Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023418 (leukemia)
 93,477 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The majority of the mRNA that specifies retrovirus glycoproteins is known to be derived from the 3' half of the genome. To examine whether the glycoprotein mRNA of murine leukemia viruses (MuLVs) might consist of portions derived from both the 5' and 3' ends of the viral genome, we performed hybridization with a 5'-specific probe and heteroduplex analysis with long reverse transcribed DNA. A 5' probe was made by purifying a discrete 50 nucleotide-long reverse transcript attached to its tRNA primer. This probe was found to hybridize to RNA of the size of glycoprotein mRNA--21S, poly(A)-containing RNA--indicating that the mRNA could have a 5' leader sequence. The 5'-specific sequences were studied by electron microscopic examination of hybrids between 21S RNA and the two longest discrete cDNA species synthesized in the endogenous reverse transcriptase reaction. One of these species, 8.8 kb long, is only made in the absence of actinomycin D, but it does not contain any self-complementary sequences, and therefore appears to be a complete transcript of the viral genome. The shorter of the two species, 8.2 kb long, is synthesized whether or not actinomycin D is present; it must terminate 500--600 nucleotides internal to the 5' end of the template RNA. The structures observed in heteroduplexes of 21S RNA and these DNAs indicated the presence of a leader sequence approximately 500 nucleotides long at the 5' end of the 21S RNA. Sequences comprising this leader segment in the 21S RNA mapped at the 5' end of the genome RNA; the rest of the 21S RNA consisted of sequences from the 3' portion of the genome. Analysis of heteroduplexes with 8.2 kb DNA suggested that actinomycin D could block the reverse transcription of most of the sequence in the genome RNA that appears as a leader in the 21S RNA.
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PMID:Analysis of a 5' leader sequence on murine leukemia virus 21S RNA: heteroduplex mapping with long reverse transcriptase products. 7 33

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

Moloney-murine sarcoma virus (S+L- strain of M-MSV) has been nonproductively cloned in murine and non-murine host cells (S+L- cells) and the expression of Moloney leukaemia virus (M-MuLV) 30000 mol. wt. core protein (p30) and envelope glycoprotein (gp69/71) were studied by radioimmunoassay. Antigenic determinants of the M-MuLV p30 were associated with the sarcoma virus genome in these non-productively transformed cell clones studied, while the determinants of M-MuLV gp69/71 were not. The absence of envelope-associated glycoprotein expression in sarcoma virus transformed cells was confirmation of biological studies demonstrating that rescued sarcoma virions acquire envelope-associated properties of host range, neutralization and interference from rescuing helper virus, and further evidence that the M-MuLV gp69/71 sequences have been deleted during the formation of the M-MSV. During the course of these studies, it was also found that S+L- dog cells were releasing into culture supernatant large amounts of the p30 antigenic determinant, apparently as a soluble antigen.
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PMID:Further evidence for deletion of envelope glycoprotein (gp69/71) sequences in formation of Moloney-murine sarcoma virus. 8 Apr 47

The XC syncytia formation observed when ecotropic murine leukemia virus producer cells were cocultivated with XC cells was specifically inhibited by anti-MuLV gp69/71 antibodies with type- or group-specific activities. Thus, the major glycoprotein of budding viruses was probably responsible for the fusion with XC cells. Since this inhibition is specific for anti-gp69/71, it provides a simple, sensitive and convenient way to type ecotropic type C viruses and to detect anti-gp69/71. The micromethod we have developed has been applied to the detection of type-specific anti-GLV gp69/71 natural antibodies in the serum of normal mice.
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PMID:Specific inhibition of XC syncytia formation by anti-MuLV gp69/71 antibodies. 8 15

Antiserum directed against murine leukemia virus also reacts with several external proteins present in rat cells transformed by a temperature-sensitive Rous sarcoma virus. Reaction of iodinated cell extracts with anti-MLV (murine leukemia virus) serum revealed the presence of a 200,000 dalton iodinated component detectable also by metabolic labelling with glucosamine only in serum-starved cultures restricted in the expression of transformation. A similar assay with iodinated cells that express the transformed phenotype revealed the preferential recognition of two components with an approximate molecular weight of 100,00 daltons as well as an additional 65,000-dalton external component. Growth of the transformed non-producer NT3-KR cells in the presence of inducers of C-type viruses leads to an increased synthesis of a 100,000-dalton glycoprotein (gp100) recognized by the anti-MLV serum which is also recognized by the antiserum in NRK-MSV-MLV transformed producer cells, in addition to a virus-like glycoprotein of 71,000 dalton (gp71). Absorption of the anti-MLV serum with monolayers of NT3-KR cells eliminated the ability of the serum to recognize the gp100 but not the gp71 from NRK-MSV-MLV-transformed producer cells. The mediation of post-translational changes in growth control is suggested by the transformation-dependent alteration in the molecular weight of the non-virion surface proteins recognized by anti-MLV serum in the rat cells used in this study.
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PMID:Antiserum to murine leukemia virus recognizes novel cell surface molecules associated with growth control and transformation. 8 26

