Recombinant Human alpha-Aminoadipate Aminotransferase, CF

Kynurenine aminotransferase II (KAT‑II), also known as alpha‑Aminoadipate Aminotransferase (AADAT), catalyzes the PLP‑dependent transamination of aminoadipate to alpha‑oxoadipate in the catabolism of lysine in the liver and also is the primary brain enzyme catalyzing the transamination of kynurenine to kynurenic acid (KYNA) (1). KYNA is an endogenous antagonist of the N‑methyl‑D‑aspartate (NMDA) receptors with weaker effects on kainite and alpha‑amino‑3‑hydroxy‑5-methyl‑4‑isoxazole (AMPA) receptors, the other two ionotropic glutamate receptors (2, 3). KYNA also acts upon alpha‑7 nicotinic acetylcholine receptors ( alpha7 nAChRs) and importantly may suppress the pre-synaptic release of glutamate to confer neuroprotective effects against NMDA‑receptor mediated over‑stimulation. Also, KYNA is an endogenous ligand of the orphaned G protein-coupled receptor 35 (GPR35), found primarily in immune cells, and may induce inositol phosphate production and Ca2⁺ mobilizaiton (4). Elevated levels of KYNA have been implicated in Alzheimer's disease, Parkinson's disease, Huntington's disease, amyotrophic lateral sclerosis, epilepsy, schizophrenia and cognitive impairment (3, 5).