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Query: UMLS:C0679427 (myeloblastosis)
982 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The availability of a purified RNA-instructed DNA polymerase (reverse transcriptase) from avain myeloblastosis virus provided the opportunity to explore whether this enzyme could be used as a general tool for synthesizing DNA complements of a wide variety of natural RNAs. The results described show that this potentially useful situation is in fact realized. The avian viral transcriptase can mediate the synthesis of DNA complementary to RNAs of such widely divergent origins as Qbeta bacteriophage and Moloney sarcoma virus. These findings open up novel pathways for the experimental resolution of several interesting problems. Thus, given a purified RNA message, one should be able to synthesize the corresponding DNA genetic material. If suitably labeled, the synthetic DNA has various obvious uses, including its use via molecular hybridization as an analytical probe for the corresponding gene on the chromosomes or for its message in a complex mixture of RNA molecules. Of immediate practical interest is the import of these findings for viral oncology. They imply that for many purposes we will not be compelled to isolate or use the "reverse transcriptase" from each oncogenic virus in order to synthesize its complementary DNA. The ability of one enzyme to accept a variety of oncogenic RNAs will obviate many of the logistical difficulties that arise, particularly in attempts to illuminate the etiology of human cancer.
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PMID:Synthesis of DNA complements of natural RNAs: a general approach. 433 Sep 45

The 70S genome of two RNA tumor viruses, murine sarcoma virus and avian myeloblastosis virus, binds to Millipore filters in buffer with high salt concentration and to glass fiber filters containing poly(U). These observations suggest that 70S RNA contains adenylic acid-rich sequences. When digested by pancreatic RNase, 70S RNA of murine sarcoma virus yielded poly(A) sequences that contain 91% adenylic acid. These poly(A) sequences sedimented as a relatively homogenous peak in sucrose gradients with a sedimentation coefficient of 4-5 S, but had a mobility during polyacrylamide gel electrophoresis that corresponds to molecules that sediment at 6-7 S. If we estimate a molecular weight for each sequence of 30,000-60,000 (100-200 nucleotides) and a molecular weight for viral 70S RNA of 3-12 million, each viral genome could contain 1-8 poly(A) sequences. Possible functions of poly(A) in the infecting viral RNA may include a role in the initiation of viral DNA or RNA synthesis, in protein maturation, or in the assembly of the viral genome.
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PMID:The genome of RNA tumor viruses contains polyadenylic acid sequences. 433 37

No significant hybridization was detected of DNA from simian virus 40 or polyoma virus, and of 70S RNA from avian myeloblastosis virus, murine leukemia virus (Rauscher), murine sarcoma virus (Kirsten), RD-114B, simian sarcoma virus-1, or Mason-Pfizer virus.
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PMID:Lack of sequence homology between the 70S RNA of various RNA tumor viruses and the DNA of simian virus 40 or polyoma virus. 435 55

The mouse cell line, BALB/c 3T3, and its derivatives transformed either spontaneously or by treatment with a variety of external agents, were analyzed for cytoplasmic RNA complementary to DNA products prepared from the Kirsten strain of murine sarcoma-leukemia virus, and from an endogenous type C virus of BALB/c 3T3. Although none of these cell lines spontaneously releases complete type C virions, they all contain RNA which is partially homologous to a portion of the 35S RNA isolated from these viruses. The parental cell line, BALB/c 3T3, contains a low level of viral-related RNA, and there is an increased amount of this RNA in some of the transformed cells. The RNA detected represents only a fraction of the viral RNA found in virus-producing cells. The formation of RNA:DNA hybrids was detected by equilibrium centrifugation in Cs(2)SO(4) density gradients and by analysis with a single-strand-specific nuclease from Aspergillus oryzae. Viral DNA products prepared either from an endogenous reaction with whole virus in the presence of actinomycin D or from purified 70S viral RNA as template using avian myeloblastosis virus DNA polymerase yield comparable data. In addition, all of the BALB/c lines examined produce detectable levels of murine type C virus group-specific antigen.
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PMID:Partial transcription of murine type C viral genomes in BALB c cell lines. 435 49

A plasmid, pJL6, was constructed that contains a unique Cla I site 12 codons beyond the bacteriophage lambda cII gene initiation codon, as well as an adjacent unique Hind III site. These sites allowed us to fuse the sequences from the avian myelocytomatosis virus (MC29) v-myc gene, the avian myeloblastosis virus (AMV) v-myb gene, and the Harvey murine sarcoma virus (Ha-MuSV) v-ras gene to the amino-terminal portion of the cII gene. Transcription of the hybrid genes is controlled from the lambda PL promoter. When this promoter is derepressed, E. coli cells harboring the chimeric plasmid produce levels of fusion proteins that amount to over 5% of total cellular protein. Antibodies raised by the cII-myc fusion protein form an immunoprecipitate with the MC29 gene product, P110gag-myc. The cII-ras fusion protein is precipitated by monoclonal antibodies directed toward the Ha-MSV p21ras, binds GDP, and is capable of autophosphorylation.
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PMID:High-level expression of oncogenes in Escherichia coli. 610 Oct 25

