomal localization, do not impair its enzymatic activity but affect synthesis of the ether glycerolipid-based virulence factor lipophosphoglycan |
720841 |
2.3.1.42 | more |
enzyme amount is reduced by 90% in Zellweger syndrome |
486972 |
2.3.1.42 | more |
null mutant deltalmdat/deltalmdat, and complemented null mutant, double mutants with additional loss of glycerol-3-phosphate acyltransferase (LmGAT) are not viable, thus, these two may be the only acyltransferases |
-, 705601 |
2.3.1.42 | more |
null mutations of GAT1 andGAT2 are lethal |
486391 |
2.3.1.42 | more |
patients affected with rhizomelic chondrodysplasia punctata show reduced enzyme activity due to a defect in peroxisomal targeting, point mutation at nucleotide 848 leading to a premature stop |
486971 |