Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:2.7.7.49 (reverse transcriptase)
31,746 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Derived from the susceptible AKR.H-2bSL1 tumor cell line, a variant tumor subclone, cl.18-5, was selectively insusceptible to H-2-restricted anti-AKR/Gross virus cytotoxic T lymphocytes (CTL) due to its failure to be recognized. In this study, the expression of virus-related products by variant cl.18-5 cells was compared to that of AKR.H-2bSL1 cells and a susceptible clone, as an approach towards defining the virus-associated antigens recognized by anti-AKR/Gross virus CTL. Despite the type specificity of the CTL, cl.18-5 displayed normal levels of the group-specific antigen (gag) encoded proteins p30, p15, p12 and p10, and the gag-associated Gross cell surface antigen. These results were confirmed by fluorescence-activated cell sorter analysis employing monoclonal antibodies specific for either AKR p12 or the cell surface glycosylated form of AKR ecotropic gag product. In contrast, cl.18-5 was variably less sensitive than AKR.H-2bSL1 to the action of complement and xenogeneic antisera directed against the envelope (env) product gp70. In addition, a panel of five monoclonal antibodies to gp70, which detect distinct endogenous ecotropic viral determinants, lysed AKR.H-2bSL1, but not cl.18-5 cells. However, absorption experiments indicated that cl.18-5 did express near normal levels of these specificities, suggesting an alteration in the orientation or topographical distribution of these determinants. Consistent with an inappropriate display of env products, cl.18-5 was found to be deficient in the production of infectious ecotropic leukemia virus. The particulate fraction of the cell-free supernatant of cl.18-5 contained normal levels of reverse transcriptase activity, indicating that noninfectious viral particles were being produced. Collectively, these results point to an association between recognition by anti-AKR/Gross virus CTL and the expression of ecotropic gp70 required for infectivity of virus.
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PMID:The specificity of H-2-restricted cytotoxic T lymphocytes directed to AKR/Gross leukemia virus-induced tumors. II. Altered gp70 display and production of noninfectious virus particles by an insusceptible variant tumor. 619 7

The structural proteins as well as some features of the RNA-dependent DNA polymerase of the hamster endogenous retrovirus (HaER) were examined. The polypeptide pattern of this virus is substantially different from that of other known retroviruses in containing major polypeptides with molecular weights of 68,000, 59,000, 27,000 and 24,000 daltons. Double antibody competitive radioimmunoassays showed that the HaER particles do not share any detectable antigenic relatedness with the murine viruses' p30, but manifest a considerable relatedness with the feline leukemia virus p27 and a slight cross-reactivity with the rat virus major protein. The RNA-dependent DNA polymerase of HaER virus has a molecular size of approximately 73,000 daltons and in contrast to other mammalian retroviruses shows no significant preference for Mn2+ over Mg2+. Apart from the lack of antigenic relatedness between the HaER virus proteins and the p30 protein of murine viruses, there is also no antigenic relatedness between HaER and murine viruses insofar as their DNA polymerase is concerned.
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PMID:Hamster endogenous retrovirus (HaER)--distinct properties of structural proteins and DNA polymerase. 619 53

We have constructed a series of deletion mutations in the p30 and p10 domains of the gag gene of Moloney murine leukemia virus. Mutants with deletions in P30 were completely defective in virion particle production even though an altered gag precursor protein is synthesized. This domain is apparently critical for particle formation. A mutant in P10 was able to release virion particles into the medium, and low levels of reverse transcriptase activity could be detected in these virions. To explore the effects of these mutations on the utilization of the gag-pol precursor, we have introduced these mutants into cells already releasing defective particles from an endogenous provirus which directs the synthesis of gag gene products and not pol gene products. The P10 mutant was capable of providing pol function as judged by the incorporation of high levels of reverse transcriptase into the particles and complete complementation for XC plaque formation. In contrast, the mutants in P30 were negative in this complementation test. Thus, those gag mutants which were unable on their own to assemble virion particles were also unable to contribute the gag-pol precursor to these particles. These mutations are the first to be mapped to the gag region which affect pol function, suggesting that the gag-pol precursor must be assembled before pol is functionally separated from the gag domain. The concordance of the effects of different mutations on both particle formation and gag-pol utilization suggests that similar domains of gag (namely, domains in the P30 region) are needed for these two processes.
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PMID:Mutations in the gag gene of Moloney murine leukemia virus: effects on production of virions and reverse transcriptase. 619 13

