Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P06889 (Mol)
 630,302 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Infection of hamsters by the human liver fluke Opisthorchis viverrini elevated liver procollagen prolyl hydroxylase activity, reflecting increased collagen biosynthesis. The increase was proportional to the intensity of infection. However, the infected liver procollagen prolyl hydroxylase activity decreased after administration of praziquantel 300 mg kg-1 body weight, and approached normal levels two weeks after treatment. In the infected hamsters, praziquantel, at a curative dose, caused a transient increase in serum aminotransferase levels and a small but persistent rise in serum alkaline phosphatase. The drug, however, did not cause changes in these enzyme activities in the uninfected hamsters.
Mol Biochem Parasitol 1983 Dec
PMID:Liver procollagen prolyl hydroxylase in Opisthorchis viverrini infected hamsters after praziquantel administration. 631 7

The gltA gene from Escherichia coli, which encodes citrate synthase, has been located on a 3.24 Kb HindIII/EcoRl restriction fragment. This region contains one restriction site for BamHl and two for BglII. Defined restriction fragments from this region were cloned into suitably cleaved replicative form M13mp8 and M13mp9. The recombinants (M13gtlA1 leads to 10) were isolated as single stranded DNA and characterised on the basis of molecular weight and DNA sequence. The single stranded DNA was converted to the double stranded replicative form and used to transform E. coli strain JM103 from which bacteriophage were isolated. Infection of JM103 with different bacteriophage followed by measurement of expressed citrate synthase activity showed that the complete gltA gene must span the BamHl restriction site, that the control region was on the 5'-terminal side of this restriction site and that the coding region for citrate synthase protein commenced on the 3'-terminal side. Analysis of the DNA sequence of this region allowed us to confirm this model, to identify the start sequence for translation of the structural gene and a number of sequences controlling the initiation of transcription. Of special interest is the fact that there must be an extensive leader sequence (305 nucleotides) separating the predicted sites for initiation of transcription and translation.
Mol Gen Genet 1983
PMID:The use of bacteriophage M13 carrying defined fragments of the Escherichia coli gltA gene to determine the location and structure of the citrate synthase promoter region. 635 71

Rabbits were infected by Trypanosoma equiperdum and the splenic mRNA was isolated. In vitro translation of this RNA and immunoprecipitation with anti-light chain, anti-heavy chain, anti-mu and anti-VH antibodies demonstrated that T. equiperdum infection elicits large quantities of splenic mRNA encoding mu and kappa chains. The mu and gamma heavy chains and the kappa light chains synthesized in the cell-free translation system were specifically immunoprecipitated by antisera to heavy chain VHa and light chain kappa b allotypes. In vitro labeling of spleen cells from trypanosome-infected animals demonstrated that the biosynthetically labeled IgM has a mu chain of higher molecular weight than the mu chain synthesized by in vitro translation, a difference that is largely abolished when cellular glycosylation is blocked with the antibiotic tunicamycin. Enrichment for heavy chain or light chain mRNA was achieved by fractionating mRNA from trypanosome-infected animals on a sucrose gradient. cDNA clones carrying mu heavy chain sequences were produced using a 'one tube' protocol and identified by cross species hybridization and hybridization selection. Infection of rabbits with T. equiperdum followed by sucrose gradient enrichment of splenic mRNA has provided sufficient quantities of mRNA encoding mu heavy chain suitable for cDNA cloning.
Mol Immunol 1983 Jan
PMID:Use of Trypanosoma equiperdum infected rabbits as a source of splenic mRNA; construction of cDNA clones and identification of a rabbit mu heavy chain clone. 640 41

In the preceding paper (Amann et al. 1981) we described the in vitro construction of hybrids between Escherichia coli phage lambda NM607 imm434 and B. subtilis phage SPP1. These lambda/SPP1 hybrids have been used to infect minicells produced by E. coli strain DS410. Analysis on polyacrylamide gels of 35S-methionine labeled proteins synthesized in infected minicells revealed the expression of both lambda and SPP1 genes. Infection of E. coli minicells carrying plasmid pGY101, which encodes and expresses the repressor gene of phage 434, results in the selective expression of the cloned SPP1 DNA. This has resulted in the assignment of 26 out of a total of 46 known SPP1 polypeptides (Mertens et al. 1979) to individual SPP1 DNA fragments. In addition, several lambda/SPP1 fusion peptides whose transcription either originates from lambda promoters or from promoters located on the inserted SPP1 fragment, were identified.
Mol Gen Genet 1981
PMID:Cloning and expression of Bacillus subtilis phage SPP1 in E. coli. II. Expression of lambda/SPP1 hybrid phages in E. coli minicells. 645 36

Infection of HeLa cells with different viruses induces permeabilization of the cell membrane to protein toxins such as alpha-sarcin. This phenomenon occurs with HeLa, KB, BHK-21 and L929 cells and EMC, SFV, VSV and Polio virus and is dependent on the ability of the virus to infect the cells. Inhibitors of endocytosis and lysosomotropic agents do not affect this process. Cells become sealed to the toxin approximately four hours after the infection. Sulfhydryl reagents impair cellular permeabilization to alpha-sarcin.
Mol Biol Rep 1984 Dec
PMID:Permeability to inhibitors of protein synthesis in virus infected cells. 652 84

