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)

Radioimmunological techniques were applied to the quantitation of the translational products of the gag, pol, and env genes of mammalian type C viruses. Analysis of the viral proteins associated with simian sarcoma-associated virus (SSA V) and SSA V-infected cells revealed in each that the level of reverse transcriptase was less than 1% of that of the major viral structural protein, p30. The rate of intracellular degradation of reverse transcriptase in SSA V-infected cells was found to be no greater than that of several viral structural proteins, indicating that the lower levels of viral enzyme resulted from its decreased synthesis. By screening individual cells infected at limiting SSA V dilution, it was possible to isolate a clone (clone 16), which demonstrated levels of viral p12, p30, and gp70 similar to those found in wild-type SSA V-infected cells, and which released noninfectious virions in large quantity. The noninfectious virions and clone 16 cells were shown to lack immunologically or enzymologically detectable reverse transcriptase. With serial passage of clone 16 cells, reverse transcriptase activity became spontaneously detectable in tissue culture fluids, concomitant with the appearance of infectious virus. The reverse transcriptase associated with this virus was indistinguishable from SSA V polymerase, indicating that the genetic alteration restricting SSA V pol gene expression in clone 16 cells was reversible. These results further demonstrate the strict requirement of reverse transcriptase for establishment of type C virus infection. Possible mechanisms to account for the patterns of type C viral gene expression detected in SSA V-infected cells are discussed.
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PMID:Differential synthesis of mammalian type C viral gene products in infected cells. 7 58

A virus-specific protein of approximately 180,000 daltons has been identified in cells transformed by avian sarcoma virus. The protein, designated P180, includes immunological determinants of both viral core proteins and reverse transcriptase. Its tryptic peptides represent essentially the sum of those of the precursor of the core proteins (Pr76gag) and reverse transcriptase. Thus P180 must arise from the uninterrupted translation of gag and pol. The kinetics of its formation and decay suggest that P180 is the precursor of reverse transcriptase.
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PMID:A joint produce of the genes gag and pol of avian sarcoma virus: a possible precursor of reverse transcriptase. 7 87

A strategy based on the identification of type-specific antigenic determinants in the transitional products of gag (p15, p12, and p30 proteins), pol (reverse transcriptase), and env (gp70 glycoproteins) genes of mammalian type C viruses has been used to study genetic recombination between these RNA viruses. By this approach, recombinants involving exogenous and endogenous mouse type C viruses have been identified and genetically mapped. Analogous techniques have been applied to investigate the genetic relationships between different classes of endogenous virus that exist within the same mouse cells. Proteins of the inducible class of xenotropic virus were shown to exhibit extensive antigenic homology with the gag but not the env gene products of the ecotropic virus class. Instead, the env gene-coded glycoproteins of the inducible and noninducible xenotropic virus classes possessed striking antigenic relatedness. These results, as well as supporting findings from molecular hybridization, favor the concept that the inducible xenotropic virus of mouse cells arose by a recombinational mechanism involving the progenitors of the other two endogenous virus classes.
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PMID:Genetic recombination between mouse type C RNA viruses: a mechanism for endogenous viral gene amplification in mammalian cells. 7 13

The patterns of oncovirus protein biosynthesis are essentially similar for avian and mammalian viruses. In each case the four major internal structural proteins are synthesized as a precursor polypeptide of about 75 000 daltons, the product of the gag gene. Translation occurs on genome-sized mRNA. This polyprotein is cleaved in a series of steps to give the mature proteins. The mechanism and localization of cleavage have not yet been clarified. Viral reverse transcriptase, the product of the pol gene, also is translated on genome-sized mRNA as a precursor, which is a "read-through" product of the neighbouring gag gene. The two major envelope proteins are translated as a glycosylated precursor of apparent molecular weight about 90 000 from the env gene located on a sub-genomic RNA species. The precursor is transported to the plasma membrane where it may mark the site of virus budding. It is cleaved in transport or on the membrane, but the resulting two mature envelope proteins remain tied by disulfide bonds. Sarc, the protein product of the src gene that is responsible for transformation, is translated from a different viral mRNA than the structural proteins. Sarc has not been definitively characterized in any system.
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PMID:The biosynthesis of oncovirus proteins. 7 78