The p30 antigen from Rauscher leukemia virus (R-MuLV) was separated into two fractions by chromatography on either phosphocellulose or DEAE-cellulose. The p30-I and p30-II were indistinguishable immunologically or by isoelectrofocusing and gel electrophoresis. An ATPase activity was tightly associated with p30-II that could not be separated by ion-exchange chromatography, isoelectrofocusing, or glycerol velocity gradient sedimentation. The ATPase hydrolyzed the gamma phosphate from only ATP or dATP. Immunoglobulin directed against R-MuLV p30 completely inhibited the p30-II associated ATPase. Glycerol velocity gradient analysis showed that p30-I sedimented as a 30-kDa species while the p30-II and its associated ATPase sedimented as a 60-kDa species. The p30-II was converted entirely to a 30-kDa form by treatment with 0.2% (w/v) lithium dodecyl sulfate, suggesting that it represented a complexed species of p30. Finally, p30-II was found to stimulate the activity of R-MuLV reverse transcriptase, but p30-I had no effect on the activity of the enzyme. These results suggested the existence of at least two different forms of p30 in R-MuLV.
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PMID:Characterization of a p30 fraction from Rauscher leukemia virus which has an associated ATPase activity. 620 91

We have analyzed the RNA genome of RadLV/VL3, a highly oncogenic murine leukemia virus. This virus is produced by a permanent cell line derived from a radiation leukemia virus-induced thymic lymphoma of C57BL/Ka mice. Two distinct RNA components were found in the virions: a 70S dimer containing two 8 kb RNA subunits and a 54S dimer containing two 5.6 kb RNAs. A nononcogenic retrovirus, BL/Ka(B), endogenous in the same strain of mice, contains only 8 kb viral RNA subunits. The linkages between both RadLV/VL3 dimers have identical thermal stabilities. Both dimers can serve as primer templates for reverse transcriptase and both produce very similar "strong-stop" cDNAs 147 +/- 1 bases long. Sequences at the 5' end of the 5.6 kb subunit contain the genes for the viral proteins p15 and p12, but the gene for p30 is either absent or partially deleted. In vitro translation of the 5.6 kb RNA yields a 100,000 molecular weight protein containing antigenic determinants which react with antibody to p15 but not with antibody to p30. In addition, cells producing RadLV/VL3 virus synthesize a novel of 1.6 kb poly(A)-containing cytoplasmic RNA which shows very little if any homology with BL/Ka(B) viral sequences.
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PMID:Radiation leukemia virus contains two distinct viral RNAs. 624 93

Reticuloendotheliosis virus (REV) is known to be capable of transforming chicken bone marrow cells in vivo and embryo fibroblasts in vitro. As with spleen necrosis virus, we have found that sequences related to REV are found in DNA of several uninfected avian species. For example, about 15% of the [3H]cDNA synthesized in the endogenous reverse transcriptase reaction reassociated with DNA of uninfected chickens. Kinetic analysis revealed only a few (less than five) such sequences per haploid genome, and the thermal stability of the reassociated duplex indicated less than perfect complementarity. Comparison of REV propagated in an avian cell line with REV grown in a canine line has revealed clear differences between the two isolates. Viral RNA and [3H]cDNA of REV isolated from the transformed chicken bone marrow cell line appear to consist of at least three sequence classes. The most numerous of these classes is highly related to REV propagated in canine cells. Only slightly less abundant is a class unrelated to RNA isolated from the canine virus but highly related to sequences found in normal uninfected avian cellular DNA. A third component is present at about 1% the level of the most numerous class. Although REV appears to be unrelated to the other known avian retroviruses, distant relatedness between p30's of REV and various mammalian type C viruses has recently been reported. We have asked whether REV-related sequences can be detected in various mammalian DNAs and viral RNAs. Hybridization experiments performed at low stringency have revealed no such sequences.
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PMID:Analysis of the nucleic acid components in reticuloendotheliosis virus. 624 35

This study describes the biological properties of a strain of virus isolated from tissues of a goat with leukoencephalomyelitis-arthritis. The agent is a retrovirus, having a virion-associated reverse transcriptase enzyme and an antigenic determinant(s) which cross-reacts with the p30 of visna-maedi viruses. Morphogenesis of the virus is also similar to visna virus in terms of virus assembly and the multinucleated giant cell formation which accompanies replication of the latter virus. Despite its cytopathogenic property the goat agent was not lytic in goat cell culture, causing instead a productive infection which persisted through multiple subcultures of the cells. The virus replicated incompletely in sheep cell cultures but could be rescued from the latter, weeks after inoculation, by co-cultivation with goat cells. Our data suggest that this strain of goat leukoencephalitis virus is a variant of the ovine retroviruses with a host range limited to the goat.
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PMID:Biological characterization of the virus causing leukoencephalitis and arthritis in goats. 625 88

