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Results 1 - 8 of 8
EC Number
General Information
Commentary
Reference
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
malfunction
patients with GABA-T deficiency show severe, nonspecific neurological manifestations, including psychomotor retardation, epilepsy, hypotonia, and hyperreflexia
metabolism
GABA metabolism
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
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
physiological function
isoform GABA-T1 plays the predominant role in GABA metabolism in vegetative tissue
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
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
Results 1 - 8 of 8