Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.1.3.1 (alkaline phosphatase)
 47,916 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A series of deletions removing progressively larger parts of the 5' flanking region of the Escherichia coli pepD gene was constructed. After fusing the resulting promoter fragments to the chromosomal malPQ operon, their activities were determined by assaying for amylomaltase, the product of the malQ gene. Transcription from the pepD promoter region in exponentially growing cells was estimated to be about 5 times less efficient than transcription from the induced lac promoter. Approximately 115 bp preceding the translation start site of the pepD gene are important for regular promoter functioning, whereas the more distal sequences could be deleted without any significant effects. In bacterial cultures containing limiting amounts of inorganic phosphate, the rate of de novo synthesis of peptidase D, simultaneously with the derepression of alkaline phosphatase, increased about fivefold as a consequence of phosphate starvation. This regulation was shown to occur at the transcriptional level by the use of chromosomal pepD promoter-malPQ fusions. The inducibility by phosphate limitation was conserved in all of the deletion clones in which the pepD promoter region was still functional. As demonstrated by the use of phoB, R, and M mutants, the modulation of pepD expression is independent of the genetic system controlling the pho regulon.
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PMID:The promoter region of the Escherichia coli pepD gene: deletion analysis and control by phosphate concentration. 131 42

We describe here an easy method of determining prolidase (EC 3.4.13.9) in plasma after preincubation with Mn2+ for 24 h at 37 degrees C to maximize prolidase activity. The mean activity in 338 patients who were either in hospital or outpatients was 900 U/L +/- 520 (2 SD), unrelated to sex or age. In 25 of these 338 samples tested, prolidase activity was between 1500 and 2000 U/L. It exceeded 2000 U/L in eight, all of whom were patients with chronic liver disease. Plasma prolidase activity was normal in cytolytic syndromes such as liver or heart disease. Of the 27 patients with cirrhosis, only five exhibited prolidase activity greater than 2000 U/L. Plasma prolidase activity was uncorrelated with six biochemical indexes to liver function (the aminotransferases, alkaline phosphatase, glutamyltransferase, total bilirubin, and serum albumin) or with the degree of cirrhotic fibrosis. We believe that plasma prolidase activity may be high only in the early stage of fibrosis. This hypothesis would be consistent with the data on rat-liver collagenolytic activities during CCl4 administration. Monitoring of plasma prolidase activity might be useful in evaluating fibrotic processes in chronic liver disease in the human.
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PMID:Plasma prolidase activity: a possible index of collagen catabolism in chronic liver disease. 669 25

The developmental characteristics of liver injury induced by a delayed-type hypersensitivity (DTH) mechanism against picryl chloride were examined for 9 consecutive weeks in 3 mouse strains, BALB/c, Kunming and ICR mice. The changes of most biochemical parameters were similar in these three strains, namely, the activities of serum transaminases, lactic dehydrogenase, and prolidase were elevated significantly on day 1, during the first several weeks, and almost throughout the duration, respectively, of liver injury. The content of liver hydroxyproline was also increased after 1-9 weeks of liver injury. In addition, a significant decrease of liver weight, serum alkaline phosphatase and albumin level was observed in BALB/c and Kunming mice. Similar changes in liver histology were also found in the three strains. The hepatocellular necrosis and inflammatory infiltration into the portal area were the predominant features on day 1 and were still distinct during the subsequent several weeks. The mild or moderate hepatocellular degeneration, regeneration and connective tissue hyperplasia were observed after 1 or 3 weeks. A bridging necrosis between portal and portal was observed in several BALB/c and ICR mice, reflecting the possibility of exacerbation of liver injury. These results suggest that the liver injury could be caused and sustained by a one-shot DTH reaction to picryl chloride. The chronicity of the biochemical and histopathological characteristics may be helpful in elucidating the mechanisms of chronic development of liver injury.
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PMID:One-shot delayed-type hypersensitivity reaction in the mouse liver causes a sustained liver injury to picryl chloride. 919 86

