Mouse 4-Aminobutyrate Aminotransferase, Mitochondrial (ABAT) ELISA Kit

Product specifications

ELISA Kits

4-Aminobutyrate Aminotransferase, Mitochondrial (ABAT)

Mouse

Colorimetric

Quantitative

Optimal dilutions/concentrations should be determined by the end user.

96 tests

Lyophilized

ELISA

Serum, plasma, tissue homogenates, cell culture supernatants and other biological fluids.

Shipped within 5-15 working days. The validity for this kit is 6 months.

Shipped at 4 °C. Upon receipt, store the kit according to the storage instruction in the kit's manual.

No

GABA-AT,GABAT,NPD009,GABA transaminase

Elisa kits for ABAT

RUO

Validity: The validity for this kit is 6 months.
This product is for research use only.   The range and sensitivity is subject to change. Please contact us for the latest product information. For accurate results, sample concentrations must be diluted to mid-range of the kit. If you require a specific range, please contact us in advance or write your request in your order comments.   Please note that our ELISA and CLIA kits are optimised for detection of native samples, rather than recombinant proteins. We are unable to guarantee detection of recombinant proteins, as they may have different sequences or tertiary structures to the native protein.

Descripción

4-Aminobutyrate Aminotransferase (ABAT), also known as GABA transaminase, is a mitochondrial enzyme that plays a crucial role in the metabolism of gamma-aminobutyric acid (GABA), the primary inhibitory neurotransmitter in the central nervous system. ABAT catalyzes the conversion of GABA to succinic semialdehyde, which is subsequently converted to succinate and enters the tricarboxylic acid (TCA) cycle, linking GABA metabolism to energy production. This process is critical for maintaining GABAergic tone and neurotransmitter balance in the brain. Dysregulation of ABAT activity has been implicated in neurological and psychiatric disorders, including epilepsy, anxiety, depression, and schizophrenia, where altered GABA levels contribute to pathophysiology. Mutations in the ABAT gene can result in disorders such as GABA-transaminase deficiency, characterized by severe developmental delays, seizures, and hypotonia. ABAT is also a target for anticonvulsant drugs like vigabatrin, which inhibit its activity to increase GABA levels and reduce neuronal excitability. Beyond its role in the nervous system, ABAT has emerging significance in cancer biology, as its expression is altered in certain tumors, influencing metabolic pathways and tumor progression.

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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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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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