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At least 1,369 records · Page 76Linked to original sources
PubMed1970

DNA complementary to viral RNA in leukemic cells induced by avian myeloblastosis virus.

Nucleic acid hybridization studies were made between 71S-AMV-RNA and DNA from leukemic myeloblasts and from normal chicken cells. There was homology between the viral RNA and chicken cell DNA and to a greater extent between viral RNA and leukemic cell DNA. Leukemic cell DNA hybridized approximately twice as much viral RNA as did normal chicken DNA. Thermal melting studies showed that the viral RNA bound to normal and leukemic cell DNA consists of long polynucleotides (T(m) = 87 degrees and 92 degrees C, respectively, in 2x saline citrate). This suggests that the leukemic cells contain a DNA template of the viral RNA.

Animals↗
PubMedDate not supplied

Preparation of stereoregulated antisense oligodeoxyribonucleoside phosphorothioate and interaction with its complementary DNA and RNA.

Diastereoisomeric specificity of oligodeoxyribonucleoside phosphorothioate (OPT) in DNA/OPT and RNA/OPT hybrid formation was investigated. The difference in the configuration between RRRR and SSSS was reflected in the conformation and the stability of the DNA/OPT and RNA/OPT hybrids. Therefore, findings of this report rationalize the antisense effect by non-stereoregulated OPT and the difference of diastereoisomerism in susceptibility to RNase H.

Circular Dichroism↗
PubMed1996

Gel shift assay: demonstration of enhanced binding of oligo(delta)-L-ornithine-oligodeoxynucleotide conjugates to complementary DNA and RNA.

An increase in melting temperature for DNA:DNA duplexes had been observed previously (Zhu et al. Antisense Res. Dev. 3:349-356, 1993) when an oligo(delta)ornithine moiety was covalently appended to a short oligodeoxynucleotide. We now report the analysis of duplex formation by electrophoretic gel shift analysis. In the particular example studied, an increase in Tm of 4 degrees C was found to correspond to about a fivefold increase in binding constant. A similar enhancement by the appended cationic peptide was observed when the target strand was RNA. The use of a competitive assay format for avoidance of adsorptive loss at low concentrations (< 10(-7)M) of the oligonucleotide-oligo(delta)ornithine conjugate is presented.

Base Sequence↗
PubMed1992

Bacteriophage P4 immunity controlled by small RNAs via transcription termination.

Satellite bacteriophage P4 immunity is encoded within a short DNA region 357 bp long containing the promoter PLE and 275 bp downstream. PLE is active both in the early post-infection phase, when genes necessary for P4 lytic cycle are transcribed from this promoter, and in the lysogenic condition, when expression of the above genes is prevented by prophage immunity. In order to understand how P4 immunity is elicited, we have characterized the transcription pattern during the establishment and the maintenance of the satellite phage P4 lysogenic condition. We found that prophage transcription starting at PLE ends prematurely and the transcripts do not extend beyond 300-400 nucleotides downstream of PLE. Thus P4 immunity acts by causing premature transcription termination rather than by repressing transcription initiation. The P4 immunity region is transcribed in the prophage, but it does not seem to be translated; this region contains two elements (seqA and seqB) of a palindromic sequence. In addition to transcripts about 300 nucleotides long, P4 prophage produces a family of shorter transcripts, about 80 nucleotides long, containing seqA or seqB. Evidence is presented suggesting that SeqB RNA is the trans-acting immunity factor, and that interaction of SeqB RNA with the complementary nascent RNA containing seqA may be involved in bringing about premature transcription termination.

Coliphages↗
PubMed1997

Molecular Epidemiology of Lyme Disease Spirochetes Based on a Probe Complementary to Ribosomal RNA.

Lyme disease is caused by the spirochete, Borrelia burgdorferi, a bacteria which infects many vertebrates including humans. Borrelia have been isolated from many parts of the world, and there is interest to identify common genetic markers to improve molecular methods of diagnosis, and to aid in understanding varied manifestations of the disease. A total of 48 Borrelia burgdorferi strains, including: 38 isolated from ticks (Ixodes dammini, I. persulcatus, I. ricinus and I. pacificus), 3 from animals (dog, bird and hamster), and 7 from human clinical cases (skin, CSF, plasma and blood) from different geographic areas, were studied by DNA/DNA hybridization and rRNA gene restriction patterns by using a biotinylated pKK3535 probe (Altewegg M., Mayer L.W., 1989). The migration patterns of rRNA gene-restriction fragments after clevage by Hind III separate these strains into 5 ribotypes of Borrelia burgdorferi: Type I (38 American,2 European strains); Type II (13 American strains); Type III (3 Asian and 1 European strains); Type IV (1 European and 2 Asian strains) and Type V (1 Asian strain). The use of ribotyping has provided an additional tool to investigate the differences or common patterns which cause various Lyme disease syndromes.

Journal Article↗
PubMed1982

Mouse DNA sequences complementary to small nuclear RNA U1.

