1.14.11.8: trimethyllysine dioxygenase
This is an abbreviated version!
For detailed information about trimethyllysine dioxygenase, go to the full flat file.
Word Map on EC 1.14.11.8
-
1.14.11.8
-
carnitine
-
gamma-butyrobetaine
-
autism
-
inborn
-
proliferator-activated
-
hydroxymethyltransferase
-
transporter-2
-
aldolase
- 1.14.11.8
- carnitine
- gamma-butyrobetaine
-
autism
-
inborn
-
proliferator-activated
- hydroxymethyltransferase
-
transporter-2
- aldolase
Reaction
Synonyms
6-N-trimethyllysine dioxygenase, epsilon-N-trimethyllysine hydroxylase, epsilon-trimethyllysine 2-oxoglutarate dioxygenase, eta-N-trimethyllysine hydroxylase, Nepsilon-trimethyllysine hydroxylase, oxygenase, trimethyllysine di-, TML dioxygenase, TML hydroxylase, TML-alpha-ketoglutarate dioxygenase, TMLD, TMLH, TMLH-a, TMLH-b, trimethyllysine alpha-ketoglutarate dioxygenase, trimethyllysine hydroxylase
ECTree
Advanced search results
Engineering
Engineering on EC 1.14.11.8 - trimethyllysine dioxygenase
Please wait a moment until all data is loaded. This message will disappear when all data is loaded.
D244E
the Km-value of the variant enzyme for N6,N6,N6-trimethyl-L-lysine is 3.7fold lower than the Km-value of the wild-type enzyme, the Km-value of the variant enzyme for 2-oxoglutarate is 2.7fold higher than the Km-value of the wild-type enzyme
T269A
the Thr269Ala variant displays high enzymatic activity (96% at 0.10 mM, 76% at 0.003 mM) for the conversion of (2S)-Nepsilon-trimethyllysine to (2S,3S)-3-hydroxy-Nepsilon-trimethyllysine
W221F
the variant displays considerably reduced enzymatic activity (32%), implying that the OH group of Tyr404 contributes to stronger interaction with the trimethylammonium group of (2S)-Nepsilon-trimethyllysine
Y217D
the variants does not display any enzymatic activity within limits of detection
Y217E
the Thr269Ala variant displays high enzymatic activity (96% at 0.10 mM, 76% at 0.003 mM) for the conversion of (2S)-Nepsilon-trimethyllysine to (2S,3S)-3-hydroxy-Ne-trimethyllysine
additional information
construction of senescence marker protein-30/gluconolactonase knockout mice, which cannot synthesize L-ascorbate in vivo, the mutant mice nevertheless produce normal levels of carnitine when fed an L-ascorbate lacking diet