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)

The usage of substrate inhibitor analysis made it possible to estimate the levels of excretion of plasma proteinases, including plasma kallikrein in the urinary DValLeuArgpNA (S-2266)- and DProPheArgpNA (S-2302)-amidase activity in patients with latent and nephrotic types of chronic glomerulonephritis (CGN). The soya bean trypsin inhibitor, an inhibitor of plasma kallikrein and other plasma proteinases, such as that of the blood coagulative factors XIa and XIIa, and the high selective plasma kallikrein inhibitor DPhePheArgCH2Cl were used as those differentiating kallikreins of tissue and plasma origin. The S-2266 and S-2302-amidase activity of the urine from healthy subjects was shown to be determined by only tissue (renal) kallikrein. The urine from the patients with a latent CGN type displayed the activity of plasma proteinases, but plasma kallikrein made no significant contribution to the urine amidase activity in these patients. With a nephrotic CGN type, great quantities of trypsin-like proteinases were secreted from the plasma through the glomerular filter into the urine, the proportion of plasma kallikrein in the urinary S-2266 and S-2302-amidase activities being approximately 27%. The compensatory and pathogenetic role of plasma kallikrein is discussed if there is lower excretion of tissue (renal) kallikrein in CGN with the nephrotic syndrome.
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PMID:[A substrate inhibitor analysis of the urinary excretion of tissue and plasma kallikreins in patients with chronic glomerulonephritis]. 227 58