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1 g treatment with the glial cell toxin, alpha-aminoadipic acid.
2 AI lysine modification to chlorolysine and 2-aminoadipic acid.
3 and rate of the metabolism of an L-[1-13C]-2-aminoadipic acid ([13C]AAA) tracer and of whole-body L-[
5 llysine, ALL) and its oxidized end-product 2-aminoadipic acid (2-AAA) were determined as a function o
6 n to glutamate was also blocked by L-2-alpha aminoadipic acid, a selective astrocyte toxin, and paxil
7 rogenase in liver and plasma levels of alpha-aminoadipic acid (AAA), both of which act as indicators
10 , including lysine and its metabolite, alpha-aminoadipic acid (alpha-AA), a predictor for developing
11 oxylate (P6C), pipecolic acid (PA) and alpha-aminoadipic acid (alpha-AAA) in plasma, serum, dried blo
13 increase in arterial concentrations of alpha-aminoadipic acid arising from increased conversion from
14 However, we find that the activity of alpha-aminoadipic acid-delta-semialdehyde (AAS) dehydrogenase
16 h a glutamate transporter substrate (l-alpha-aminoadipic acid) increased the neuronal firing rate, su
18 either of the selective glial toxins L-alpha-aminoadipic acid (L-AA) or fluorocitrate (FC) blocked mG
20 ) exhibited elevated serine, tyrosine, and 2-aminoadipic acid levels, indicating enhanced amino acid
22 kainate (KA), dihydrokainate (DHK) and alpha-aminoadipic acid produced less than 30% inhibition at 1
23 cid, asparagine, fructose, arachidonic acid, aminoadipic acid, sorbitol, retinol, tryptophan, niacina
24 is pathway catalyzes the conversion of alpha-aminoadipic acid to alpha-aminoadipic-delta-semialdehyde