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1 hesis of NAD (+) and clearing the neurotoxin quinolinate.
2 he phthalate catabolic pathway cometabolizes quinolinate.
5 e enzymatic product subsequently cyclizes to quinolinate, an intermediate in the biosynthesis of nico
7 elis complex is approximated by PRPP and the quinolinate analogue phthalate bound to the active site.
8 formation of nicotinate mononucleotide from quinolinate and 5-phosphoribosyl-1-pyrophosphate (PRPP).
10 ntrastriatal injection of either malonate or quinolinate and systemic administration of 3-NP resulted
16 cted outside the needle track 10 hours after quinolinate injection and, on average, 20% of neurons ex
17 ced hippocampal cell death, are resistant to quinolinate, malonate, and 3-nitropropionic acid (3-NP).
19 of two metabolic pathways: the tryptophan to quinolinate pathway and the bacterial 2-nitrobenzoic aci
24 e biosynthetic pathway including NtPMT1a and quinolinate phosphoribosyltransferase (NtQPT2), and lowe
27 tion of a bottleneck enzyme in this pathway, quinolinate phosphoribosyltransferase (QPRT) may contrib
29 tructural similarities between phthalate and quinolinate: phthalate is a competitive inhibitor of thi
30 When supplied as the sole NAD precursor, quinolinate promoted B. bronchiseptica growth, and the a
31 metabolism of tryptophan and accumulation of quinolinate (QA) as a metabolic node in glioblastoma and
39 entified by MutMap in the encoding region of Quinolinate Synthase (QS) gene required for the de novo
41 chosen the [4Fe-4S] cluster-dependent enzyme quinolinate synthase to illustrate each one of these pro
43 study concludes that all currently annotated quinolinate synthases harbor a [4Fe-4S] cluster, that th
44 the biosynthetic pathway from tryptophan to quinolinate, the universal de novo precursor to the pyri
45 sis by limiting the conversion of downstream quinolinate to NAD(+), a profile recapitulated in aging
46 ratios of 3-sialyllactose to xanthosine and quinolinate to X-16397 and our previously reported urina
47 e, fumarate, hypoxanthine, acetone, leucine, quinolinate, valine, O-acetylcarnitine, citrate, and tri
49 metabolites (kynunerate, 8-methoxykyunerate, quinolinate) were higher in patients who developed AKI.