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 secondary structural features in the 70S RNAs of the Prague strain of avian Rous sarcoma virus, subgroup A (PR-RSV-A), and Moloney murine leukemia virus (M-MuLV) were compared by electron microscopy. The PR-RSV-A genome contained two subunits joined by a linkage structure as in the genomes of M-MuLV and other mammalian retroviruses. In both viral genomes, a highly reproducible hairpin occurred at about 70 nucleotides from the 5' end of each subunit and contained 320 +/- 8 nucleotides. The stable point of linkage between the subunits in both viral genomes involved fewer than 50 nucleotides and occurred at 466 +/- 9 nucleotides from the 5' end. This places the linkage about 350 nucleotides further toward the 3' end of the subunit than the binding site of primer tRNA. Another structural feature common to both genomes was a loop in each subunit. In M-MuLV, the loop contained 3.9 +/- 0.10 kilobases (kb) and occurred at a distance of 2.2 +/- 0.05 kb from the 5' end. In PR-RSV-A, the loop was smaller (2.3 +/- 0.10 kb) and further (3.3 +/- 0.10 kb) from the 5' end. When M-MuLV RNA was heated to 70, 85, or 90 degrees C and cooled, the hairpin consistently reformed at the 5' end. No other structures typical of the native molecules reappeared. In RNA samples heated to 70 degrees C, a new loop reproducibly occurred near the 5' end of each subunit, but this loop was not found in samples heated to higher temperatures. Based on all of these findings, we conclude that the genome of PR-RSV-A shares several features with M-MuLV and other mammalian retroviruses and that the primer tRNA molecules are not involved in the linkage of the two subunits in either genome. We also conclude that the dimer linkage and the loops in subunits are typical of the native molecules and that their formation requires a special environment.
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PMID:Secondary structural features in the 70S RNAs of Moloney murine leukemia and Rous sarcoma viruses as observed by electron microscopy. 626 Sep 92

Both lymphocytes and fibroblasts that have been transformed by ABelson murine leukemia virus contain 6- to 12-fold increased levels of the rare modified amino acid phosphotyrosine in their proteins. This observation, coupled with the fact that the p120 protein encoded by this virus has been shown to undergo an apparent autophosphorylation to yield phosphotyrosine in vitro, suggests that Abelson virus encodes a protein kinase that phosphorylates tyrosine in transformed cells. These results are similar to those obtained previously with Rous sarcoma virus and suggest, by analogy, that the modification of cellular polypeptides through the phosphorylation of tyrosine may be involved in cellular transformation by Abelson virus. p120 isolated from transformed cells contains phosphoserine, phosphothreonine, and phosphotyrosine. The phosphotyrosine is found at two sites in the protein. p120 therefore may be a protein kinase that undergoes autophosphorylation in vivo.
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PMID:Evidence that the Abelson virus protein functions in vivo as a protein kinase that phosphorylates tyrosine. 626 13

Transformation of chicken cells by Fujinami sarcoma virus (FSV), PRC II or Y73 (three independently isolated avian sarcoma viruses that are replication-defective and lack the Rous sarcoma virus src gene) resulted in significant elevation (4-13 fold) of phosphotyrosine levels in cellular protein. The gag-related proteins encoded by these avian sarcoma viruses (ASVs) were all associated with tyrosine-specific protein kinase activity when assayed in immune complexes and were phosphorylated at both tyrosine and serine residues in vivo. Both the phosphotyrosine level in protein of FSV-infected cells and the protein kinase activity assayed in immune complexes containing the FSV protein P140 were temperature-sensitive. The presumed transforming proteins of these ASVs were compared with those of Rous sarcoma virus (RSV), Abelson murine leukemia virus and the Snyder-Theilen and Gardner-Arnstein strains of feline sarcoma virus (FeSV), which have previously been associated with tyrosine-specific protein kinase activity. FSV and PRC II proteins were shown to be structurally related to one another and to the FeSV proteins by tryptic peptide mapping and by immunological studies. No homology was observed, however, between the transforming proteins of RSV, Y73, Abelson murine leukemia virus and the FSV/PRC II/FeSV class, suggesting there may be at least four classes of retroviruses whose transformation mechanisms involve aberrant phosphorylation of cellular protein at tyrosine residues.
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PMID:Transforming proteins of some feline and avian sarcoma viruses are related structurally and functionally. 626 83

Agents identified as adenovirus CELO were isolated from organ suspensions of 1500 Japanese quails (JQ) in 4 experiments. No contaminating viruses were found in examinations of cell cultures prepared from the kidneys of 80 JQ. Negative results were obtained in examinations of 163 antigens from JQ organs in the COFAL test. Agents identified as mycoplasma were isolated in 16 cases from 736 specimens of the virus-containing fluid used for manufacture of measles virus. According to the results of the CFT, 59 antigens prepared from Japanese quail embryo cell cultures contained no oncornavirus antigens and were negative in the COFAL test. Among 1848 JQ sera examined for the presence of antibody to leukemia-sarcoma complex viruses only 2 sera were found in 1976 to contain antibody to Rous sarcoma virus. No antibody to Marek disease virus in 414 serum samples or to Newcastle disease virus in 554 sera were detected. Among 500 sera tested 30.8% contained antibody to adenovirus CELO.
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PMID:[Study of viral contamination of Japanese quail and cell cultures from their embryos]. 626 56