Cells infected by Rous-associated virus 61 (RAV-61) contained a precursor-like protein, pr90, that was specifically precipitated by antiserum directed against envelope glycoproteins, gp85 and gp35. Tryptic peptide mapping showed that pr90 contained tryptic sequences of both gp85 and gp35. Pactamycin mapping experiments indicated that the two glycoproteins are translated from the env-mRNA in the order (5') gp85--gp35. The pactamycin mapping experiments also indicated a translational order of p10--(p27, p12)--p15 for the gag proteins; this agreement with the order previously reported from tryptic mapping studies on precursor pr76 of avian myeloblastosis virus implied that the stoichiometry of the core proteins was unchanged when virions were assembled in the presence of pactamycin. The reverse transcriptase proteins, unlike those of the env and gag genes, fell on the right side of the pactamycin map. This result is in accord with the idea that most, if not all, of the reverse transcriptase protein is translated by read-through of the gag(pol) message rather than by translation of a hypothetical pol-mRNA devoted solely to synthesis of that protein.
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PMID:Proteins of Rous-associated virus 61, an avian retrovirus: common precursor for glycoproteins gp85 and gp35 and use of pactamycin to map translational order of proteins in the gag, pol, and env genes. 7 10

Clones of cells were isolated from single virus-single cell infections of NIH/3T3 cells with Moloney murine leukemia virus. Approximately one third of such clones aberrantly expressed viral gene functions. One clone produced virus with altered plaque morphology, while others failed to produce particles able to make plaques on XC cells. In addition, clones that made particles lacking reverse transcriptase were found, and these did not synthesize the reverse transcriptase precursor Pr180 gag-pol. One clone (M23) lacked any detectable glycoprotein or reverse transcriptase. Despite these defects, each clone released particles of type C morphology, suggesting that gag gene function alone may be sufficient for particle production. All the particles contained viral RNA of 60-70S that was composed of the normal 35S size subunits except for M23, which had a deletion in the viral genome of approximately 1000-1500 nucleotides. A variety of defective clones were also isolated following infection of rat cells with Moloney virus. It is apparent that the murine leukemia virus genome is ofter mutated by spontaneous processes generating a wide range of phenotypes.
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PMID:High frequency of aberrant expression of Moloney murine leukemia virus in clonal infections. 8 Feb 81

The genetic compositions of two independently derived preparations of the Bratislava-77 strain (B77) of Rous sarcoma virus were analyzed after each was passaged seven or more times in duck embryo fibroblasts. RNase, T1-resistant oligonucleotide fingerprint analysis of virion RNA from both preparations of duck-passaged B77 revealed the presence of two large noncontiguous deletions. Approximately 75% of the RNAs contained a deletion which spans oligonucleotides 304 to 4 on the viral genome (about 3,500 nucleotides) and encompasses all of the B77 polymerase gene. More than 90% of the RNAs also contained a deletion which spans src-specific oligonucleotides 6 and 5(about 2,200 nucleotides) and is identical to the deletion observed in transformation-defective B77. Virion RNA from duck-passaged B77 also contained two oligonucleotides (D1 and D2) not observed in the RNA of B77 virus grown on chicken embryo fibroblasts. Analysis of the virion RNA of duck-passaged B77 by denaturing agarose gel electrophoresis revealed four major subunits with molecular weights of 3.40 x 10(6), 2.65 x 10(6), 2.25 x 10(6), and 1.55 x 10(6). Whereas the 3.40- and 2.65-megadalton (Mdal) RNA species comigrated with the nondefective and transformation-defective RNAs of B77 propagated on chicken embryo fibroblasts, no counterparts to the 2.25- and 1.55-Mdal RNAs were observed in the RNA of B77 grown on chicken embryo fibroblasts. Oligonucleotide fingerprint analysis of these RNA species revealed that the 2.65-Mdal RNA contains the src-specific deletion and that 2.25-Mdal RNA contains the polymerase region deletion; both of these deletions were observed in the 1.55-Mdal RNA, which was the major RNA subunit species detected in duck-passaged B77. The new oligonucleotides (D1 and D2) observed in the duck-passaged virus were present in the 2.25- and 1.55-Mdal RNA species in vitro and in vivo and directs the synthesis of a 130,000-dalton protein (p130). p130 contains antigenic determinants specific for p27 (gag gene) and gp85 (env gene) but does not contain sequences which cross-react with antisera directed against the alpha beta form of RNA-dependent DNA polymerase (pol gene). This RNA, therefore, is generated by a fusion of the gag and env genes of Rous sarcoma virus B77.
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PMID:Deletion mutant of the Bratislava-77 strain of Rous sarcoma virus containing a fusion of the group-specific antigen and envelope genes. 9 86

