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Query: UNIPROT:P06889 (Mol)
 630,302 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Rats were immunized with mouse lymphocytes enriched by the absorption-elution technique with specific suppressor T-cells (STC) immune to antigens of the H-2 complex. The anti-suppressor sera (ASS) obtained being absorbed with mouse erythrocytes and lymph node cells killed in the presence of complement about 30 per cent of the STC-enriched cell population and inactivated the STC in vitro function in a selective fashion, not affecting the function of other T-cell subclasses, killers and MIF-producers, immune to the same H-2 antigens. The STC inactivating ASS action occurred partly in the absence of complement irrespective of the STC strain origin, STC immunological specificity in the H-2 system and the intensity of the STC activity. This ASS action was abolished by exhaustion of antibodies only with STC containing cell suspensions. In contrast, intact (non-enriched) mouse STC appeared to be able to induce a mixture of rat antibodies inactivating partly all three T-cell subclasses assayed. Infections of ASS to mice prevented them from the in vivo STC generation and gave rise to inhibition of the syngeneic tumor growth in the specifically preimmunized mice.
Mol Biol (Mosk)
PMID:[Selective inactivation of specific T-suppressors immune to H-2 complex antigens and prevention of their generation in vivo by antisuppressor xenogenic antibodies]. 645 78

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

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

The imidazoquinolineamine derivative 1-(2-methyl propyl)-1H-imidazole [4,5-c]quinoline-4-amine (imiquimod) has been shown to induce alpha interferon (IFN-alpha) synthesis both in vivo and in peripheral blood mononuclear cells in vitro. In this study, we show that, in these cells, imiquimod induces expression of several IFNA genes (IFNA1, IFNA2, IFNA5, IFNA6, and IFNA8) as well as the IFNB gene. Imiquimod also induced the expression of interleukin (IL)-6, IL-8, and tumor necrosis factor alpha genes. Expression of all these genes was transient, independent of cellular protein synthesis, and inhibited in the presence of tyrosine kinase and protein kinase C inhibitors. Infection with Sendai virus led to expression of a similar set of cytokine genes and several of the IFNA genes. Imiquimod stimulates binding of several induction-specific nuclear complexes: (i) the NF-kappa B-specific complexes binding to the kappa B enhancer present in the promoters of all cytokine genes, but not in IFNA genes, and (ii) the complex(es) binding to the A4F1 site, 5'-GTAAAGAAAGT-3', conserved in the inducible element of IFNA genes. These results indicate that imiquimod, similar to viral infection, stimulates expression of a large number of cytokine genes, including IFN-alpha/beta, and that the signal transduction pathway induced by both of these stimuli requires tyrosine kinase and protein kinase activity.
Mol Cell Biol 1995 Apr
PMID:Stimulation of interferon and cytokine gene expression by imiquimod and stimulation by Sendai virus utilize similar signal transduction pathways. 753 79

We introduced a plant selection marker, nptII, to the left of border A in the Agrobacterium Ti plasmid pTiA6. Infection of tobacco leaf discs with the modified Agrobacterium strain gave rise to kanamycin-resistant calli which grew in a hormone-dependent manner. Southern hybridization analysis of DNA isolated from four transformants indicated initiation of DNA transfer at or near border A and absence of T-DNA sequences. These results demonstrate that DNA transfer events starting at a left border on a native Ti plasmid and moving away from the T-DNA region occur and that they can be detected by designing a suitable selection strategy.
Plant Mol Biol 1995 Sep
PMID:Transfer of non-T-DNA portions of the Agrobacterium tumefaciens Ti plasmid pTiA6 from the left terminus of TL-DNA. 754 33

Infection of human cells with oncogenic adenovirus type 12 (Ad12) induces four specific chromosome fragile sites. Remarkably, three of these sites appear to colocalize with tandem arrays of genes encoding small, abundant, ubiquitously expressed structural RNAs--the RNU1 locus encoding U1 small nuclear RNA (snRNA), the RNU2 locus encoding U2 snRNA, and the RN5S locus encoding 5S rRNA. Recently, an artificial tandem array of the natural 5.8-kb U2 repeat unit has been shown to generate a new Ad12-inducible fragile site (Y.-P. Li, R. Tomanin, J. R. Smiley, and S. Bacchetti, Mol. Cell. Biol. 13:6064-6070, 1993), demonstrating that the U2 repeat unit alone is sufficient for virally induced fragility. To identify elements within the U2 repeat unit that are required for virally induced fragility, we generated cell lines containing artificial tandem arrays of the entire 5.8-kb repeat unit, an 834-bp fragment spanning the U2 gene alone, or the same 834-bp fragment from which key U2 transcriptional regulatory elements had been deleted. The U2 snRNA coding regions within each artificial array were marked by an innocuous single base change (U to C at position 87) so that the relative expression of supernumerary and endogenous U2 genes could be monitored by a primer extension assay. We find that artificial arrays of both the 5.8- and the 0.8-kb U2 repeat units are fragile but that arrays lacking either the distal sequence element or both the distal and the proximal sequence elements of the promoter are not. Surprisingly, variations in repeat copy number and/or transcriptional activity of the artificial arrays do not appear to correlate with the degree of Ad12-inducible fragility. We conclude that U2 transcriptional regulatory elements are required for virally induced fragility but not necessarily U2 snRNA transcription per se.
Mol Cell Biol 1995 Nov
PMID:Adenovirus type 12-induced fragility of the human RNU2 locus requires U2 small nuclear RNA transcriptional regulatory elements. 756 77

Recombinant bacteriophages provide efficient delivery systems for introducing reporter genes into specific bacterial hosts. We have constructed mycobacteriophage L5 recombinants carrying the firefly luciferase gene inserted into the tRNA region of the phage genome. Infection of Mycobacterium smegmatis by these phages results in expression of the luciferase gene and light emission. Fortuitously, the luciferase gene is expressed continuously in lysogens surviving infection. Synthesis of luciferase from a mycobacterial promoter created by cloning enables the detection of extremely small numbers of M. smegmatis cells. These reporter phages can be used to discriminate between drug-sensitive and drug-resistant strains of M. smegmatis, and may provide tools for the rapid identification and classification of antimycobacterial agents.
Mol Microbiol 1995 Mar
PMID:L5 luciferase reporter mycobacteriophages: a sensitive tool for the detection and assay of live mycobacteria. 762 62


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