A mouse genomic library was screened for sequences complementary to U1 nuclear RNA. Out of the eight clones tested, none contained more than one copy of U1. Six of them were identical and one of those (clone 0U1-XIII) was further analyzed. This latter clone contained no other gene for discrete species of small size RNA in the 8 Kb EcoRI fragment encoding U1. A 248 bp Bg1II fragment from 0U1-XIII encompassing the full length of U1 as well as flanking regions on both sides has been subcloned and sequenced in M13 phage. Although the coding region was 96.5% homologous to rat U1a RNA, there is no direct evidence that this clone is a true gene. 3' and 5' flanking sequences of this as well as other published clones have been searched for homologies and the results of this search are discussed.

Animals↗
PubMed1975

Characterization of the mRNA of influenza virus.

The kinetics of the appearance of influenza mRNA, the distribution of mRNA between free and membrane-associated polyribosomes, its poly(A) content, and the extent to which the genome was transcribed into mRNA early in infection were determined. Polyribosomes were prepared from influenza virus-infected cells labeled for 30-min periods at various times after infection with [3H]uridine. Most of the 3H-labeled RNA extracted from these polyribosomes sedimented as a heterogeneous 8S to 20S peak in sucrose gradients, and it was largely complementary to virion RNA. By the following criteria, the complementary RNA had properties normally ascribed to mRNA: (i) it labeled rapidly with [3H]uridine; (ii) after glutaraldelyde treatment, it banded with polyribosomes in CsCl density gradients; and (iii) it contained poly(A). In chick cells at 37 C, virus mRNA was first detectable at 45 min postinfection and reached its maximal rate of appearance at 2 to 2.5 h postinfection. The free and membrane-bound polyribosomes of infected cells were separated and were found to contain the same classes of mRNA. There was no absolute segregation of mRNA sequences into either polyribosome class although each probably contained distinct ratios of the different mRNA's. From 45 min postinfection onwards, both membrane-bound and free polysomal poly(A)-containing RNA contained sequences complementary to at least 80% of the genome RNA, whereas poly(A)-minus RNA contained sequences complementary to 90 to 100% of the genome. There was no evidence for the temporal control of transcription of influenza mRNA. At 31 C, when virus development was slowed relative to 37 C,complementary RNA first appeared at 1 h postinfection. At this time, total polysomal RNA contained sequences complementary to the whole genome.

Base Sequence↗
PubMed1973

Synthesis of (3H)DNA complementary to ovalbumin messenger RNA: evidence for limited copies of the ovalbumin gene in chick oviduct.

Accumulation of ovalbumin messenger RNA in chick oviduct is absolutely dependent upon estrogen. After estrogen treatment, ovalbumin comprises 60-65% of the total oviduct protein. We used maximally stimulated animals to extract and partially purify the ovalbumin messenger RNA. The final product was enriched about 100-fold in activity with respect to this specific messenger RNA. This ovalbumin messenger RNA fraction was used to direct the synthesis of a complementary [(3)H]DNA in the presence of RNA-dependent DNA polymerase isolated from avian myeloblastosis virus. The complementary [(3)H]DNA (specific radioactivity, 8 x 10(7) cpm/mug) was a faithful transcript since about 90% would hybridize back to the original messenger RNA template. Ovalbumin complementary [(3)H]DNA was reannealed with an excess of chick-oviduct total DNA. The kinetics of this reaction indicate that only one copy of the ovalbumin gene exists in each haploid genome. These data suggest that estrogen may affect the oviduct genome to stimulate production of large numbers of ovalbumin messenger RNA molecules from a single copy of the ovalbumin gene.

Animals↗
PubMed2002

Cell proteins TIA-1 and TIAR interact with the 3' stem-loop of the West Nile virus complementary minus-strand RNA and facilitate virus replication.

It was reported previously that four baby hamster kidney (BHK) proteins with molecular masses of 108, 60, 50, and 42 kDa bind specifically to the 3'-terminal stem-loop of the West Nile virus minus-stand RNA [WNV 3'(-) SL RNA] (P. Y. Shi, W. Li, and M. A. Brinton, J. Virol. 70:6278-6287, 1996). In this study, p42 was purified using an RNA affinity column and identified as TIAR by peptide sequencing. A 42-kDa UV-cross-linked viral RNA-cell protein complex formed in BHK cytoplasmic extracts incubated with the WNV 3'(-) SL RNA was immunoprecipitated by anti-TIAR antibody. Both TIAR and the closely related protein TIA-1 are members of the RNA recognition motif (RRM) family of RNA binding proteins. TIA-1 also binds to the WNV 3'(-) SL RNA. The specificity of these viral RNA-cell protein interactions was demonstrated using recombinant proteins in competition gel mobility shift assays. The binding site for the WNV 3'(-) SL RNA was mapped to RRM2 on both TIAR and TIA-1. However, the dissociation constant (K(d)) for the interaction between TIAR RRM2 and the WNV 3'(-) SL RNA was 1.5 x 10(-8), while that for TIA-1 RRM2 was 1.12 x 10(-7). WNV growth was less efficient in murine TIAR knockout cell lines than in control cells. This effect was not observed for two other types of RNA viruses or two types of DNA viruses. Reconstitution of the TIAR knockout cells with TIAR increased the efficiency of WNV growth, but neither the level of TIAR nor WNV replication was as high as in control cells. These data suggest a functional role for TIAR and possibly also for TIA-1 during WNV replication.