A nonconditional mutant of B-tropic murine leukemia virus (MuLV), defective in polymerase, has been isolated by cloning chronically infected cells. The cell clone containing the mutant produced virus particles which were noninfectious. However, superinfection of the cells by replication-competent XC-negative viruses resulted in the rescue of virus capable of forming plaques in a modified XC test, termed the "complementation plaque assay" (A. Rein and R. H. Bassin, J. Virol. 28:656-660, 1978). Analysis of the noninfectious virions produced without superinfection demonstrated that they contained only 2 to 5% of the wild-type level of reverse transcriptase activity. Purification of this activity indicated that it was associated with a smaller molecule than that produced by wild-type virus. Cells producing the mutant virions did not contain the gag-pol precursor, Pr180gag-pol; however the cells contained proteins of 147K and 114K daltons precipitable with anti-pol serum. All of the normal structural proteins as well as 70S genomic RNA could be detected in the mutant particles. An interference test indicated that a functional ecotropic glycoprotein was synthesized by the mutant. These results indicate that the mutant has a unique defect in the pol gene.
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PMID:Mutant of B-tropic murine leukemia virus synthesizing an altered polymerase molecule. 9 71

Extracts from lymphoid and fibroblast cell lines transformed by Abelson murine leukemia virus (A-MuLV) contain a protein of molecular weight 120,000 (P120). Immunoprecipitation with specific sera shows that P120 contains regions homologous to the 5'-terminal segment of the MULV gag gene complex--p15, p12, and at least part of p30--but lacks detectable determinants of p10, reverse transcriptase, and the envelope glycoprotein. P120 is phosphorylated and has an intracellular half-life of 3--6 hr. In vitro translation of virion RNA from A-MuLV, with Moloney MuLV as helper, yields a product of molecular weight 120,000 with serological reactivity similar to that of the cellular P120. Translation of the RNA from the helper gave no P120. P120 is expressed in all lymphoid and fibroblastic cell lines we have tested that were transformed by A-MuLV but is not detectable in a lymphoid line in which the A-MuLV genome was established by infection but was not responsible for the transformation. Expression of P120 is selectively retained in clones of A-MuLV-transformed lymphocytes that convert to a nonproducer state after loss of expression of helper MuLV intracellular precursors. These results suggest that the P120 product of the A-MuLV genome may be responsible for maintenance of the transformed phenotype of lymphoid and fibroblast cells transformed by the virus.
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PMID:Identification of an Abelson murine leukemia virus-encoded protein present in transformed fibroblast and lymphoid cells. 20 68

Cell clones nonproductively transformed by the replication-defective Abelson strain of murine leukemia virus (AbLV) were analyzed for type C viral antigen expression by competition immunoassay. AbLV-transformed mink non-producer lines were found to express a 110,000- to 130,000-molecular weight polyprotein containing murine leukemia virus gag proteins p15 and p12 covalently linked to nonstructural AbLV-coded component(s) of around 80,000-100,000 molecular weight. This polyprotein lacked detectable antigenic cross-reactivity with other virion-coded gag gene proteins such as p30, p10, the viral reverse transcriptase (RNA-dependent DNA polymerase), or the major viral envelope glycoprotein, gp70. By analogy to earlier data on feline and avian sarcoma viruses, these results suggest that a portion of this polyprotein might represent the AbLV src gene product and that in translation it is initially linked in precursor form to gag structural proteins. Superinfection of mink cells nonproductively transformed by AbLV--with either a wild mouse amphotropic type C virus isolate, 4070-A, or with the endogenous cat virus, RD114--led to production of pseudotype virus containing high concentrations of the AbLV-coded precursor polyprotein.
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PMID:Cells nonproductively transformed by Abelson murine leukemia virus express a high molecular weight polyprotein containing structural and nonstructural components. 21 10


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