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)

The DNA content of lymphocytes and of basal cells from normal hairless mouse epidermis was measured by microflow fluorometry (MFF). To obtain a relatively pure suspension of epidermal basal cells a combined mechanical and enzymatic method was used. The admixture of differentiating cells into the basal cell fraction after cell separation was 13%. The results were compared with those obtained with conventional Feulgen microspectrophotometry applied to basal cells and dermal lymphocytes in histologic sections. The results from both cytophotometric methods were in good agreement and clearly demonstrated the improved resolution obtained by using microflow fluorometry. When the lymphocytes were not treated with pepsin before being stained with ethidium bromide for MFF, the modal DNA value was consistently below that of the basal cells from the same specimen. Pepsin treatment of lymphocytes, however, increased their fluorescence intensity to the value of epidermal basal cells. The modal DNA value of Feulgen-stained dermal lymphocytes in histologic sections was consistently below that of epidermal basal cells from the same section. The advantage of pepsin treatment for obtaining higher resolution of DNA measurements of basal and differentiating epidermal cells and of lymphocytes was evaluated. The cell cycle distribution of basal cells from epidermis in different states of proliferative activity was determined. Changes in the proportion of cells in S phase were parallel to changes in the 3H-Tdr labeling index.
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PMID:Separation of mouse epidermal basal and differentiating cells for microflow fluorometric measurements: a methodologic study. 82 57

Patients who had cranial injuries and those who were less severely injured had a normal gastric acid output. Pepsin output decreased throughout the first 72 hours after trauma. Gastric juice protein output was slightly increased. Gastric mucosal cell renewal as estimated by gastric juice DNA was increased. Patients who were more severely injured and those with intra-abdominal trauma had markedly increased gastric acid, pepsin, and protein output after increased gastric mucosal cell exfoliation but a relatively decreased gastric mucosal cell renewal between 36 and 72 hours after trauma. It is concluded that the gastric mucosa must be protected by antacids and/or gastric aspiration before 24 hours after trauma and continued through at least 72 hours. This study supports the importance of acid-pepsin damage during gastric mucosal cell exfoliation and decreased renewal in trauma patients and indicates the timing and value of prophylactic treatment.
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PMID:Prospective studies of gastric secretion in trauma patients. 110 89

Familial multiple endocrine neoplasia type 1 (MEN 1) is an autosomal dominant disorder characterized by the combined occurrence of tumors of the parathyroid glands, the endocrine pancreas, and the pituitary gland. MEN 1 tumors have previously been shown to be associated with the loss of alleles on chromosome 11, and deletion mapping studies together with family linkage studies have localized the MEN 1 gene to 11q13. A detailed genetic map around the MEN 1 locus is required to facilitate further characterization and cloning of the gene (MEN1). We have characterized a panel of seven rodent-human somatic cell hybrids which contain fragments of human chromosome 11 with breakpoints in the pericentromeric region by using eight DNA sequences (D11S149, PGA, PYGM, D11S97, INT2, D11S37, D11S533, and D11S147) to define the region containing MEN1. This will facilitate the rapid localization of additional DNA sequences in this region. In addition, we have used a highly polymorphic repetitive degenerate hexanucleotide sequence, designated D11S533, for segregation studies in one family with MEN 1. These molecular genetic approaches will help to define a precise 1 to 2 centiMorgan map around MEN1.
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PMID:Molecular genetic mapping of the multiple endocrine neoplasia type 1 locus. 136 97