Preparations of purified Rauscher murine leukemia virus were found to contain an endodeoxyribonuclease after disruption of the virus with nonionic detergents. The enzyme makes single-strand breaks in linear or covalently closed circular phage double-stranded DNA molecules. The enzyme was partially purified by ion-exchange chromatography on DEAE- and carboxymethyl-Sepharose columns followed by electrophoresis in DNA-containing polyacrylamide gels. The enzyme was separated from reverse transcriptase (p80pol), and the final endonuclease preparation contained no detectable reverse transcriptase activity. The DEAE-Sepharose column-purified endonuclease activity contained a polypeptide of about 40,000 Mr that we term p40. Peptide mapping experiments demonstrated that p40 shares methionine-labeled tryptic peptides with Pr200gag-pol and Pr135pol. Six major methionine-labeled tryptic peptides derived from p40 were found in Pr200gag-pol, but only five of these were detected in Pr135pol. The four core proteins (p30, p15, pp12, and p10) and p80pol plus p40 account for most, but not all, of the peptide sequences of Pr200gag-pol. The endonuclease-associated p40 is similar in size and precursor origin to the avian retrovirus-coded endonuclease (p32). In view of these similarities to the avian p32 endonuclease and its association with partially purified Rauscher murine leukemia virus-associated endonuclease preparations, we propose that p40 is the Rauscher murine leukemia virus-coded endonuclease.
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PMID:Endodeoxyribonuclease activity associated with Rauscher murine leukemia virus. 626 Sep 82

HTLV strain CR (HTLVCR) is a retrovirus which was isolated from a human T-cell lymphoma cell line. A protein of molecular weight 24,000 p24, was purified from this virus. Several results indicate that this p24 is an internal core protein of HTLVCR. (i) The p24 copurified with viral cores. (ii) It was labeled with 125I after disruption of the virus, but not when undisrupted virus was iodinated. (iii) The amount of p24 was directly proportional to the amount of HTLVCR. (iv) In chromatographic properties, the HTLVCR p24 behaved similarly to the major structural protein (24,000- to 30,000-molecular-weight protein) of other retroviruses. A rabbit antiserum raised against disrupted HTLVCR precipitated the labeled p24, and the precipitation was competed for by unlabeled HTLVCR and by cytoplasmic proteins from cells producing HTLVCR, but not by proteins from normal human cells, including normal growing human T-cells, and several cultured human cutaneous T-cell lymphoma lines. Proteins from several mammalian type B, type C, and type D viruses also failed to compete in this precipitation. Moreover, HTLVCR did not react in homologous and interspecies assays for p30 antigens of several mammalian type C and type D viruses. These observations agree with immunological comparisons between reverse transcriptase of HTLVCR and other retroviruses and nucleic acid sequence homology studies which indicate that the various HTLVCR isolates represent new retroviruses found in some human T-cell neoplasias.
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PMID:Immunological properties of a type C retrovirus isolated from cultured human T-lymphoma cells and comparison to other mammalian retroviruses. 626 63

Recombinant viruses were generated in tissue culture between Rauscher murine leukemia virus (MuLV) temperature-sensitive (ts) mutants restricted at different steps in virus replication and a mouse endogenous xenotropic virus, BALB:virus-2. Mutants used included ts 28, a late mutant which releases noninfectious viruses at 39 degrees C, and ts 29, a double mutant with a ts lesion in its reverse transcriptase and a late block affecting virus budding. Immunological typing of the translational products of clonal recombinant viruses made it possible to establish their partial genetic maps and localize regions of the viral genome affected by different ts lesions. Recombinants involving Rauscher MuLV ts 28 invariably contained BALB-virus-2 p15, p12, and p30 proteins, localizing the late defect in replication by this mutant to the 5' moiety of the viral gag gene. All ts 29-derived recombinants contained the entire BALB:virus-2 gag and pol genes. Substitution of the pol gene is in agreement with the reported thermolability of Rauscher MuLV ts 29 reverse transcriptase (Tronick et al., J. Virol. 16:1476-1482, 1975). Substitution of the gag gene suggests that internal structural proteins are actively involved in the virus budding processing. Rauscher MuLV recombinants were used to establish the genetic map of the Rauscher MuLV genome by T1 oligonucleotide fingerprinting analysis. Detection of Rauscher MuLV T1 oligonucleotides in representative recombinant viruses, whose protein phenotypes were established by immunological techniques, permitted their assignment to specific regions of the viral genome. The genetic map of Rauscher MuLV generated in these studies should be useful for identifying and characterizing the viral gene(s) involved in leukemogenesis.
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PMID:Recombinants between temperature-sensitive mutants of rauscher murine leukemia virus and BALB:virus-2: genetic mapping of the Rauscher murine leukemia virus genome. 626 12


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