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Biomedical subjects

K Fujinaga

Publications and source records attributed to K Fujinaga.

At least 217 records · Page 12Linked to original sources
PubMed1972

The mechanism of viral carcinogenesis by DNA mammalian viruses: RNA transcripts containing viral and highly reiterated cellular base sequences in adenovirus-transformed cells (DNA-RNA hybridization-viral-cell mRNA).

Virus-specific RNA was isolated from cells transformed by human adenovirus 2 and 7 by multiple hybridizations with and elutions from homologous viral DNA; RNA molecules purified by this selection procedure hybridized efficiently with both viral DNA (24-50%) and DNA from untransformed cells (12-27%). Virus-specific RNA isolated in the same manner from cells productively infected with adenoviruses did not hybridize significantly with cellular DNA. These findings suggest that RNA molecules containing covalently-linked viral and cellular sequences are transcribed in cells transformed by human adenoviruses. The high efficiency of hybridization with DNA from untransformed cells implies that viral DNA is integrated adjacent to highly reiterated cellular DNA sequences.

Adenoviridae↗
PubMed1972

Virus-specific ribonucleic acid in the nucleus and cytoplasm of rat embryo cells transformed by adenovirus type 2.

Nuclei were isolated from rat embryo cells transformed by adenovirus type 2. Nuclear and cytoplasmic virus-specific ribonucleic acids (RNA) were characterized and quantitated by deoxyribonucleic acid (DNA)-RNA hybrid formation with adenovirus DNA. The results indicate that most, if not all, virus-specific RNA molecules are synthesized in the cell nucleus and subsequently transported into cytoplasm where they degrade with a half-life of 1 to 2 hr. No difference in base sequences between nuclear and cytoplasmic virus-specific RNA species can be detected by hybridization competition experiment with viral DNA.

Adenoviridae↗
PubMed1970

Mechanism of viral carcinogenesis by DNA mammalian viruses. VII. Viral genes transcribed in adenovirus type 2 infected and transformed cells.

DNA-RNA hybridization-competition experiments were used to compare the virus-specific RNA sequences synthesized during productive infection with human adenovirus type 2 with those synthesized in virus-free adenovirus type 2 transformed cells. The "early" virus-specific RNA present at six hours after infection, prior to the onset of viral DNA synthesis, represents 8-20 percent (2 to 10 genes) of the viral genome. All viral RNA sequences synthesized early are also present "late," at 18 hours after infection. The base sequences transcribed in transformed cells are homologous to approximately 50 per cent of the sequences transcribed early after infection. Thus only 4 to 10 per cent of the viral genome, representing 1 to 5 viral genes, are transcribed in adenovirus type 2 transformed cells. The virus-specific RNA synthesized 18 hours after infection was not found in transformed cells, suggesting that either these late viral genes are not present or are not transcribed in adenovirus type 2 transformed cells.

Adenoviridae↗
PubMed1970

Mechanism of carcinogenesis by RNA tumor viruses. I. An RNA-dependent DNA polymerase in murine sarcoma viruses.

A highly active and stable DNA polymerase was found in purified preparations of two murine sarcoma viruses. Enzyme activity is not detected in most virus preparations unless they are treated with low concentrations of a nonionic detergent such as Nonidet P-40. The incorporation of labeled thymidine triphosphate requires all four deoxyribonucleoside triphosphates and either Mg(2+) or Mn(2+). Enzyme activity is proportional to virus concentration and is linear with time up to 90 min. That the template is RNA is suggested by the reduction in polymerase activity upon treatment of murine sarcoma virus with RNase, and by the absence of detectable amounts of DNA in the virus. That the product is DNA is shown by the incorporation of all four deoxyribo-nucleoside triphosphates into an acid-insoluble product which is stable in alkali, is destroyed by DNase, sediments in alkaline sucrose gradients with a sedimentation coefficient of 7 S, and bands in isopycnic CsCl gradients with a mean buoyant density of 1.700.

Animals↗
PubMed1970

Mechanism of carcinogenesis by RNA tumor viruses. 3. Formation of RNA, DNA complex and duplex DNA molecules by the DNA polymerase (s) of avian myeloblastosis virus.

DNA polymerase activity can be unmasked in avian myeloblastosis virus (AMV) by treatment with the nonionic detergent Nonidet P-40. Two products are formed: (1) RNA.DNA hybrid molecules and (2) duplex DNA molecules. The kinetics of dTTP incorporation into DNA are biphasic: an initial rapid reaction for 4 min at 37 degrees C with a minimal polymerization rate of 10-20 nucleotides per see, and a second reaction at about half the initial rate. Viral RNA.DNA complexes are detected as early as 30 sec after the initiation of DNA synthesis; DNA free of template is formed subsequently. Most of the free AMV DNA forms an RNA.DNA hybrid when annealed with viral RNA. Over half of the free AMV DNA product is inferred to be double-stranded, since it is retained on hydroxyapatite columns after elution with 0.12 M phosphate buffer, and is resistant to Escherichia coli exonuclease I. Adenovirus or calfthymus DNA added to unmasked AMV stimulates DNA synthesis 4-16 times if there is no treatment with RNase, and 40-130 fold if RNase treatment precedes the enzyme assay. It is possible that two polymerases are present, or that a single enzyme forms both the RNA.DNA hybrid and the double-stranded product.

Alpharetrovirus↗
PubMed1969

The mechanism of viral carcinogenesis by DNA mammalian viruses. VI. A new class of virus-specific RNA molecules in cells transformed by group C human adenoviruses.

A new class of virus-specific RNA molecules was found in cells transformed by group C human adenovirus types 2, 5, and 6. RNA isolated from virus-free rat embryo cells transformed by adenovirus 2, 5, and 6 hybridized with all group C adenovirus DNA's (adenovirus 1, 2, 5, and 6) equally well, but not appreciably with group A and B adenovirus DNA's. Most likely no viral genes common to group A, B, and C adenoviruses are transcribed in adenovirus-transformed cells. Group C adenoviruses are closely related since they share 83 to 93 per cent of their base sequences as shown by DNA-DNA homology measurements. Group C DNA's share only 10 to 26 per cent of their base sequences with group A and B DNA's. Moreover, the shared sequences are not transcribed detectably in adenovirus transformed cells.Virus-specific RNA isolated from group C transformed cells contains 49 to 51 per cent G + C, but viral DNA's possess a 7 to 9 per cent higher G + C content. These differences suggest that only a portion of the viral genome with an average G + C content of 49 to 51 per cent is transcribed in group C adenovirus transformed cells.

Adenoviridae↗