A helper-independent Friend leukemia virus was used to infect bone marrow cultures. This virus induces myeloblastic leukemia in mice after a long latency period. Infection of the bone marrow cultures resulted in the in vitro production of myeloblastic leukemogenesis after a long latency period. Three steps were observed in the evolution of the infected cultures, and permanent cell lines were derived at each step. This allowed us to individualize three successive events in the course of the myeloblastic transformation: (i) an abnormal responsiveness to the physiological hormone granulo-macrophagic colony-stimulating factor, (ii) the acquisition of growth autonomy, and (iii) the acquisition of in vivo tumorigenicity.
Mol Cell Biol 1984 Jan
PMID:Multistep virus-induced leukemogenesis in vitro: description of a model specifying three steps within the myeloblastic malignant process. 658 94

Infection of human cells by adenovirus results in multiple alterations of host gene expression. To examine the effects of viral infection on the expression of a single gene, a line of human cells was developed which is resistant to growth in methotrexate and which contains amplified RNA and protein specific for dihydrofolate reductase (DHFR). Cytogenetic evidence indicated the presence of amplified DNA. Adenovirus infection of these cells caused an induction and subsequent decline in the synthesis of DHFR protein. The maximum DHFR induction occurred 16 to 19 h after infection and reached a level 2.5-fold greater than that observed in uninfected cells. Induction of DHFR protein synthesis was accompanied by concomitant increases in the level of steady-state DHFR-specific cytoplasmic RNA. The relative rate of DHFR mRNA production (i.e., the appearance of DHFR-specific mRNA sequences in the cytoplasm) also increased 2.5-fold during induction. Later in infection, the relative rate of DHFR protein synthesis declined, reaching a level below that observed in uninfected cells. This decline was accompanied by a similar decline in the steady-state levels of DHFR RNA and in the relative rate of synthesis of DHFR mRNA. These data suggest that adenovirus infection controls DHFR gene expression by increasing and subsequently decreasing the relative rate at which DHFR-specific mRNA sequences appear in the cytoplasm and enter the pool of mRNA available for translation.
Mol Cell Biol 1983 May
PMID:Control of cellular gene expression during adenovirus infection: induction and shut-off of dihydrofolate reductase gene expression by adenovirus type 2. 686 43

Tuftsin, a physiological tetrapeptide derived from the Fc region of leukophilic IgG possesses a variety of immunopotentiating properties including the ability to act as an immunotherapeutic agent against the experimental tumors, L1210 leukemia and Cloudman S-91 melanoma. Although the mechanism of action of tuftsin in vivo is not known, several types of leukocytes have been shown to become cytotoxic effector cells following activation with tuftsin. These cells presently include macrophages, natural killer cells, and granulocytes. The possibility that tuftsin can also activate other types of effector cells have not been ruled out. We feel this small peptide has a high potential (largely unrecognized) as an antitumor immunopotentiating agent. It is naturally occurring in man and appears to be relatively non-toxic. Its exact sequence (Thr-lys-Pro-Arg) is known and it can be chemically synthesized. Methods are also available to monitor the levels of tuftsin in body fluids. These properties along with its ability to control infectious disease make this agent one of the more promising immunopotentiators.
Mol Cell Biochem 1981 Dec 04
PMID:Antitumor effect of tuftsin. 689 73

P1 infected minicells synthesize approximately 50 phage-encoded polypeptides. Phage expression is temporally controlled, demonstrating phage polypeptides synthesized both early and late after infection. The P1 repressor, gpcl1 (Mr = 33,000), repressor bypass polypeptide, gpreb A (Mr = 27,500) and cistron 10 product, (gp10) (Mr = 64,000), have been identified by infection of minicells with P1 amber mutants. The beta-lactamase gene product (gpbla) carried by the closely related P7 and the chloramphenicol acetyl-transferase gene product (gpcat) carried by P1 Cm (in Tn9) have been demonstrated. Infection of minicells by P1virs or P1c4 mutants results in increased synthesis of gpreb A and a second polypeptide designated gpreb B (Mr = 40,000). The P1vir11 mutation leads to increased synthesis of a small polypeptide (Mr = 3,500) but does not affect the amount of gpc1 synthesized.
Mol Gen Genet 1980 Apr
PMID:Identification of the repressor and repressor bypass (antirepressor) polypeptides of bacteriophage P1 synthesized in infected minicells. 699 77

The effect of 9 monosaccharides which constitute cell surface carbohydrates on the infection of bovine embryonic skin and muscle (BESM) cells by Trypanosoma cruzi trypomastigotes and Toxoplasma gondii tachyzoites was assayed. Most of the monosaccharides tested stimulated the infection of BESM cells by T. gondii; none of the monosaccharides were inhibitory. In contrast (at a concentration of 50 mM or greater) the monosaccharides inhibited non-specifically the infection of BESM cells by T. cruzi trypomastigotes whereas the other 8 monosaccharides were ineffective. The inhibition was due to an effect on the trypomastigotes and not on the vertebrate cells. It is proposed that there is a wheat-germ agglutinin-like lectin on the T. cruzi trypomastigote surface which recognizes and attaches to an N-acetylglucosamine-containing receptor on the vertebrate cell surface prior to infection. Infection of vertebrate cells by T. gondii tachyzoites appears to be mediated by other cell surface components. If monosaccharides are involved in infection by tachyzoites, they are ones not commonly found on animal cell surfaces. Alternatively, infection of vertebrate cells by T. cruzi and T. gondii is effected by different mechanisms.
Mol Biochem Parasitol 1982 May
PMID:Influence of monosaccharides on the infection of vertebrate cells by Trypanosoma cruzi and Toxoplasma gondii. 704 90


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