Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: HUMANGGP:003721 (Poly)
11,742 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. The decreased ability of polysomes isolated from the gastrocnemius of rats bearing the Walker 256 carcinoma to incorporate L-[14C]leucine into protein persisted in the presence of 5-10-5 M aurin tricarboxylic acid and 1-10-2 M NaF. 2. Poly(U)-directed phenylalanine incorporation by such polysome preparations was less than that of similar preparations from normal rats. 3. The ability of gastrocnemius polysomes from tumour-bearing rats to react with puromycin was markedly decreased. Cycloheximide inhibited peptidyl puromycin formation by polysome preparations from both normal and tumour-bearing rats. 4. The ability of recombined 60 S and 40 S subunits prepared from polysomes of tumour-bearing rats to carry out poly(U)-directed polyphenylalanine synthesis was much reduced when assayed over a wide range of magnesium concentrations. Cross-over experiments with subunits from normal and tumour-bearing animals suggested that this was due to a defect in the smaller ribosomal subunit.
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PMID:Muscle protein biosynthesis in the tumour-bearing rat. A defect in a post-initiation stage of translation. 112 27

The relationship between cell morphology, proliferation, and contact inhibition was studied in normal and malignant human cells which varied in their sensitivity to contact inhibition. Their ability to proliferate was examined under conditions where the cells were constrained into different shapes by plating onto plastic surfaces coated with poly(2-hydroxyethyl methacrylate). Poly(2-hydroxyethyl methacrylate) can precisely vary the shape of cells without toxicity. Cell proliferation was quantitated by cell counts and labeling indices were determined by autoradiography. The normal JHU-1 foreskin fibroblasts and IMR-90 lung fibroblasts exhibited contact-inhibited growth with a saturation density of 2.9 X 10(5) and 2.0 X 10(5) cells/cm2, respectively. These cells also exhibited stringent dependency on cell shape with a mitotic index of less than 3% at poly(2-hydroxyethyl methacrylate) concentrations at which the cells were rounded versus a labeling index of 75-90% when the cells were flat. The malignant bladder carcinoma line RT-4 exhibited partial contact-inhibited growth. Its dependency on cell shape was less stringent than that of normal cells with a mitotic index of 37-40% when rounded and 79% when flat. The malignant fibrosarcoma line, HT1080, was not contact inhibited and was entirely shape independent with a mitotic index of 70-90% regardless of cell shape. Treatment of HT1080 cells with low concentration of human fibroblast interferon (less than 40 units/ml) restored shape-dependent proliferation while having little effect on normal cells. Subantiproliferative doses of interferon were also shown to restore contact-inhibited proliferation control to malignant cells previously lacking it. The concordant restoration of contact inhibition and shape-dependent proliferation in malignant cells by interferon suggest that these two types of proliferation controls represent a manifestation of common regulatory mechanisms. However, since these effects occurred at interferon concentrations below that required to produce an antiproliferative effect, these actions of interferon may be distinct from the antiproliferative action.
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PMID:Shape-dependent regulation of proliferation in normal and malignant human cells and its alteration by interferon. 242 83

Poly(A)+ RNA was isolated from 9 specimens of human primary hepatic carcinoma, 1 non-tumorous liver tissue adjacent to cancer and 1 normal liver tissue samples. The Oligo-dT cellulose-purified poly(A)+ RNAs were subjected to formaldehyde agarose gel electrophoresis, Northern transfer and hybridization with various oncogene probes. Two RNA species, 5.6 kb and 2.2 kb were identified by N-ras gene hybridization in 6 out of 9 mRNA samples from primary hepatic carcinoma specimen. N-ras specific mRNA was not detectable in mRNA samples from normal human liver and tumor surrounding cirrhotic tissue. No detectable hybridization of mRNA from hepatoma and normal liver with Ki-ras or Ha-ras was observed. As human N-ras gene has been identified in DNA of mouse transfectants transformed with PHC DNA, it strongly suggests that N-ras gene might be responsible for the transforming activity of part of cases of human liver cancer.
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PMID:Expression of N-ras gene in human primary hepatocarcinoma. 301 23