Chicken myeloblasts transformed by avian myeloblastosis virus (AMV) in the absence of nondefective helper virus (termed nonproducer cells) were found to release a defective virus particle (DVP) that contains avian tumor viral gag proteins but lacks envelope glycoprotein and a DNA polymerase. Nonproducer cells contain a Pr76 gag precursor protein and also a protein that is indistinguishable from the Pr180 gag-pol protein of nondefective viruses. The RNA of the DVP is 7.5 kilobases (kb) long and is 0.7 kb shorter than the 8.2-kb RNAs of the helper viruses of AMV, MAV-1 and MAV-2. Comparisons based on RNA.cDNA hybridization and mapping of RNase T1-resistant oligonucleotides indicated that DVP RNA shares with MAV RNAs nearly isogenic 5'-terminal gag and pol-related sequences of 5.3 kb and a 3'-terminal c-region of 0.7 kb that is different from that found in other avian tumor viruses. Adjacent to the c-region, DVP RNA contains a contiguous specific sequence of 1.5 kb defined by 14 specific oligonucleotides. Except for two of these oligonucleotides that map at its 5' end, this sequence is unrelated to any sequences of nondefective avian tumor viruses of four different envelope subgroups as well as to the specific sequences of fibroblast-transforming avian acute leukemia and sarcoma viruses of four different RNA subgroups. The specific sequence of the DVP RNA is present in infectious stocks of AMV from this and other laboratories in an AMV-transformed myeloblast line from another laboratory, and it is about 70% related to nucleotide sequences of E26 virus, an independent isolate of an AMV-like virus. Preliminary experiments show DVP to be leukemogenic if fused into susceptible cells in the presence of helper virus. We conclude that DVP RNA is the leukemogenic component of infectious AMV and that its specific sequence, termed AMV, may carry genetic information for oncogenicity. Thus we have found here a transformation-specific RNA sequence, unrelated to helper virus, in a highly oncogenic virus that does not transform fibroblasts.
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PMID:Genetic structure of avian myeloblastosis virus, released from transformed myeloblasts as a defective virus particle. 615 39

The RNA-dependent DNA polymerase (the reverse transcriptase) was solubilized from three related strains of avian sarcoma virus (ASV B77, ASV tsLA334, and ASV QV2) as well as avian myeloblastosis virus (AMV) and a chicken endogenous virus (RAV-O), by a combination of non-ionic detergent treatment and CsCl step-gradient centrifugation, and was subsequently separated into individual enzyme forms by poly(C)-agarose column chromatography. The newly developed two-step method allowed us to purify the three molecular forms (alpha-, alpha beta- and beta-form) of highly active enzyme rapidly and quantitatively from all the five virus strains examined. The molar ratio of the three enzyme forms differed among the virus strains: For the three sarcoma viruses, the major species was the alpha beta-form enzyme, the putative holoenzyme, and the alpha- and beta-form enzymes were less than a few percent and 15-25%, respectively, while the alpha-form enzyme content was higher for the two leukosis viruses than for the three sarcoma viruses. Both the total DNA polymerase activity and the content of the two enzyme subunits in purified virions of the three sarcoma virus was in the following order: ASV tsLA334 greater than ASV B77 greater than ASV QV2, which paralleled the virus yield at a permissive temperature in roller bottle cultures of chick embryo fibroblasts. No alteration was found in the thermolability of DNA polymerases between tsLA334, which carries ts mutations affecting both virus growth and cell-transformation, and other viruses.
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PMID:Reverse transcriptase associated with avian sarcoma-leukosis viruses. I. Comparison of intra-virion content of multiple enzyme forms. 617 23

A RNA-directed DNA polymerase was partially purified from a human homologous, mixed mesodermal sarcoma by DEAE-cellulose chromatography after sucrose density centrifugation. The enzyme transcribed poly(rA) most effectively but also transcribed poly(rI), poly(dA) and poly(rG) and to a lesser extent, poly(rmC). It was unable to transcribe poly(rU). The product with poly(rA) as template contained large material (greater than 28S) in addition to some proper size product demonstrating a slippage reaction. This pattern of transcription, while similar to avian myeloblastosis virus DNA polymerase, reveals qualitative differences making direct extrapolation from studies with animal oncornaviruses to human cancer difficult. In this paper, the detection and purification of RNA-directed DNA polymerase from a patient with an uncommon uterine sarcoma is reported along with the template specificities of the enzyme.
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PMID:Template specificities of a RNA-directed DNA polymerase from a human homologous mixed mesodermal sarcoma. 619 Dec 64