Amino Acid Sequence↗
PubMed1995

Differential expression of cytokeratin mRNA in hamster squamous epithelia as observed by in situ hybridization using human cytokeratin cRNA probes.

In this hybridohistochemical study, we investigated the expression of cytokeratin (CK) mRNA in the keratinizing squamous epithelium of hamster cheek pouch and esophagus, using eight different digoxigenin-labelled RNA probes complementary to human CK mRNAs. CK 4, CK 6, CK 8, CK 14, and CK 15 RNA probe obviously hybridized with hamster counterpart mRNA(s) in the cheek pouch as well as in the esophageal epithelium. However, using the CK 10-specific RNA probe, only the cheek pouch epithelium exhibited a positive reaction. We were not able to detect any positive signal for the CK 18 or for the CK 19 RNA probe. We observed three different CK mRNA distribution patterns in the cheek pouch epithelium, and four in the esophageal epithelium. The differences in expression and distribution pattern of CK mRNAs between the two types of epithelia suggest that the hamster CK polypeptide family comprises at least six different species. We also conclude that human cRNA probes for CK mRNAs may provide a way to detect changes in CK expression and distribution during induced non-neoplastic and neoplastic changes in the hamster cheek pouch model. This may also help to elucidate the molecular pathogenesis of squamous-cell carcinoma.

Animals↗
PubMed2003

[Inhibition of lens epithelial cell cycle and PCNA mRNA expression by an antisense oligonucleotides complementary to the messenger RNA of proliferating cell nuclear antigen].

OBJECTIVE: To determine whether antisense oligonucleotides complementary to the messenger RNA of proliferating cell nuclear antigen (PCNA ASODN) inhibit the proliferation of bovine lens epithelial cell (BLEC) by changing the cell cycle and down-regulating the expression of PCNA mRNA and PCNA protein. METHODS: BLECs were cultured in vitro, and the second passage cells were used in this experiment. PCNA ASODN (30 micro mol/L), PCNA SODN (sense oligonucleotides, 30 micro mol/L), basic fibroblast growth factor (bFGF, 10 micro g/L), bFGF (10 ng/ml) + ASODN (30 micro mol/L), bFGF (10 micro g/L) + SODN (30 micro mol/L) were introduced respectively into the medium, and the same amount of PBS was added into the medium as a control. After 24 hours, the cell cycle and the PCNA expression were counted by flow cytometry, and the expression of PCNA mRNA was indicated by Northern ELISA hybridization. RESULTS: PCNA ASODN could decrease the rate of the cells of S phase and down-regulate the expression of PCNA mRNA and PCNA protein. Comparing with the control group, after 24 hours, the rate of cells of S phase was decreased from 15.67% to 7.96%, the expression of PCNA mRNA from 0.266 to 0.176 and the expression of PCNA protein from 55.27% to 12.32%. PCNA ASODN could also inhibit the proliferation of BLEC induced by bFGF, comparing with the bFGF group, the rate of cells of S phase was decreased from 23.4% to 19.9%, the expression of PCNA mRNA from 0.576 to 0.357 and the expression of PCNA protein from 76.4% to 35.48%. CONCLUSIONS: Our results demonstrate that the PCNA ASODN decreases expression of PCNA mRNA and PCNA protein, and stops the cell to enter and progress through S phase. These results provide an important impetus to initiate in vivo studies to determine the feasibility of antisense strategies in the prevention of posterior capsular opacification.

Animals↗
PubMed1988

Antisense RNA directed against the 3' noncoding region prevents dormant mRNA activation in mouse oocytes.

Primary mouse oocytes contain untranslated stable messenger RNA for tissue plasminogen activator (t-PA). During meiotic maturation, this maternal mRNA undergoes a 3'-polyadenylation, is translated, and is degraded. Injections of maturing oocytes with different antisense RNA's complementary to both coding and noncoding portions of t-PA mRNA all selectively blocked t-PA synthesis. RNA blot analysis of t-PA mRNA in injected, matured oocytes suggested a cleavage of the RNA.RNA hybrid region, yielding a stable 5' portion, and an unstable 3' portion. In primary oocytes, the 3' noncoding region was susceptible to cleavage, while the other portions of the mRNA were blocked from hybrid formation until maturation occurred. Injection of antisense RNA complementary to 103 nucleotides of its extreme 3' untranslated region was sufficient to prevent the polyadenylation, translational activation, and destabilization of t-PA mRNA. These results demonstrate a critical role for the 3' noncoding region of a dormant mRNA in its translational recruitment during meiotic maturation of mouse oocytes.

Animals↗