Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P00790 (PGA)
 2,475 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Antiserum raised in rabbits against the FBP obtained from CML cells, and the purified binder labeled with 125I, have been used for an RIA which can measure an immunologically similar protein in human serum. The concentration of the binding protein in normal serums ranged from 1.2 to 9.3 ng/ml, with a mean +/- S.E.M. of 3.8 +/- 0.4 ng/ml. Elevated values of the binder protein were measured in the serums from patients with folate deficiency, vitamin B12 deficiency, liver disease, uremia, myeloproliferative disease, chronic lymphocytic leukemia, and various types of cancer and in the serum from pregnant women. The concentration of the binder protein and the capacity of the serum to specifically bind isotopically labeled PGA correlated poorly, indicating that the binding protein concentration and degree of saturation by endogenous serum folate vary independently in many instances.
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PMID:The identification and measurement of a folate-binding protein in human serum by radioimmunoassay. 27 99

Prostaglandins A1, B1, E2, Falpha and PRA have been measured by radioimmunoassay in peripheral or renal venous blood of different groups of hypertensive and control subjects. PGA1 and PGE2 were significantly increased in renal, renovascular, labile and essential hypertension. PGFalpha was significantly increased only in patients with unilateral renal atrophy and in some patients with renovascular and essential hypertension. There was a significant positive correlation between PRA and PGA1 or B1, but not with PGE2 or Falpha. The increase of PGA and PGE represents a secondary antihypertensive, diuretic and natriuretic mechanism, the increase of PGF a direct hypertensive mechanism.
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PMID:Prostaglandins and high blood pressure. 35 39

Microsomal fractions of cells isolated from chick epiphyseal cartilage catalyzed the synthesis of prostaglandins from radiolabeled delta8,11,14-eicosatrienoic and from arachidonic acids. In addition, the microsomal supernatants contained both 15-hydroxyprostaglandin dehydrogenase and prostaglandin 15-keto delta13,14-reductase activities. Two major classes of prostaglandins (E and F) were synthesized; however, a major product which chromatographically behaves as PGA was also isolated. Synthetase activities were analyzed for pH optima and response to known stimulators and inhibitors of prostaglandin systhesis. The different activators had varying stimulatory effects on prostaglandin synthesis; the anti-inflammatory drugs were all strongly inhibitory. Synthetase activity in the growth plate was highest in the zone of hypertrophy, declining substantially in the more heavily calcified regions. Degradative enzyme activities were highest in the zone of maturation and significantly lower in the adjacent hypertrophic zone. The net effect of these opposing activities would be to elevate prostaglandin levels at the zone of hypertrophy, a finding which suggests that prostaglandins may play a role in the modulation of epiphyseal cartilage metabolism.
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PMID:Biosynthesis and metabolism of prostaglandins in chick epiphyseal cartilage. 41 62

The binding sites for methylfolate of the FABP in serum are fully saturated in the physiological state. When the FABP of serum from pregnant subjects is stripped of its endogenous folate, it is capable of binding an average of 549 +/- 12 pg/ml (range 464 to 723) of 14C-methylfolate, compared with 736 +/- 57 pg/ml (range 491 to 1610) of 3H-PGA. When 3H-PGA is added to untreated serum, an average of 258 +/- 6 pg/ml (range 218 to 325) is bound by FABP; this binding represents sites available to PGA but not to methylfolate, as well as sites from which methylfolate is displaced by 3H-PGA. This displacement averages 71 +/- 10 pg/ml (range 9 to 142), the amount which the standard technique for measurement of the UFBC for 3H-PGA overestimates the true UFBC for PGA.
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PMID:Binding of methylfolate and pteroylglutamic acid by the specific serum folate binder. 42 35

Previous studies have reported indirect evidence for the mediation of folate antagonism in the induction of malformations by diphenylhydantion. We have demonstrated that a teratogenic regimen of folate-deficiency and antagonism using 9-methyl PGA in the rat produces significantly decreased rates of oxygen consumption in the maldeveloping embryos. The present study reports similar reductions in oxygen uptake by mouse embryos from mothers treated with teratogenic doses of diphenylhydantoin, and documents a significant depression of the actual folate levels in such embryos. The differences are less significant with lower doses of diphenylhydantoin, and do not occur with a nonteratogenic dose.
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PMID:Folate antagonism following teratogenic exposure to diphenylhydantoin. 45 36

