|Other Names||4-aminobutyrate aminotransferase, mitochondrial, (S)-3-amino-2-methylpropionate transaminase, GABA aminotransferase, GABA-AT, Gamma-amino-N-butyrate transaminase, GABA transaminase, GABA-T, L-AIBAT, ABAT, GABAT|
|Format||The synthetic peptide was lyophilized with 100% acetonitrile and is supplied as a powder. Reconstitute with 0.1 ml deionized water for a final concentration of 1 mg/ml.|
|Storage||Maintain refrigerated at 2-8°C for up to 6 months. For long term storage store at -20°C.|
|Precautions||This product is for research use only. Not for use in diagnostic or therapeutic procedures.|
|Function||Catalyzes the conversion of gamma-aminobutyrate and L- beta-aminoisobutyrate to succinate semialdehyde and methylmalonate semialdehyde, respectively. Can also convert delta-aminovalerate and beta-alanine.|
|Cellular Location||Mitochondrion matrix.|
|Tissue Location||Liver > pancreas > brain > kidney > heart > placenta|
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Provided below are standard protocols that you may find useful for product applications.
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.
Chakrabarti, B., et al. Autism Res 2(3):157-177(2009)Inada, T., et al. Pharmacogenet. Genomics 18(4):317-323(2008)Wu, C., et al. Proteomics 7(11):1775-1785(2007)
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