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prolidase deficiency/alaniini
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5 tuloksia
Characterization of prolidase activity in erythrocytes from a patient with prolidase deficiency: comparison with prolidase I and II purified from normal human erythrocytes.
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OBJECTIVE
The purpose of this study was to investigate the effect of various amino acids and their metabolites on the activities of prolidase I and II from human erythrocytes compared to those in a patient with prolidase deficiency.
METHODS
Prolidase I and II from human erythrocytes were purified by
Effects of amino acids and its metabolites on prolidase activity against various iminodipeptides in erythrocytes from normal human and a patient with prolidase deficiency.
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BACKGROUND
The characteristics of prolidase in erythrocytes from controls and patient with prolidase deficiency were investigated.
METHODS
The erythrocytes were isolated from the heparinized blood of normal human and a patient with prolidase deficiency. Effects of various amino acids and their
Characteristics of prolinase against various iminodipeptides in erythrocyte lysates from a normal human and a patient with prolidase deficiency.
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The effect of various amino acids and MnCl2 on prolinase activity in erythrocyte lysates from a healthy individual and a patient with prolidase deficiency was investigated. A concentration of 0.1 mM MnCl2 increased prolinase activity in normal erythrocytes against pro-gly, pro-glu, pro-leu, pro-ser
Different effects of sulfur amino acids on prolidase and prolinase activity in normal and prolidase-deficient human erythrocytes.
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BACKGROUND
Prolidase and prolinase activity is known to be enhanced significantly in some diseases. Recently, the effect of amino acids on prolidase and prolinase activity in normal and prolidase-deficient human erythrocytes was investigated. It was reported that both enzymes were enhanced by
Identification and analysis of a novel mutation in PEPD gene in two Kashmiri siblings with prolidase enzyme deficiency.
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Prolidase deficiency (PD) is a rare inborn disorder of collagen metabolism characterized by chronic recurrent cutaneous ulceration. We report a novel 3 bp insertion in the 12th exon of the PEPD gene in two Kashmiri siblings with prolidase deficiency phenotype. This mutation results in addition of an
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