The development of the exocrine pancreas has been determined quantitatively in 31 infants with cystic fibrosis (CF) both with and without meconium ileus and in 29 control infants. In the normal pancreas, the ratio of acinar to connective tissue volume is 0.5 at 32 weeks postconceptional age (PCA) and increases linearly to 2.0 at 52 weeks PGA. In cystic fibrosis infants, with or without meconium ileus, the ration is 0.5 at 35 weeks PCA anddecreases linearly to 0.3 at 52 weeks PCA. The volume of acinar and duct lumens is greater in CF than control infants but is independent of age or acinar volume. The development of the exocrine pancreas in infants with CF with and without meconium ileus diverges from the normal pattern: There is consistent lack of exocrine tissue before or a full-term birth, which persists throghout the age range of this study. CF infants above 42 weeks PCA can be discriminated from controls on the basis of the quantitative assessment of acinar volume.
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PMID:Quantitative evaluation of the development of the exocrine pancreas in cystic fibrosis and control infants. 45 30

Prostaglandins (PGs) participate in the inflammatory response, but the contribution of endogenously synthesized PGs to edema formation and increased vascular permeability is not known. Using a 10% scald burn in the rat, we measured water content (as percent, wet minus dry/wet weight) and 131I-RISA leakage (counts/g dry tissue) in scalded and normal skin at 30 minutes and 3 hr post injury. Four groups (10 rats/group) in each time period studied: control; scald; scald, 5 mg/kg indomethacin; scald, 10 mg/kg indomethacin. Indomethacin was administered intravenously 30 minutes before the scald; RISA was injected intravenously 30 min before termination of the study. In all indomethacin-treated groups immunoreactive plasma PGA was significantly lower (p less than 0.05) than in scalded, untreated groups. All scalded groups showed significantly higher RISA counts and water content than did the control group (p less than 0.01). At 30 min post-injury the indomethacin -treated groups did not differ from the untreated scald group (p greater than 0.20). In the 3 hour study all scalded groups had significantly higher content and RISA counts than control (p less than 0.01). Thus PGs produced during thermal trauma do not greatly contribute to the edema formation and increase in vascular permeability.
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PMID:Effect of inhibiting prostaglandin synthesis on edema formation and albumin leakage during thermal trauma in the rat. 50 95

Ten tryptophan residues per one protein molecule were found to be present in the enolase from human and swine muscle. In Tris buffer, N-bromosuccinimide (NBS) inactivated the enolases after oxidation of all 10 tryptophan residues. The presence of 2-phosphoglycerate (2-PGA) partially protected the activity, and in the presence of 2-PGA together with Mg2+ full protection was observed. In phosphate buffer, only 6 tryptophan residues could be oxidized, but the enzyme was fully inactivated. 2-PGA made possible the oxidation of all 10 tryptophan residues, concomitant with full inactivation. In either case, Mg2+ had no effect. The Km values and pH optima were the same for the native and partially NBS-modified enolases.
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PMID:The reaction of N-bromosuccinimide with enolase. 61 Feb 83

Plasma prostaglandins were determined by radioimmunoassay in 92 pregnant and 14 nonpregnant women. There was significant elevation of PGA-like material in the first trimester of pregnancy (1744 pg/ml) over that seen in nonpregnant women (576 pg/ml) with continuation of that elevation in the second and third trimesters. No significant difference existed among PGE levels of the nonpregnant group (251 pg/ml) and the first two trimesters of pregnancy (384 pg/ml and 294 pg/ml); the PGE level of the third trimester group (443 pg/ml) was significantly elevated over that of the nonpregnant group. PGF levels remained constant during all trimesters (135 pg/ml, 144 pg/ml, and 130 pg/ml) but exhibited plasma concentrations significantly higher than the nonpregnant group (78 pg/ml). Potential role (s) of prostaglandins as mediators of cardiovascular and renal changes of pregnancy are discussed.
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PMID:Plasma prostaglandins in pregnancy. 61 37

The earlier radioimmunoassays were mainly intended for the measurement of prostaglandins of the E-F-A or B type in blood plasma/serum or urine. Many recent studies, however, explain the use of radioimmunoassay to measure the prostaglandin content of tissues, and many other studies are concerned with the prostaglandin production in a single cell type, or in a few cell types, rather than the whole tissue. To date, however, by far the greatest number of quantitative prostaglandin studies have been carried out on blood plasma or serum, while assay for primary prostaglandins are now fairly seldom applied to the peripheral circulation, unless it is to study the prostaglandin production in vivo. It has been proposed that prostglandins of the A type are circulating hormones in contrast to other prostglandins, and a number of laboratories have developed quantitative methods for the measurements of PGA compounds. The sensitivity and specificity of the prostaglandins radioimmunoassays have increased considerably in later years through the use of labelled ligands of better quality; on the other hand, the accuracy of many radioimmunoassays seems to be very low when they are applied to biologic materials.
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PMID:Radioimmunoassay of prostaglandins. 62 74


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