Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.5.1.4 (deaminase)
 5,113 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Tryptophan and some indolic metabolites were studied in urine, plasma and dialysate of uraemic patients using thin-layer- and high-pressure liquid chromatography. Some new metabolites: indole-3-carboxylic acid, indole-3-carbaldehyde, indolelactic acid and N-acetyltryptophan were detected. Levels of the latter two metabolites in urine, dialysate and especially plasma suggest increased transamination of tryptophan and a possible defect in renal amino acid acylase in uraemia.
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PMID:Indolic tryptophan metabolism in uraemia. 93 25

Deacetylations of N-acetylhistidine and N-acetyltryptophan were examined in vivo by their administration to mice and rats. N-Acetylhistidine accumulated preferentially in the kidney and was converted to histidine effectively by acylase I. Similar deacetylation of N-acetyltryptophan by acylase III was also observed. Acylase I and III activities in mouse kidney increased in parallel remarkably at the period of weaning. A hypothesis that the acylase system in mammalian kidneys is a mechanism acquired to utilize amino acids from exogenous and endogenous acyl derivatives including those derived from protein hydrolysis was offered.
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PMID:In vivo deacetylation of N-acetyl amino acids by kidney acylases in mice and rats. A possible role of acylase system in mammalian kidneys. 735 28