Integration of retroviral DNA appears to occur randomly in host genomes, suggesting that retroviruses can act as insertion mutagens. We have confirmed this prediction by showing that the nontransforming retrovirus, Moloney murine leukemia virus (M-MuLV), can insert its provirus within the selectable target provided by a single provirus in a clonal rat cell line (B31) transformed by Rous sarcoma virus (RSV). Analysis of over 60 morphological revertants of M-MuLV-superinfected B31 cells revealed two lines with inserts of M-MuLV proviruses within the RSV provirus but outside the transforming gene of RSV (src), at sites 0.6 and 4.0 kb from the 5' end. The inserts did not inactivate initiation of RSV RNA synthesis but did affect elongation or processing, or both, generating species with the 5' end of RSV RNA linked to sequences that presumably derive from the inserted M-MuLV DNA. In one mutant line, most of the insert was excised at low frequency, apparently by homologous recombination between repeated sequences at the ends of M-MuLV DNA. After excision, RSV src mRNA was present in normal amounts, and the cells resumed a transformed appearance. In at least four independent lines, large portions of the left end of the RSV provirus (from 1 to 6 kb) and variable amounts of leftward flanking cellular DNA (from 0.5 to 10-15 kb or more) were deleted, without nearby insertions of M-MuLV NA. The deletions removed the putative promoter for synthesis of RSV RNA; in the two cases examined, no RSV RNA was detected. These deletions may represent a second mutational effect of the superinfection by M-MuLV.
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PMID:Retroviruses as mutagens: insertion and excision of a nontransforming provirus alter expression of a resident transforming provirus. 626 4

Reticuloendotheliosis virus strain T (REV-T) is a highly oncogenic avian retrovirus which causes a rapid neoplastic disease of the lymphoreticular system. Upon infection, this virus gives rise to two species of unintegrated linear viral DNA, which are 8.3 and 5.5 kilobase pairs long and represent the helper virus (REV-A) and the oncogenic component (REV-T), respectively. Restriction endonuclease cleavage maps of these two DNA components indicate that REV-T DNA has a large portion of the genome deleted with respect to REV-A DNA and a substitution about 0.8 to 1.5 kilobase pairs long that is unrelated to REV-A DNA. These additional sequences comprise the putative transforming region of REV-T (rel). A chicken spleen cell line transformed by REV-T produced virus which upon infection gives rise to three species of unintegrated linear viral DNA (8.3, 5.5, and 3,3 kilobase pairs). We isolated the proviruses of the 8.3- and 3.3-kilobase pair species from this cell line by cloning in the phage vector Charon 4A. Restriction enzyme mapping showed that the two proviral clones are proviruses of REV-A and a variant of REV-T, respectively. A subclone of the variant REV-T provirus specific for the rel sequences of REV-T was used as a hybridization probe to demonstrate that the rel sequences are different from the putative transforming sequences of Schmidt-Ruppin Rous sarcoma virus strain A, avain myelocytomatosis virus, avian myeloblastosis virus, avian erythroblastosis virus, Abelson murine leukemia virus, and Friend erythroleukemia virus. In addition, the rel-specific hybridization probe was used to identify a specific set of sequences which are present in uninfected avian DNAs digested with several restriction enzymes. The corresponding cell sequences are not arranged like rel in REV-T.
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PMID:Characterization of reticuloendotheliosis virus strain T DNA and isolation of a novel variant of reticuloendotheliosis virus strain T by molecular cloning. 627 17

