Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:Q9NRP7 (fused)
 58,367 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Human VA-2 cells infected with baboon type C virus were cloned and fused to Syrian hamster cells, and 33 primary hybrid colonies were obtained. These cells segregated human chromosomes and retained the complete hamster genome. Assays for type C viral p30 antigen and reverse transcriptase were performed in conjunction with analyses of 30 gene-enzyme systems representing 22 different human chromosomes. The results comfirmed that a gene, Bevi, previously assigned to human chromosome 6, dominantly controls baboon type C virus expression in hybrid cells. Representative hybrid colones were studied by nucleic acid hybridization techniques for the presence of integrated proviral DNA using complementary 3H-DNA transcripts of the baboon viral RNA genome. For each of 12 clones examined, there was a concordance between the presence of human chromosome 6, the presence of baboon type C proviral DNA sequences and virus expression. Clones which segregated chromosome 6 as judged by isozyme and karyological analyses lost detectable proviral DNA sequences and failed to produce virus. No syntenic association between the replication of baboon virus and the presence of 21 other human chromosomes was deteced. We conclude that Bevi is a preferred integration site for the baboon type C provirus in the human genome.
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PMID:A gene (Bevi) on human chromosome 6 is an integration site for baboon type C DNA provirus in human cells. 8 Feb 84

A cloned DNA transcript of ovalbumin mRNA was cut a few nucleotides away from the initiator codon, and fused in phase to the beginning of the Escherichia coli beta-galactosidase gene. The hybrid gene has been cloned in E. coli where it produces large amounts of an ovalbumin-like protein.
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PMID:Synthesis of an ovalbumin-like protein by Escherichia coli K12 harbouring a recombinant plasmid. 8 Jul 51

By recombinant DNA methods, the chicken ovalbumin structural gene has been fused to Escherichia coli lac transcriptional and translational control regions. When a plasmid containing the hybrid gene was introduced into E. coli, a protein identified as ovalbumin by immunoreactivity and sodium dodecyl sulfate/polyacrylamide gel electrophoresis was synthesized. The chicken ovalbumin made in bacteria was full length (43,000 daltons) and constituted 1.5% of the cellular protein. In addition, the microbially synthesized ovalbumin was secreted through the cell membrane into the periplasmic space of E. coli. The ability of the E. coli secretory apparatus to recognize chicken ovalbumin, which is normally synthesized and secreted in hen oviducts, suggests that common features exist in the secretion-recognition mechanisms found in these two organisms. The bacterial synthesis of significant amounts of chicken ovalbumin demonstrates that the E. coli cellular machinery may be utilized to synthesize a higher eukaryotic protein which is relatively stable in the bacterial intracellular environment.
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PMID:Chicken ovalbumin is synthesized and secreted by Escherichia coli. 10 96

Fulvocin C is a bacteriocin from Myxococcus fulvus Mx f16. It has a molecular weight of 4672 and is one of the smallest bacteriocins known. Four disulfide bonds give the molecule a tight structure, so that its native form was not attacked by chymotrypsin or pronase. Fulvocin C was stable in various organic solvents and could tolerate 80 degrees C in aqueous solution without loss of activity. The killing effect of fulvocin C was observed only at concentrations higher than 0.25 mumol/1. Macromolecular synthesis (DNA, RNA, protein) was affected very gradually. Viability in growing cultures decreased slowly from 100 to 25% during one generation (8 h). Cell division was affected early. After one generation v-shaped cell pairs had accumulated in the culture. Electron microscopic pictures revealed extended membrane systems connected with the inner membrane. The most striking effect was that often the outer membranes of neighbouring cells seemed to have fused laterally. With further incubation many cells lost their rod shape and empty bags became predominant.
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PMID:Purification and effects of fulvocin C, a bacteriocin from Myxococcus fulvus Mx f16. 10 92

Integration of the tetracycline resistance transposon Tn10 into lacI of a lacI-lacZ gene fusion permits the isolation of deletions that excise DNA from one end of Tn10 and fuse Tn10 genes with lacZ in such a manner that chimeric proteins with beta-galactosidase activity are produced. The synthesis of the chimeric proteins is under the same control as the transposon genes. Thus, regulation of expression of Tn10 genes can be investigated by measuring beta-galactosidase activity. Analysis of Tn10-lacZ fusions revealed different deletion endpoints within Tn10; lacZ has been fused to at least three different Tn10 genes or operons. Two of these genes are under the control of a tetracycline repressor.
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PMID:A genetic approach to analysis of transposons. 10 39

Simple, rapid colorimetric tests for lysogenic induction (the derepression of a latent bacterial virus) are described. A quantitative test and a more rapid semiquantitative test are based on the assay of the beta-galactosidase synthesized from lacZ gene fused to an operon under lambda repressor control. These biochemical "inductests" are suitable for screening programs designed to detect agents that damage DNA and that are of potential interest in carcinogenesis and cancer chemotherapy.
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PMID:A colorimetric assay of lysogenic induction designed for screening potential carcinogenic and carcinostatic agents. 16 85