Poly-N-acetyllactosamines were prepared from Ehrlich carcinoma cells cultured in the presence of [14C]galactose. Methylation analysis indicated that 31% of the galactose was in the non-reducing end. Of it, 77% was cleaved by alpha-galactosidase, and 56% was released as a disaccharide by endo-beta-galactosidase C. Methylation analysis confirmed that the released disaccharide was mostly Gal alpha 1----3Gal. Therefore, Gal alpha 1----3Gal structure, not Gal alpha 1----3(Gal alpha 1----6)Gal structure, was the major alpha-galactosyl structure in the poly-N-acetyllactosamines synthesized. Furthermore, alpha-galactosidase digestion did not change the content of disubstituted galactosyl residues. Thus, Gal alpha 1----3(Gal alpha 1----6)Gal structure, which was suggested to be the sole non-reducing terminal structure of poly-N-acetyllactosamines of Ehrlich carcinoma cells, was not detected in significant amounts under the present experimental conditions.
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PMID:Poly-N-acetyllactosamines synthesized by cultured Ehrlich carcinoma cells: application of endo-beta-galactosidase C for analysis of the terminal structure. 314 15

This paper describes an investigation into the effect of alpha-1-antichymotrypsin (ACT) on DNA primase. DNA primase was partially purified from human stomach carcinoma cells. It was found that poly(dC)-dependent DNa primase activity was inhibited by ACT and the inhibition was proportional to the concentration of the inhibitor. The inhibitory effect of ACT remained even after ACT lost most of its chymotrypsin-inhibitory activity by heat treatment. Poly(dT)-dependent primase activity was enhanced by the presence of ACT. The enhancement was effective up to a concentration of 1mg/ml.
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PMID:Effect of alpha-1-antichymotrypsin on activity of DNA primase isolated from human stomach adenocarcinoma cells. 326 45

cDNA clones complementary to mRNA of neoplastic cells of human stomach tissue were used to examine quantitative changes in the mRNA levels of specific genes in neoplastic cells. Poly(A)+ RNA from poorly differentiated adenocarcinoma cells of a female patient with stomach cancer was used for construction of a complementary DNA (cDNA) library. Screening of the 18,000 colonies utilizing 32P-cDNAs derived from normal human tissue and stomach carcinoma tissue samples was used to select clones likely to represent sequences preferentially expressed in stomach carcinoma cells. Twenty-six recombinants were initially selected and further analysis of these clones indicated that eight (4-3D, 9-2D, 9-4G, 29-1G, 29-6F, 37-1B, 115-5A and 52-5F) contain sequences preferentially expressed in stomach carcinoma cells. We have identified the 9-4G, 29-1A, and 29-6F genes which are differentially expressed in human neoplasia.
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PMID:Preferentially expressed genes in stomach adenocarcinoma cells. 342 17

Mouse bladder tumor (MBT-2), derived from a carcinogen-induced transitional cell carcinoma of the bladder, has proven a useful model for study of pathogenesis and prediction of cytotoxic drug sensitivity of human bladder carcinoma. To define optimal conditions for activity of the potent interferon inducer polyriboinosinic-polyribocytidylic acid [poly(I) X poly(C)] in this model, studies of dose, timing, and combinations with a cytotoxic drug were initiated. Poly(I) X poly(C) inhibited MBT-2 growth when 10(5) or 10(6) tumor cells were implanted. Tumor growth reduction was relatively more pronounced in mice inoculated with higher numbers of MBT-2 cells (10(6] than in mice inoculated with an intermediate dose (10(5] or small dose (10(4]. In mice inoculated with 10(5) MBT-2 tumor cells, poly(I) X poly(C) (2.5 or 10 mg/kg i.p.) on Days 5 to 19 every other day reduced tumor size markedly. It had no effect, however, on tumor incidence or the time of their first detection. Treatment for a shorter period (alternate days from Days 11 to 19) resulted in less inhibition of tumor growth. Once treatment was discontinued, tumors grew progressively. Polyriboadenylic:polyribouridylic acid [poly(A) X poly(U)] (10 mg/kg) which inhibited tumor growth but to a lesser degree than poly(I) X poly(C) induced lower, less sustained levels of serum interferon. Cyclophosphamide, injected i.p. on Day 1, resulted in inhibition of tumor incidence and growth in direct proportion to the dose administered (25 to 200 mg/kg), but it was curative only at greater than or equal to 30% lethal doses. When combined with poly(I) X poly(C) (2.5 or 10 mg/kg), cyclophosphamide (50 mg/kg) had an additive antitumor effect. Optimal inhibition of MBT-2 tumor growth occurred by combining cyclophosphamide (100 mg/kg) with poly(I) X poly(C) (2.5 mg/kg); eight of 14 mice were tumor free on Day 60.
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PMID:Antitumor effects of polyribonucleotides for mouse transitional cell carcinoma enhanced by cyclophosphamide. 396 50

