Target intelligence / Profile preview

4-aminobutyrate transaminase (GABA-T)

Target
GABA-T
Molecular classification
Enzyme, Transaminase
01

Overview

4-aminobutyrate transaminase (GABA-T), also known as GABA transaminase, is a mitochondrial enzyme (EC 2.6.1.19) that plays a critical role in the catabolism of gamma-aminobutyric acid (GABA), the primary inhibitory neurotransmitter in the central nervous system. As a key component of the GABA shunt pathway, GABA-T converts GABA and α-ketoglutarate into succinic semialdehyde and glutamate. By regulating the breakdown of GABA, this enzyme controls its synaptic concentrations and modulates inhibitory tone in the brain. Pharmacological inhibition of GABA-T, for instance by vigabatrin, is a strategy used in antiepileptic therapies to increase GABA levels and enhance inhibitory neurotransmission.

Other names
GABA transaminase4-aminobutyrate aminotransferaseEC 2.6.1.19
02

Mechanism of action

Inhibition of GABA transaminase (GABA-T) leads to increased GABA levels in the central nervous system, thereby enhancing inhibitory neurotransmission. For example, vigabatrin irreversibly inhibits GABA-T.

03

Biological functions

Neurotransmitter metabolism (GABA catabolism)Regulation of neurotransmitter levels (GABAergic tone)Involvement in GABA shunt pathway
04

Disease associations

Epilepsy (pharmacological target)Neurodegenerative disease (dysregulation)Psychiatric disorders (dysregulation)
05

Safety considerations

Vigabatrin: visual field defects and retinal toxicity (associated with drug targeting GABA-T)Disrupted GABA catabolism leading to metabolic/neurological dysfunction, seizures, encephalopathy (due to deficiency or excessive inhibition)
06

Interacting drugs

Vigabatrin
07

Biomarkers

Elevated or reduced levels of GABA in cerebrospinal fluid or brain

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