Flow cytometric DNA analysis of nuclear suspensions from formalin-fixed, paraffin-embedded tissue often fails to detect aneuploid cell populations present in corresponding fresh tissue. Nuclear suspensions were prepared by 8 different modifications and standard Hedley's method using 50-microns sections of tissue blocks from 8 breast and 8 colonic carcinomas, all previously known to be DNA aneuploid by analysis of fresh tumor. Pepsin solutions of three different enzymatic activities were used to release nuclei using three different tissue digest formats. DNA aneuploidy was demonstrated overall in 7 of 72 different colon tumor experiments and 25 of 72 breast cancer experiments. Modifications yielded aneuploid populations not detected by the standard Hedley method; DNA aneuploidy of 4 breast and 2 colon cancers was detected by modifications compared to 2 breast and 1 colon cancer demonstrated by the standard. No single method consistently demonstrated DNA aneuploidy. High histogram baselines, presumably from debris, contributed to the marked loss of sensitivity in detecting most DNA aneuploid populations. Detection of DNA aneuploidy was most closely associated with specific cases, regardless of the method of nuclear suspension preparation. Recovery of DNA aneuploid nuclei seems to depend primarily on tissue processing or innate characteristics of the tumor cells, not on the method used to prepare the nuclear suspension.
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PMID:Comparison of eight modifications of Hedley's method for flow cytometric DNA ploidy analysis of paraffin-embedded tissue. 152 60

The effects of prostaglandins (PGs) A and J, which are anti-tumor eicosanoids, on the proliferation of cultured vascular smooth muscle cells were investigated. Serum-stimulated DNA synthesis was potently inhibited by PGA1, PGA2, PGJ2, and delta 12-PGJ2 in similar dose-dependent fashions. The effects of PGA1 and PGA2 were reversible when they were removed from the culture media, whereas recoveries were only partial in the cells treated with PGJ2 and delta 12-PGJ2. PGs were effective even if they were added immediately before entry into S phase. Inhibition of DNA synthesis was sustained when hydroxyurea, which blocks cell cycle at the G1/S border, was added after the removal of PGA2, and vice versa; PGs blocked DNA synthesis when they were added after the removal of hydroxyurea. Levels of c-myc mRNA formed two peaks during the G1 phase, at 1-2 h and at 8-12 h. The PGs did not affect the first elevation, but enhanced the second and sustained it up to 18-24 h, whereas in controls, c-myc mRNA decreased quickly after entry into S phase. The rate of degradation of c-myc mRNA was much smaller in PG-treated cells than in nontreated cells. We conclude, therefore, that PGA and PGJ inhibit a crucial event(s) in the cell cycle occurring at the G1/S border, but that this inhibition is not accompanied by the reduction in c-myc gene expression in contrast with some types of tumor cells treated with PGs.
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PMID:Prostaglandins A and J arrest the cell cycle of cultured vascular smooth muscle cells without suppression of c-myc expression. 157 2

In a series of bronchial and bladder carcinomas, p53 protein expression was examined. Samples from formalin-fixed, paraffin-embedded tissue (routine-treated) were compared with parallel samples of fresh tissue and tissue fixed in paraformaldehyde and ethanol. The expression of p53 was measured by immunofluorescence staining and dual parameter flow cytometry, with simultaneous monitoring of DNA content. For each tumor, p53 fluorescence with different fixatives was expressed relative to fresh tissue. The p53 fluorescence signals were on average brighter from routine-treated tissue than from fresh tissue. The tissue fixed in paraformaldehyde showed no difference from fresh tissue. In the ethanol-fixed tissue, however, fluorescence signals were reduced by nearly 70%, and the fraction of detectable p53 positive cells in tumor tissue was reduced by more than 50%. This loss of fluorescence was probably due to a leakage of the antigen from nucleus to cytoplasm. Pepsin treatment did not influence p53 fluorescence. Within the same tumor, the S-phase fraction in p53 positive cells was significantly higher than in p53 negative cells (13.1 +/- 2.0% vs. 6.5 +/- 0.8%). This pattern was not influenced by formalin fixation or pepsin treatment. Our study demonstrates that in measuring a nuclear antigen, tissue handling may influence the results, and care should be taken to optimize the preparation procedure. Using the antibody PAb 1801, p53 expression measured in archival material is not reduced as compared to fresh tissue.
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PMID:Influence of tissue preparation techniques on p53 expression in bronchial and bladder carcinomas, assessed by immunofluorescence staining and flow cytometry. 178 31

