EC Number   |
General Information |
Reference  |
|---|
    2.6.1.19 | metabolism |
GABA metabolism |
698627 |
| 2.6.1.19 | physiological function |
GABA-T acts in salt responses in linking N and C metabolisms in roots, GABA-T is the most responsive step of GABA metabolism upon NaCl stress |
702914 |
| 2.6.1.19 | physiological function |
isoform GABA-T1 plays the predominant role in GABA metabolism in vegetative tissue |
704882 |
| 2.6.1.19 | malfunction |
patients with GABA-T deficiency show severe, nonspecific neurological manifestations, including psychomotor retardation, epilepsy, hypotonia, and hyperreflexia |
704969 |
| 2.6.1.19 | malfunction |
constitutive overexpression lines of GABA-T are generated in Arabidopsis. Brief cold treatments increases leaf GABA concentrations in both the WT and transgenic line OX1, but the concentrations in OX1 is consistently lower. These findings confirm that GABA-T limits the catabolism of GABA when its production is stimulated by stress, and suggest a bioengineering strategy for improving the availability of succinate semialdehyde for the Krebs cycle or GLYR1, a potential redox-modulating reaction during stress |
721953 |
| 2.6.1.19 | physiological function |
mutations in the enzyme cause an autosomal recessive neurometabolic disorder and mitochondrial DNA depletion syndrome (MDS). ABAT functions in the mitochondrial nucleoside salvage pathway to facilitate conversion of dNDPs to dNTPs. Inhibition of ABAT by Vigabatrin causes depletion of mtDNA in photoreceptor cells that is prevented through addition of dNTPs in cell culture media |
738002 |
| 2.6.1.19 | physiological function |
loss of GABA transaminase increases sleep, and affects metabolism such that flies lacking GABA transaminase fail to survive on carbohydrate media. GABA degradation product glutamate, rather than succinic semialdehyde, accounts for the metabolic phenotype of the mutants. Inhibition of GABA transaminase affects energetic pathways. Mutants display a general disruption in bioenergetics. The effects of GABA transaminase on sleep do not depend upon glutamate, indicating that GABAT regulates metabolic and sleep homeostasis through independent mechanisms |
738656 |
| 2.6.1.19 | physiological function |
Arabidopsis thaliana GABA-T functionally complements a Saccharomyces cerevisiae Uga1 mutant lacking GABA transaminase activity, despite mitochondrial localization of the Arabidopsis thaliana enzyme and cytosolic localization of the yeast enzyme. Recombinant GABA-T rescues mutant yeast's GABA growth defect, thermosensitivity and limiting production of reactive oxygen species, but GABA-T is about half as efficient in doing so Saccharomyces cerevisiae Uga1 gene product |
739761 |
| 2.6.1.19 | physiological function |
production of glutaric acid depends on the expression of native gabT (EC 2.6.1.48) and gabD of Corynebacterium glutamicum, or on heterologous expression of davT (EC 2.6.1.48) and davD (EC 1.2.1.20) from Pseudomonas putida encoding 5-aminovalerate aminotransferase, and glutarate semialdehyde, respectively |
754623 |
| 2.6.1.19 | more |
homology structure modeling using pig ABAT as template (PDB ID 6B6G) |
758692 |