OK10, a defective leukemia virus, is produced as a defective particle by so-called nonproducer transformed quail fibroblasts. OK10 defective viral particles contain an 8-kilobases (kb)-long genomic RNA, lack any detectable reverse transcriptase activity, and are not infectious. We studied the genetic content of OK10 RNA extracted from both virions and infected cells. As shown by RNA-cDNA hybridizations in stringent conditions, about 77% (6.4 kb) of the OK10 8.0kb RNA was related to avian leukosis viruses in the three structural genes gag, pol, and env, as well as in the c region. The remainder of the OK10 genome-encoding capacity (</=1.6 kb) was homologous to the MC29-specific transforming sequence myc(m) and therefore has been named myc(o). EcoRI restriction analysis of the OK10 integrated proviral DNA with different probes indicated the presence of only one provirus in the OK10 QB5 clone, which agreed with the gene order: 5'-gag-Deltapol-myc(o)-Deltaenv-c- 3'. Heteroduplex molecules formed between the viral OK10 8.0-kb RNA and the 6.8-kb SacI DNA fragment of the Prague A strain of Rous sarcoma virus confirmed that structure and indicated that the myc(o) sequence formed a continuous RNA stretch of 1.4 to 1.6 kb long between Deltapol and Deltaenv. We also examined the myc(o)-containing mRNA's transcribed in OK10-transformed cells. OK10-transformed quail fibroblasts (OK10 QB5) transcribed two mRNA species of 8.0 and 3.6 kb containing the myc(o) sequence. The genetic content of the 3.6-kb species made it a possible maturation product of the genome size 8-kb species by splicing out the gag and pol sequences. In OK10-transformed bone marrow cells (OK10 BM), a stable bone marrow-derived cell line producing OK10, the myc(o) sequence was found in four RNA species of 11.0, 8.0, 7.0, and 3.6 kb. Again, the genetic content of these mRNA's indicated that (i) the 3.6-kb species could be spliced out of the 8.0-kb-genome size mRNA and (ii) the 11.0-kb-long mRNA could represent a read-through of the OK10 provirus, the corresponding maturation product being, then, a 7.0-kb mRNA. The 7.0- and 3.6- kb mRNA's both contained the myc(o) sequence, but no sequences related to the gag or pol gene. In conclusion, whereas the myc sequences have been generally thought to be expressed through a gag-onc fusion protein, as for MC29 and CMII viruses, our experiments indicate that they could also be expressed as a non-gag-related product made from a subgenomic mRNA in the OK10-transformed cells.
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PMID:Subgenomic mRNA in OK10 defective leukemia virus-transformed cells. 628 57

Different variants of Moloney murine sarcoma virus (MSV) were examined by nucleotide sequencing to compare the junctions between the acquired cellular sequence, v-mos, and the adjacent virus-derived sequences. These variants included 124-MSV, m1-MSV, and HT1-MSV and also the purportedly independent isolate Gazdar MSV. These four strains have an identical 5' junction between the murine leukemia virus env gene and the v-mos gene. This junction lies within the sixth codon of the chimeric env-mos coding region that encodes the transforming gene product. In contrast, at the 3' junction between the v-mos gene and the murine leukemia virus env gene, the three variants examined here were all different. A small deletion was found in the COOH-terminal portion of the m1-MSV env-mos coding region, indicating that the COOH terminus of this transforming gene product must be different from that of 124-MSV or HT1-MSV. The data presented here are consistent with the thesis that a virus closely related to HT1-MSV was the primordial Moloney MSV, and that all other related strains evolved from it by deletion or rearrangement. The variability observed in the Moloney MSV family is discussed in terms of possible mechanisms for the initial capture of mos sequences by the parental retrovirus and also in comparison with other transforming retrovirus families, such as Abelson murine leukemia virus and Rous sarcoma virus.
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PMID:Recombinational junctions of variants of Moloney murine sarcoma virus: generation and divergence of a mammalian transforming gene. 630 Apr 24

We have identified p10 as a fifth gag protein of avian sarcoma and leukemia viruses. Amino-terminal protein sequencing of this polypeptide purified from the Prague C strain of Rous sarcoma virus and from avian myeloblastosis virus implies that it is encoded within a stretch of 64 amino acid residues between p19 and p27 on the gag precursor polypeptide. For p10 from the Prague C strain of Rous sarcoma virus the first 30 residues were found to be identical with the predicted amino acid sequence from the Prague C strain of Rous sarcoma virus DNA sequence, whereas for p10 from avian myeloblastosis virus the protein sequence for the same region showed two amino acid substitutions. Amino acid composition data indicate that there are no gross composition changes beyond the region sequenced. The amino terminus of p10 is located two amino acid residues past the carboxy terminus of p19, whereas its carboxy terminus probably is located immediately adjacent to the first amino acid residue of p27.
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PMID:Amino-terminal amino acid sequence of p10, the fifth major gag polypeptide of avian sarcoma and leukemia viruses. 630 Apr 42

It has recently been shown by mass spectral analysis (Henderson et al., Proc. Natl. Acad. Sci. U.S.A. 80:339-343, 1983) that the p15gag protein of murine leukemia viruses contains a novel post-translational modification, an amino-terminal myristyl (tetradecanoyl) amide. In this report we show that p15gag is the only structural protein to contain this fatty acid. In addition, the gag precursor polyproteins of type B, C, and D retroviruses have been examined for the presence of myristic acid by metabolic labeling and immunoprecipitation studies. In a panel of mammalian type C retroviruses we found that the precursor polyprotein Pr65gag homologs, but not the glycosylated forms (gPr80gag homologs), were specifically labeled after a 5-min incubation of infected cells with [3H]myristic acid. The gag precursor polyprotein was also labeled in mouse mammary tumor virus and in Mason-Pfizer monkey virus, but Pr76gag of Rous sarcoma virus failed to incorporate [3H]myristate. Under similar conditions, [3H]palmitate was not found to be incorporated into any viral gag proteins. Thus, myristylation appears to be a common feature of mammalian type B, C, and D retroviruses but not of avian retroviruses.
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PMID:In vivo modification of retroviral gag gene-encoded polyproteins by myristic acid. 630 7


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