Previously we detected an antigen in cells infected with the spleen focus-forming virus (SFFV) with a radioimmunoassay specific for the gp 70's of murine leukemia mink cell focus-inducing (MCF) viruses. This antigen has now been characterized in competition radioimmunoassays with limiting dilutions of antibody and in pulse-labeling studies under conditions of antibody excess. Both methods of analysis indicate that the SFFV-encoded antigen is a glycoprotein with a molecular weight of approximately 52,000. The gp52 shared immunological reactivity and methionine-containing tryptic peptides with the gp70 of a Friend MCF virus and was expressed on the surface of SFFV-infected cells as well as in the cytoplasm. The gp52 could be detected (i) in fibroblastic cell lines from several species when these cells were infected with SFFV; (ii) in several established erythroleukemic cell lines; and (iii) in the spleens of mice recently infected with SFFV. Although it shared immunochemical properties with the gp70 of Friend MCF virus, the gp52 could be distinguished from the MCF gp70 (i) by its apparent lack of group and interspecies immunological determinants compared with MCF virus-derived gp70's; (ii) by its failure to be released from cells infected with SFFV or SFFV plus helper virus; (iii) by its molecular weight; and (iv) by tryptic peptide analysis. The results indicate that SFFV codes for an MCF gp70-related gp52 which is apparently no longer a virion structural protein like the MCF gp70 from which it was originally derived.
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PMID:Characterization of a protein found in cells infected with the spleen focus-forming virus that shares immunological cross-reactivity with the gp70 found in mink cell focus-inducing virus particles. 9 Jan 66

Cell lines obtained by in vitro transformation of bone marrow with Abelson murine leukemia virus (A-MuLV) can be divided into three classes: producers, releasing reverse transcriptase-containing particles and infectious virus; nonproducers, releasing no viral particles; and defective producers, the most common phenotype, releasing particulate reverse transcriptase in the absence of infectious virus. When such cell lines were analyzed 1 to 2 weeks after their isolation, however, all produced infectious virus. Because these cell lines were carried in culture, many ceased to release infectious virus but produced defective virions. One defective producer, SWR4, has been extensively studied. The particles it produces have the same density as that of virions of Moloney murine leukemia virus (M-MuLV). The particles contain no 35 to 70S RNA, as determined by analysis of [3H]uridine-labeled particles, and exhibit no endogenous reverse transcriptase activity. Although the reverse transcriptase enzyme is of normal size, the major structural protein of the defective virions has a molecular weight of 28,000 (p28), in contrast to the p30 of M-MuLV, and no viral glycoprotein was evident. The defective particles do not appear to arise either from the helper virus or from Abelson virus. An alteration of the protein of the helper virus is an unlikely source of p28 because particles produced by lymphoid cells transformed with another strain of M-MuLV as helper (M-MuLV-TB) contained p28 with an unaltered cleavage pattern, although M-MuLV-TB p30 differs from M-MuLV p30. The A-MuLV genome lacks the capacity to code for the reverse transcriptase virions. Clones of fibroblasts infected with A-MuLV only occasionally produce defective particles. The defective particles therefore probably arose from an endogenous virus that is preferentially expressed in the class of lymphoid cells transformed by A-MuLV. This interpretation implies that the majority of A-MuLV-transformed lymphoid cells completely lose expression of the helper virus genome.
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PMID:Virus production by Abelson murine leukemia virus-transformed lymphoid cells. 9 Jan 75

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

Large-scale production and concentration procedures have been standardized to study the biological properties of Rauscher leukemia virus produced from the high-passaged JLS-V9-H mouse bone marrow cell line. Virus produced early (days 4 to 6) in the harvest and refeed cycle contained higher levels of ribonucleic acid-directed deoxyribonucleic acid polymerase activity and was more infectious than Rauscher leukemia virus produced later (days 7 to 10) in the growth period. The peak of virus production as detected by physical assays (virus particle count, protein, and p30 antigen) was highest at day 6, whereas the optimum biological and ribonucleic acid-directed deoxyribonucleic acid polymerase activity occurred 24 h earlier. When product characterization values of each concentrate were adjusted to a specific activity (i.e., per milligram of protein) basis, virus particle counts averaged 4 x 10(11) through days 5 to 9, and the peak infectivity occurred at day 4, whereas ribonucleic acid-directed deoxyribonucleic acid polymerase activity was highest at day 4 (endogenous) and 5 (exogenous). Sodium dodecyl sulfate-polyacrylamide gel analysis revealed only slight differences in the polypeptide pattern of Rauscher leukemia virus harvested from cultures of varying age, although Rauscher leukemia virus produced between days 3 and 5 contained more glycoprotein than either earlier or later harvests.
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PMID:In vitro production of Rauscher murine leukemia virus: influence of culture age on biological properties. 9 28

The occurrence of fatal spontaneous leukemia in AKR mice could be drastically reduced by passive immunization with goat antibody against isolated murine Friend virus glycoprotein gp71, possessing high group specific reactivity. The success depended on the time of antibody application. The best results were achieved when mothers and babies were inoculated.
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PMID:[Spontaneous leukemia of AKR mice. Successful passive immunization with goat antibodies against isolated glycoprotein gp71 of Friend leukemia virus]. 14 18


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