Fibroblast strains from 12 patients with xeroderma pigmentosum had lower than normal rates of DNA repair, as determined by autoradiographic studies of ultraviolet-induced unscheduled nuclear DNA synthesis. The nuclei in binuclear cells, obtained by fusing fibroblasts from certain pairs of these strains, had a greater rate of DNA repair than the nuclei of either strain's unfused mononuclear cells. These results indicate that complementary corrections of the strains' repair defects had occurred in the fused cells. Four complementation groups were found, indicating that at least four mutations caused decreased DNA repair among these 12 strains. The unfused mononuclear cells of each group had a characteristic rate of repair that differed from the rates of the other groups.
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PMID:Genetic heterogeneity in xeroderma pigmentosum: complementation groups and their relationship to DNA repair rates. 16 28

UV survival curves of adenovirus 2 using fused, complementing xeroderma pigmentosum (XP) fibroblast strains as virus hosts showed a component with an inactivation slope identical to that given by normal cells. This component was not observed when the fibroblasts were not fused or when fusion involved strains in the same complementation group. Extrapolation of this component indicated that at zero dose 3% of the viral plaque-forming units had infected cells capable of normal repair. These results suggest that 3% of the cells were complementing heterokaryons, a value similar to that actually observed by autoradiographic analysis of UV-induced unscheduled DNA synthesis. Thus, heterokaryons formed from XP fibroblasts belonging to different complementation groups are as capable of restoring biological activity to UV-damaged adenovirus 2 as are normal cells.
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PMID:Complementing xeroderma pigmentosum fibroblasts restore biological activity to UV-damaged DNA. 16 4

Cytological and chemical analysis of heterokaryons, the immediate product of cell fusion, offer new possibilities for studying the factors responsible for genetic regulation in eukaryotic cells. In comparison with proliferating cell hybrids the heterokaryon state offers the important advantage that a heterokaryon contains two complete genomes since chromosome loss does not occur, but since segregation and recombination are absent, heterokaryons cannot be used for gene mapping in the same way as proliferating cell hybrids. However, if two cell types carrying different genetic defects are fused the analysis can be used for studies of gene complementation. The biological information obtained with heterokaryons has emphasized the role of the cytoplasm in the control of nuclear activity. When a G1 nucleus is brought into contact with the cytoplasm of an S phase cell the G1 nucleus is stimulated to synthesize DNA. If the nucleus is brought into a mitotic cell, the chromatin of the G1 nucleus is forced to condense into prematurely condensed chromosomes. Inactive nuclei such as the dormant chick erythrocyte nucleus will be stimulated to initiate RNA and DNA synthesis when brought into contact with an active cytoplasm by cell fusion. Specific nuclear proteins have been shown to be responsible for this process of reactivation. Other inactive nuclei such as the nuclei of macrophages and spermatozoa have likewise been shown to be reactivated by fusion with active cells. The degree of activation in all of these cases appears to be determined by the state of the active cell. Inactive nuclei are activated to the same level as the active nucleus but seldom beyond this level. If differentiated cells are fused with undifferentiated cells, usually the differentiated character is lost rapidly after fusion. This observation is in agreement with several studies on proliferating cell hybrids indicating some type of negative control of differentiated properties. In heterokaryons obtained by fusion of cells of a similar type of histotypic differentiation usually coexpression of the differentiated markers is observed.
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PMID:Heterokaryons in the analysis of genes and gene regulation. 16 48

Cultures of the rat skeletal muscle myoblast cell line, L6, were treated with the mutagen ethylmethanesulfonate and grown in the presence of alpha-amanitin, an inhibitor of RNA polymerase II in vitro. One clonal cell line, Ama102, resistant tc the cytotoxic action of 2 mu-g/ml of alpha-amanitin was isolated and extensively characterized. Ama102 cells were about 30-fold more resistant to alpha-amanitin than their Ama+ parent cells based on a comparison of the concentration of alpha-amanitin required to reduce their plating efficiencies to similar extents. The RNA polymerase activities from Ama+ and Ama102 cells were solubilized and separated by DEAE-Sephadex chromatography. Whereas all of the Ama+ RNA polymerase II activity was inhibited by 0.1 mu-g/ml of alpha-amanitin, about 30% of the activity in the Ama102 RNA polymerase II peak was resistant to this concentration of alpha-amanitin and was inhibited only by much higher concentrations (25 mu-g/ml) of alpha-amanitin. This alpha-amanitin-resistant activity in Ama102 cells was identified as a bona fide RNA polymerase II by its chromatographic behavior on DEAE-Sephadex, salt optimum, preference for denatured DNA as template, insensitivity to inhibition by potassium phosphate, thermal inactivation kinetics, and inactivation by anti-RNA polymerase II antiserum. Both RNA polymerase IIa and IIb from Ama102 cells exhibited the partial alpha-amanitin resistance, as did this activity when purified further on phosphocellusose. Unlike the parental Ama+ cells, Ama102 cells neither fused at confluence nor showed an increase in the specific activity of creatine kinase. The altered sensitivity of the Ama102 RNA polymerase II to alpha-amanitin appears to account for the drug-resistant phenotype of these cells.
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PMID:Isolation and characterization of an alpha-amanitin-resistant rat myoblast mutant cell line possessing alpha-amanitin-resistant RNA polymerase II. 16 92


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