8006-I is an antibacterial antibiotic with a rather broad spectrum of activity. The minimum inhibitory concentrations for the most sensitive bacteria are in the range of one to ten micrograms/ml. Yeasts are not affected by concentrations up to 100 micrograms/ml. Some filamentous fungi like Fusarium oxysporum and Mucor miehei are inhibited at 100 micrograms/ml. In Ehrlich carcinoma ascitic cells the incorporation of uridine and leucine and to a lesser extent that of thymidine is reduced. In isolated nuclei of these cells the incorporation of UTP into RNA is inhibited. At low concentrations, the incorporation of uracil into trichloroacetic acid-precipitable material is almost completely inhibited in cells of Bacillus subtilis; at higher concentrations all macromolecular syntheses are affected. No reduction of respiration of the cells is observed. The antibiotic exhibits weak hemolytic activity and lytic activity towards bacteria. In vitro an inhibition of both DNA- and RNA polymerase from Escherichia coli is observed. Poly(U)-directed poly(Phe) synthesis is not affected.
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PMID:8006-I, an antibiotic from Amblyosporium spongiosum (Pers.) Hughes sensu Pirozynski. II. Biological properties. 617 18

We have been working on poly(ADP-Rib) since our discovery of it. This lecture will review recent findings on this polymer obtained in our laboratory. Poly (ADP-Rib) has long been thought to be a linear homopolymer attached to nuclear protein. The ribose-ribose bond of poly(ADP-Rib) was shown to be an alpha(1" leads to 2') ribosidic bond. There are two molecular forms of poly(ADP-Rib), namely low molecular weight (L) and high molecular weight (H) poly(ADR-Rib) molecules. The L and H fractions of poly(ADP-Rib) are separable by gel filtration, sucrose density gradient centrifugation and polyacrylamide gel electrophoresis. Physicochemically the L and H forms differ in their molecular size, solubility in high salt, rate of hydrolysis by venom phosphodiesterase and circular dichroism (CD) spectrum. However, the two forms have a similar ultraviolet (UV) absorption spectrum, both show a similar hyperchromicity on heating to 98 degrees C or hydrolysis with snake venom phosphodiesterase and give similar results on ordinary chain length determination. The great discrepancy in size observed by physicochemical methods and by the ordinary chain length method indicates the presence of a branching structure in poly(ADP-Rib). The branching structure was proved by demonstrating the presence of a unique compound, 2'[1"-ribosyl-2"(1"'-ribosyl)]adenosine-5',5",5"'-tris(phosphate) and by electron microscopy. The amount of poly(ADP-Rib) was determined by our new method, consisting of tritium labeling and high performance liquid chromatography. The merit of this method is that it can determine the recovery of poly(ADP-Rib) exactly and that its sensitivity is high. The amount of poly(ADP-Rib) changed dramatically when human promyelocytic leukemia cells were induced to differentiate by dimethyl sulfoxide or 12-O-tetradecanoylphorbol-13-acetate. The use of inhibitors of poly (ADP-Rib) polymerase in combination with bleomycin, a DNA damaging antitumor drug, potentiated the antitumor activity of bleomycin against Ehrlich ascites carcinoma cells in vivo.
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PMID:Poly(ADP-ribose): structure, quantification, and biological significance. 619 2

Poly(A) RNA was isolated from a rat medullary thyroid carcinoma that exhibited high levels of immunoreactive cholecystokinin (CCK). Double-stranded cDNA was synthesized from the poly(A) RNA and inserted into the Pst I site of pBR322. Bacterial colonies containing CCK cDNA were identified using the hybridization probe d(T-C-C-A-T-C-C-A-N-C-C-C-A-T-G-T-A-G-T-C). The sequence of the probe was deduced from the known amino acid sequence of porcine CCK-8, Asp-Tyr-Met-Gly-Trp-Met-Asp-Phe-NH2. The nucleotide sequence of the cDNA complementary to the mRNA of rat preprocholecystokinin was determined. The cDNA contains 33 nucleotides in the 5'-noncoding region, 199 nucleotides in the 3'-noncoding region, and 345 nucleotides coding for a precursor to CCK, which is 115 amino acids (Mr, 12,826). Examination of the rat CCK gene revealed a suggested transcriptional control sequence analogous to the "TATA" sequence located 33 nucleotides upstream from a proposed transcriptional start site. The amino acid sequence of CCK-39 is flanked by both amino-terminal and carboxyl-terminal extensions. Analysis of CCK mRNA showed that it is approximately equal to 750 nucleotides long. CCK mRNA of the rat brain and intestine appeared to be identical in size to the CCK mRNA of the carcinoma.
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PMID:Cloning and sequence analysis of a cDNA encoding rat preprocholecystokinin. 619 87


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