Avian myelocytomatosis virus (MC29V) is a retrovirus that transforms both fibroblasts and macrophages in culture and induces myelocytomatosis, carcinomas, and sarcomas in birds. Previous work identified a sequence of about 1,500 nucleotides (here denoted onc(MCV)) that apparently derived from a normal cellular sequence and that may encode the oncogenic capacity of MC29V. In an effort to further implicate onc(MCV) in tumorigenesis, we used molecular hybridization to examine the distribution of nucleotide sequences related to onc(MCV) among the genomes of various avian retroviruses. In addition, we characterized further the genetic composition of the remainder of the MC29V genome. Our work exploited the availability of radioactive DNAs (cDNA's) complementary to onc(MCV) (cDNA(MCV)) or to specific portions of the genome of avian sarcoma virus (ASV). We showed that genomic RNAs of avian erythroblastosis virus (AEV) and avian myeloblastosis virus (AMV) could not hybridize appreciably with cDNA(MCV). By contrast, cDNA(MCV) hybridized extensively (about 75%) and with essentially complete fidelity to the genome of Mill Hill 2 virus (MH2V), whose pathogenicity is very similar to that of MC29V, but different from that of AEV or AMV. Hybridization with the ASV cDNA's demonstrated that the MC29V genome includes about half of the ASV envelope protein gene and that the remainder of the MC29V genome is closely related to nucleotide sequences that are shared among the genomes of many avian leukosis and sarcoma viruses. We conclude that onc(MCV) probably specifies the unique set of pathogenicities displayed by MC29V and MH2V, whereas the oncogenic potentials of AEV and AMV are presumably encoded by a distinct nucleotide sequence unrelated to onc(MCV). The genomes of ASV, MC29V, and other avian oncoviruses thus share a set of common sequences, but apparently owe their various oncogenic potentials to unrelated transforming genes.
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PMID:Avian retroviruses that cause carcinoma and leukemia: identification of nucleotide sequences associated with pathogenicity. 624 77

We purified the p19 proteins from the Prague C strain of Rous sarcoma virus, avian myeloblastosis virus, B77 sarcoma virus, myeloblastosis-associated virus-2(0), and PR-E 95-C virus and measured their binding affinities for 60S viral RNA by the nitrocellulose filter binding technique. The apparent association constants of the p19 proteins from Rous sarcoma virus Prague C, avian myeloblastosis virus, and B77 sarcoma virus for homologous and heterologous 60S RNAs were similar (1.5 x 10(11) to 2.6 x 10(11) liters/mol), whereas those of myeloblastosis-associated virus-2(0) and PR-E 95-C virus were 10-fold lower. The sizes and relative amounts of the virus-specific polyadenylic acid-containing RNAs in the cytoplasms of cells infected with Rous sarcoma virus Prague C, myeloblastosis-associated virus-2(0), and PR-E 95-C virus were determined by fractionating the RNAs on agarose gels containing methylmercury hydroxide, transferring them to diazobenzyloxymethyl paper and hybridizing them to a 70-nucleotide complementary DNA probe. In cells infected with Rous sarcoma virus Prague C we detected 3.4 x 10(6)-, 1.9 x 10(6)-, and 1.1 x 10(6)-dalton RNAs, in PR-E 95-C virus-infected cells we detected 3.4 x 10(6)-, 1.9 x 10(6)- and 0.7 x 10(6)-dalton RNAs, and in cells infected with myeloblastosis-associated virus-2(0) we detected 3 x 10(6)- and 1.3 x 10(6)-dalton RNAs. Each of these RNA species contained RNA sequences derived from the 5' terminus of genome-length RNA, as evidenced by hybridization with the 5' 70-nucleotide complementary DNA. The ratios of subgenomic mRNA's to genome-length RNAs in cells infected with myeloblastosis-associated virus-2(0) and PR-E 95-C virus were three- to five-fold higher than the ratio in cells infected with Rous sarcoma virus Prague C. These results suggest that more processing of viral RNA in infected cells is correlated with lower binding affinities of the p19 protein for viral RNA, and they are consistent with the hypothesis that the p19 protein controls processing of viral RNA in cells.
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PMID:Correlation of RNA binding affinity of avian oncornavirus p19 proteins with the extent of processing of virus genome RNA in cells. 625 34


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