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)

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

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

[3H]tyrosine-labeled viral precursor polyproteins and known mature viral proteins derived from the Rauscher murine leukemia virus gag and pol genes were examined by two-dimensional tryptic peptide mapping. Pr200gag-pol was found to contain peptide sequences of the viral core proteins p30, p15, p12, and p10, as well as peptide sequences found in the cell-associated reverse transcriptase. Intermediate reverse transcriptase precursor Pr125pol lacked peptide sequences of the four-core proteins but contained reverse transcriptase-specific tryptic peptides plus two additional tyrosine-containing tryptic peptides not related to gag or pol gene products. Methionine-containing tryptic peptide analysis also suggested the presence of additional protein material in Pr125pol (Kopchick et al., Proc. Natl. Acad. Sci. U.S.A. 75:2016-2020, 1978). Pr200gag-pol, although containing both viral core and reverse transcriptase-assoicated methionine and tyrosine tryptic peptides, also contained additional tryptic peptides. Thes are of two classes: (i) tryptic peptides associated with the Pr125pol but not Pr80pol and (ii) tryptic peptides not found in Pr125pol or in any known viral protein. One interpretation of these results is that Pr200gag-pol contains additional gene products aside from the gag and pol genes. Pr80gag and Pr65gag peptide maps were also examined and found to have sequences of all four core proteins. Pr65gag was found to contain two p30 tyrosine tryptic peptides that were absent in Pr80gag, suggesting that Pr80gag may not be the precursor to Pr65gag. Pr80gag, as expected from its larger size, also contained tryptic peptides not found in Pr65gag. Two of these additional Pr80gag tryptic peptides were found in Pr80pol as well but not in any of the viral core proteins, suggesting that Pr80gag and Pr80pol may have overlapping peptide sequences. Consistent with this finding is the conclusion that Pr80gag terminates within the pol gene. A model that describes the relationship of these recent findings to viral gene products is presented.
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PMID:Tryptic peptide analysis of gag and gag-pol gene products of Rauscher murine leukemia virus. 46 95

Translation of Rauscher murine leukemia virus (R-MuLV) 35S RNA in an mRNA-dependent cell-free protein-synthesizing system yields polypeptides identical to authentic Pr65gag, the R-MuLV gag precursor, and Pr200gag-pol, the precursor to the R-MuLV reverse transcriptase. In addition to these polypeptides, the cell-free product contains a family of polypeptides of less than 65,000 molecular weight which appear to be generated by premature termination of protein synthesis within the viral gag gene. We compared the tryptic maps of several of these less than 65,000-molecular-weight premature termination polypeptides with that of full-size Pr65gag and found a progressive loss of tryptic peptides which could be assigned to known R-MuLV gag proteins. A 40,000-molecular-weight fragment, P40gag, lacked p10 and part of p30, placing p10 at the C terminus pf Pr65gag and p30 ajacent to it. Fragments of 33,000 (P33gag) and 27,000 to 28,000 (P27/28gag) molecular weight showed a successive loss of additional p30 tryptic peptides, but no loss of either p15 or p12. An 18,000-molecular-weight fragment lost p12 but retained p15. These data suggest an R-MuLV gag gene order of NH2-p15-p12-p30-p10-COOH.
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PMID:Tryptic peptide analyses of polypeptides generated by premature termination of cell-free protein synthesis allow a determination of the Rauscher leukemia virus gag gene order. 73 99

Nasal exudate and tumour tissue from goats with enzootic nasal tumours were shown to contain a reverse transcriptase activity associated with a particle of buoyant density typical of retroviruses. The same particle contained a 25,000 Mr protein that cross-reacted with the p27 of Mason-Pfizer monkey virus (MPMV) and with p25 of sheep pulmonary adenomatosis retrovirus. It also contained a low Mr protein related to p10-12 of MPMV.
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PMID:Enzootic nasal tumour of goats: demonstration of a type D-related retrovirus in nasal fluids and tumours. 171 43

We have purified from Moloney murine leukemia virus (Mo-MuLV) a protease that has the capacity of accurately cleaving the polyprotein precursor Pr65gag into the mature viral structural proteins. Both the NH2- and COOH-terminal amino acid sequences have been determined and aligned with the amino acid sequence deduced from the DNA sequence of Mo-MuLV by other workers. The results show that: (i) the protease is located at the 5' end of the pol gene, and the first four amino acids are overlapped with the 3' end of the gag gene; (ii) the fifth amino acid residue is glutamine, which is inserted by suppression of the UAG termination codon at the gag-pol junction; and (iii) the protease is composed of 125 amino acids with calculated Mr = 13,315, and the COOH terminus of the protease is adjacent to the NH2 terminus of reverse transcriptase. The map order of the gag-pol gene is proposed to be 5'-p15-p12-p30-p10-protease-reverse transcriptase-endonuclease-3'.
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PMID:Murine leukemia virus protease is encoded by the gag-pol gene and is synthesized through suppression of an amber termination codon. 388 15

An approach toward elucidation of the mechanisms of action of mammalian leukemia viruses has been made by the generation in tissue culture of recombinant viruses between a potent murine leukemia virus (MuLV), Rauscher-MuLV, and an endogenous xenotropic mouse type-C virus, BALB:virus-2, without known malignant potential. Using a double selection system devised to select against the temperature-sensitive (ts) lesion associated with a mutant of Rauscher-MuLV and the xenotropic host range of BALB:virus-2, recombinant viruses were obtained at frequencies ranging from 0.01 to 0.1%. Recombinant viruses were identified on the basis of the type specific antigenic determinants in the translational products of gag (p15, p12, p30, and p10 proteins), pol (reverse transcriptase), and env (gp70 glycoprotein) genes. By this approach, the partial genetic maps of a large number of recombinants were obtained. The fact that p10 of Rauscher-MuLV ts 25, the mutant utilized, was the only protein uniformly lacking in recombinant viruses, localized the lesion inhibiting gag precursor cleavage in this mutant at the carboxy terminus of its gag gene. The recombinant viruses demonstrated two host range phenotypes as defined by Fv-1 host cell restriction. In each case, NB-tropic recombinants possessed the p30 of BALB:virus-2 p30. Thus, it was possible to assign the site of Fv-1 action at, or closely linked, to the viral p30. The target within the viral genome of a second host restriction was also mapped. A serum factor, previously shown to specifically inactivate xenotropic virus infectivity, was demonstrated to exert its action on the viral env gene product. The system described here allows the generation of specific recombinant genotypes that should be useful in defining those regions of the viral genome involved in leukemogenesis.
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PMID:Viral genes involved in leukemogenesis. I. Generation of recombinants between oncogenic and nononcogenic mouse type-C viruses in tissue culture. 615 14

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

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


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