Hypercalcemia and hypercalciuria observed both in humans and in animals who were on long-term theophylline therapy, prompted us to investigate whether oral theophylline treatment at optimal doses causes any adverse side effects on bone metabolism in mild asthmatics. Therefore, serum osteocalcin (BGP) and total alkaline phosphatase (TALP, EC 3.1.3.1) as bone formation markers, serum prolidase I (EC 3.4.13.9) activity as a marker for collagen metabolism, urinary deoxypyridinoline (Dpd), hydroxyproline (Hyp) and fasting urinary calcium as bone resorption markers, were measured in 18 mild asthmatics who had been treated with theophylline over 1-10 years. Among measured bone turnover markers, BGP, TALP, and Hyp levels were found to be increased in mild asthmatics; and BGP showed the greatest percent mean increase (98%) over the healthy subjects. However, these increments did not exceed the upper reference limits. Serum prolidase I activity was also increased in mild asthmatics receiving theophylline. Our results indicate that theophylline therapy at optimal doses may not exert adverse side effects on bone homeostasis, but patients receiving supratherapeutic doses of theophylline should be under close examination in order to predict future bone mass status.
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PMID:Evaluation of the effect of low-dose oral theophylline therapy on some bone turnover markers and serum prolidase I activity in mild asthmatics. 1043 80

Prolidase is a specific imidodipeptidase involved in collagen degradation. The increase in the enzyme activity is believed to be correlated with the increased intensity of collagen degradation. The aim of this study was to evaluate the serum prolidase activity and its relationship between bone turnover markers and bone mineral density (BMD) in postmenopausal osteoporosis. The study included 45 postmenopausal osteoporotic, 55 postmenopausal nonosteoporotic and 38 premenopausal healthy women. BMD was measured at the femoral neck and lumbar spine with DEXA. T score was more than 2.5 SD below the normal at the lumbar spine or femoral neck in postmenopausal osteoporotic patients. Serum levels of prolidase, C-terminal telopeptide of type I collagen (C-telopeptide), total alkaline phosphatase (ALP), osteocalcin (OC), urinary deoxypyridinoline (Dpd) and urinary creatinine were also assayed. C-telopeptide, total ALP, OC, urinary Dpd levels were significantly higher in postmenopausal osteoporotic group compared with premenopausal women. However, there was no statistical difference in serum prolidase activity between the three groups. There were also no significant correlations between serum prolidase and any biomarkers of bone turnover as well as BMD. To conclude, in postmenopausal osteoporotic women with increased bone turnover, serum prolidase concentration was not correlated with the biomarkers of bone formation or bone resorption and with BMD.
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PMID:Correlations of serum prolidase activity between bone turnover markers and mineral density in postmenopausal osteoporosis. 1653 21

The derangements in bone metabolism in patients with chronic renal failure (CRF) are summarized as uremic bone disease (UBD). In this study, we planned to determine the serum prolidase to compare it with the other biochemical markers. This study was performed on 44 patients (19 females, 25 males, mean age = 56.8 +/- 15.6 years) with endstage renal disease (ESRD). The patients were divided into three groups according to serum bone alkaline phosphatase (bAP) levels. The patients whose bAP was > or =77 U/L were accepted as having high-turnover UBD (n=18), the patients whose bAP was < or =50 U/L were accepted as having low-turnover UBD (n=14), and the patients whose bAP levels were between these two values were accepted as having bone disease with normal turnover (n=12). The serum prolidase levels did not increase in patients with ESRD. There were no significant differences between the serum prolidase levels of patients according to types of the UBD (p > 0.05). Kidney is the most prolidase-rich tissue of the human body. The serum prolidase activity is low in all patients with ESRD, irrespective of the type of UBD. Therefore, we concluded that prolidase had no value in the diagnosis of UBD.
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PMID:The role of prolidase activity in the diagnosis of uremic bone disease. 1677 Dec 40