Human ABAT (4-aminobutyrate aminotransferase, mitochondrial) ELISA Kit

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Product specifications
Category | ELISA Kits |
Reactivity | Human |
Assay Data | 4 hours |
Assay Type | Sandwich ELISA, Double Antibody |
Test Range | 15.6-1000pg/ml |
Sensitivity | 9.375pg/ml |
Size 1 | 96T |
Tested Applications | ELISA |
Sample Type | Serum, Plasma, Cell Culture Supernatant, cell or tissue lysate, Other liquid samples |
Availability | Shipped within 10-14 working days. |
Storage | 2-8 °C for 12 months |
UniProt ID | P80404 |
Alias | GABA-AT,GABAT,NPD009,GABA transaminase |
Background | Elisa kits for ABAT |
Status | RUO |
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Human ABAT (4-aminobutyrate aminotransferase, mitochondrial) ELISA Kit
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ABAT antibody
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.
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4-Aminobutyrate Aminotransferase (ABAT) Antibody
ABAT Antibody is a Rabbit Polyclonal antibody against ABAT. 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.
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