GABA (Shorten Name),
General GABA/ Gamma-Aminobutyric acid ELISA Kit
Natural and recombinant general Gamma-Aminobutyric acid
Serum, plasma, tissue homogenates, cell culture supernates and other biological fluids
E0900Ge is a ready-to-use microwell, strip plate ELISA (enzyme-linked immunosorbent assay) Kit for analyzing the presence of the A Disintegrin and Metalloprotease 30 (Gamma-Aminobutyric acid) ELISA Kit target analytes in biological samples. The concentration gradients of the kit standards or positive controls render a theoretical kit detection range in biological research samples containing Gamma-Aminobutyric acid. The ELISA analytical biochemical technique of the E0900Ge kit is based on Gamma-Aminobutyric acid antibody-Gamma-Aminobutyric acid antigen interactions (immunosorbency) and an HRP colorimetric detection system to detect Gamma-Aminobutyric acid antigen targets in samples. The ELISA Kit is designed to detect native, recombinant, Gamma-Aminobutyric acid. Appropriate sample types may include undiluted human body fluids and/or tissue homogenates, secretions. Quality control assays assessing reproducibility identified the intra-assay CV (%) and inter-assay CV(%).
The linearity of the kit was assayed by testing samples spiked with appropriate concentration of Gamma-Aminobutyric acid and their serial dilutions. The results were demonstrated by the percentage of calculated concentration to the expected.
γ-Aminobutyric acid is the chief inhibitory neurotransmitter in the mammalian central nervous system. It plays a role in regulating neuronal excitability throughout the nervous system. In humans, GABA is also directly responsible for the regulation of muscle tone. Although chemically it is an amino acid, GABA is rarely referred to as such in the scientific or medical communities, because the term "amino acid," used without a qualifier, conventionally refers to the alpha amino acids, which GABA is not, nor is it ever incorporated into a protein. In spastic diplegia in humans, GABA absorption becomes impaired by nerves damaged from the condition's upper motor neuron lesion, which leads to hypertonia of the muscles signaled by those nerves that can no longer absorb GABA.
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