The technique of cassette and site-specific mutagenesis were used to study the role of residue No. 177 in penicillin G acylase (PGA, EC 3.5.1.11). Ser is conserved at residue No. 177 in all penicillin binding proteins. We got a series of mutants in which the amino acid at residue No. 177 was replaced by other amino acids through the site-specific and cassette mutagenesis, and we characterized the mutants by colony hybridization, NIPAB paper test and DNA sequence analysis. These mutants all show no activity of enzyme, even if the Ser residue was replaced by Thr, Gly and Ala respectively. The results show that Ser residue may be essential for substrate-binding or catalysis of PGA.
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PMID:[Effect of mutagenesis at Ser 177 residue in penicillin G acylase on activity of the enzyme]. 190 33

Human pepsinogen (PGA) exhibits extensive polymorphism that can be detected both at the protein and the DNA level. We describe here two restriction fragment length polymorphisms, EcoRI and BglII, which provide for the detection of three of the most common PGA haplotypes (A, B, and C) in the United States population. The relationship of these polymorphisms to each PGA haplotype was determined by analysis of DNA from individuals exhibiting the corresponding protein phenotypes and by analysis of a series of human x mouse somatic cell hybrids containing the individual chromosome 11 homologous from heterozygous individuals exhibiting the AB and AC protein phenotypes. The use of the BglII polymorphism in combination with previously described EcoRI polymorphism provides a very informative marker of 11q13.
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PMID:Human pepsinogen A (PGA): an informative gene complex located at 11q13. 196 39

Multiple endocrine neoplasia type 1 is an autosomal dominant condition characterized by the development of parathyroid hyperplasia, pituitary adenomas, and pancreatic islet cell tumors. Recently the gene for multiple endocrine neoplasia type 1 was mapped to the long arm of chromosome 11 between the loci PGA and INT2. We tested the hypothesis that tumor development is the result of a somatic deletion that unmasks a constitutional mutation. By investigating DNA isolated from tumors and somatic tissues in 12 patients from 4 different families with multiple endocrine neoplasia type 1, we found loss of heterozygous markers mapped to 11q13 in 9 (82%) of 11 informative tumors. In contrast, we were unable to identify allelic loss from other chromosomes using a variety of informative probes. This high incidence of chromosomal deletion of 11q13 suggests that this region is important in the oncogenesis of this disorder.
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PMID:Loss of heterozygosity of markers on chromosome 11 in tumors from patients with multiple endocrine neoplasia syndrome type 1. 197 36

Liver fatty acid binding protein (L-FABP) is the principal target protein of the hepatic carcinogen N-(2-fluorenyl)acetamide (2-acetylaminofluorene) in rat liver. In addition, the cyclopentenone prostaglandins (PG), PGA, PGJ2, and delta 12-PGJ2, inhibit the growth of many cell types in vitro. This report describes the preferential binding of the growth inhibitory prostaglandins by L-FABP and the reversible inhibition of thymidine incorporation into DNA by PGA2 and delta 12-PGJ2 in primary cultures of purified rat hepatocytes. As a model ligand, [3H]PGA1 bound to L-FABP specifically, reversibly, rapidly, and with high affinity. Its dissociation constants were 134 nM (high affinity) and 3.6 microM (low affinity). The high-affinity binding of [3H]PGA1 was 9- and approximately 13-fold more avid than the binding of the conventional fatty acid ligands, oleic acid and arachidonic acid, respectively. The abilities of different prostaglandins to compete with the high-affinity binding of [3H]PGA1 correlated with their growth inhibitory activities reported previously and here. The growth inhibitory cyclopentenone prostaglandins (PGA1, PGA2, delta 12-PGJ2, and PGJ2) were the best competitive ligands, intermediate competitors were the weak growth inhibitors PGE1 and PGD2, and the poorest competitors were PGE2 and PGF2 alpha, which stimulate rather than inhibit DNA synthesis in rat hepatocytes in primary culture. The in vitro actions of L-FABP are compatible with those of a specific and dissociable carrier of growth inhibitory prostaglandins in rat hepatocytes and suggest that the carcinogen may usurp the cellular machinery of the growth inhibitory prostaglandins.
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PMID:Preferential binding of growth inhibitory prostaglandins by the target protein of a carcinogen. 225 Dec 82


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