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This study utilized ER+ IBC to identify a metagene including ABAT and STC2 (show STC2 Proteins) as predictive biomarkers for endocrine therapy resistance.
A-to-G transition at nucleotide 754 of the human ABAT gene identified in lymphoblast cDNA (c.754A>G) results in substitution of an invariant arginine at amino acid 220 by lysine (p.Arg220Lys). This point mutation results in destabilization of the binding of pyridoxal-5'-phosphate to GABA-transaminase (required for transamination of GABA to succinic semialdehyde) and thus results in GABA-transaminase deficiency.
Findings point to a possible role of ABAT gene-regulated GABA catabolism for an altered processing of somatosensory stimuli as a potential vulnerability marker for affective disorders.
direct involvement of ABAT in pathways affecting lower esophageal sphincter (LES (show FUT3 Proteins)) control in gastro esophageal reflux disease
excessive prenatal GABA exposure in the central nervous system (CNS) is responsible for the clinical manifestations of GABA transaminase deficiency [case report]
Marked differences in platelet uptake of GABA and activity of catabolic enzyme GABA-T between patients with generalized and localization-related epileptic syndromes. May indicate an impairment in function of brain GABAergic systems.
results suggest that the Cys321 residue is essential for the catalytic function of GABAT, and that it is involved in the formation of a disulfide link between two monomers of human brain GABAT
lysine 357 is essential for catalytic function of brain GABA transaminase, and is involved in binding PLP (show PLP1 Proteins) at the active site
Analysis of the autistic disorder susceptibility locus suggests an association on chromosome 16p between GRIN2A (show GRIN2A Proteins) and ABAT.
Propionate-mediated inhibition of neuronal GABA transaminase, an enzyme of the inner mitochondrial membrane, indicates entry of propionate into neuronal mitochondria.Propionate-induced inhibition of energy metabolism in GABAergic neurons may render the striatum, in which >90% of the neurons are GABAergic, particularly vulnerable to degeneration in propionic acidemia
4-aminobutyrate aminotransferase (ABAT) is responsible for catabolism of gamma-aminobutyric acid (GABA), an important, mostly inhibitory neurotransmitter in the central nervous system, into succinic semialdehyde. The active enzyme is a homodimer of 50-kD subunits complexed to pyridoxal-5-phosphate. The protein sequence is over 95% similar to the pig protein. GABA is estimated to be present in nearly one-third of human synapses. ABAT in liver and brain is controlled by 2 codominant alleles with a frequency in a Caucasian population of 0.56 and 0.44. The ABAT deficiency phenotype includes psychomotor retardation, hypotonia, hyperreflexia, lethargy, refractory seizures, and EEG abnormalities. Multiple alternatively spliced transcript variants encoding the same protein isoform have been found for this gene.
4-aminobutyrate aminotransferase, mitochondrial
, 4-aminobutyrate aminotransferase
, (S)-3-amino-2-methylpropionate transaminase
, 4-aminobutyrate transaminase
, GABA aminotransferase
, GABA transaminase
, GABA transferase
, gamma-amino-N-butyrate transaminase
, beta-alanine oxoglutarate aminotransferase