Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.1.30.2 (endonuclease)
18,621 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A Type II restriction endonuclease, designated FseI, has been partially purified from a Frankia species (NRRL 18528). This enzyme cleaves Adenovirus 2 DNA at three sites, but does not cleave the DNAs from bacteriophages lambda, T7, and phi X174, the animal virus SV40, pUC18 and pBR322. FseI recognizes the octanucleotide sequence 5' GGCCGG decreases CC 3' and cleaves as indicated by the arrow. The frequency of occurrence of FseI sites within sequenced regions of the human genome is similar to that for NotI sites.
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PMID:FseI, a new type II restriction endonuclease that recognizes the octanucleotide sequence 5' GGCCGGCC 3'. 215 36

An outbreak of epidemic keratoconjunctivitis occurred at the department of ophthalmology of a hospital in Yokohama, involving 14 inpatients, 12 outpatients, and 2 doctors. Adenovirus type 37 (Ad-37) was isolated from the conjunctival swab in 12 of 18 cases. In neutralization tests, the isolates showed some cross-reaction with adenovirus type 19 (Ad-19). The Ad-37 isolates were indistinguishable from each other and from the prototype Ad-37, but distinct from the prototype Ad-19 in the restriction endonuclease analysis of viral DNA.
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PMID:A nosocomial outbreak of epidemic keratoconjunctivitis due to adenovirus type 37. 217 12

Adenovirus type 7 is the type most frequently associated with serious disease. Eighteen different genome types of adenovirus type 7 had been reported up to October 1986. The genome type Ad7c, based on the restriction enzyme profiles of SmaI and BamHI, has been reported from Europe prior to 1969 and more recently from South Africa. Here, we report two new genome types of adenovirus 7 c that have not previously been identified and that have been isolated in South Africa between 1975 and 1986 from children with postmeasles pneumonia. The two new genome types differ from the prototype Ad7c virus in having two (Ad7c1) or one (Ad7c2) extra cleavage sites for the restriction endonuclease EcoRI. These sites have been located at 3.68kb and 5.32kb from the left terminus of the genome map published for the prototype Ad7c strain. A strain resembling the prototype Ad7c was also isolated in 1986 from a case of post measles pneumonia.
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PMID:Two new genome types of adenovirus 7c. 282 28

Adenovirus type 4 (Ad4) is the sole member of adenovirus group E based on overall DNA sequence homology, restriction endonuclease cleavage patterns, and the size of capsid proteins. We cloned the BamHI-F fragment from the left end of Ad4 in pUC13-1 between the SalI and BamHI sites in order to carry out the structural analysis of the E1A region of Ad4. The complete sequence of the BamHI-F fragment (2042 bp) has been determined. From the DNA sequence, the splice sites for the putative 12 S and 13 S mRNAs, encoded by the E1A region of Ad4 were deduced. If protein synthesis initiates at the first available AUG triplet (position 575), these 12 S and 13 S mRNAs would code for polypeptides containing 226 and 257 amino acids, respectively. Comparison of Ad4- and Ad7-13 S mRNA-coded polypeptides indicates that there is 57% homology, whereas the homology is only 38% with Ad12 and 31% with Ad2-13 S mRNA-coded polypeptides. The structural analysis in the E1 region of Ad4 also includes the coding region for the E1B 19-kDa protein. Ad4 and Ad7 shows 65% homology in the coding regions for E1B 19-kDa protein. Comparison of the DNA sequence of Ad4 with those of Ad2, Ad7, and Ad12 by using a dot matrix computer program and by Southern hybridization revealed that Ad4 bears a stronger homology with Ad7 than with Ad2 and Ad12 in this region. Hydropathy plots and alignments of the putative polypeptides coded by this region in Ad4 with those from the corresponding regions of different serotypes to reveal the highly conserved domains also support the above conclusion.
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PMID:Sequence analysis in the E1 region of adenovirus type 4 DNA. 294 81

Adenovirus-polyomavirus recombinant viruses were constructed in vitro by inserting a hybrid transcription unit composed of the adenovirus type 2 major late promoter and the early coding region of polyomavirus into the adenovirus type 5 vector Ad5 delta E1/dl309. The vector lacks the E1a and E1b transcription units and contains a unique restriction endonuclease cleavage site in their place. The polyomavirus genomic insert contained a small deletion which precluded the synthesis of functional small and middle T antigen but allowed for the synthesis of large T antigen. One recombinant virus, Ad5PyR39, which contained the hybrid transcription unit in the opposite transcriptional orientation from the overall direction of late-gene transcription, was studied in detail. Ad5PyR39 replicated efficiently without a helper virus in human 293 cells and expressed hybrid mRNAs of the expected size and composition that were translated to yield large T antigen. The large T antigen synthesized in 293 cells was the same size as that produced in mouse 3T6 cells lytically infected with polyomavirus, and this protein bound efficiently and specifically to the large-T-antigen-binding sites in polyomavirus DNA. Moreover, the large T antigen encoded by the recombinant virus proved capable of catalyzing the replication in mouse 3T6 cells of a plasmid containing the polyomavirus origin for DNA replication. Comparison of the amount of large T antigen produced in 3T6 cells infected with polyomavirus with that in 293 cells infected with Ad5PyR39, under optimal conditions for each system, revealed at least a fivefold greater yield of the protein on a per cell basis in the latter system compared with the former. Ad5PyR39 should prove to be useful to isolate large quantities of functional polyomavirus large T antigen for structural and biochemical studies.
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PMID:Construction of a helper-free recombinant adenovirus that expresses polyomavirus large T antigen. 302 52

Adenovirus type 35 (Ad35) is an uncommon group B adenovirus that has been isolated nearly exclusively from immunosuppressed hosts. In our series of 46 patients with Ad35 isolates, 36 had AIDS or AIDS-related complex (ARC), seven patients were immunocompromised because of other diseases, and three patients were "normal." Neither patients with AIDS or ARC made specific antibody to Ad35, whereas antibody was present in one immunocompetent host and one renal transplant recipient. All isolates were identified as Ad35 by using genomic analysis with the restriction endonuclease SmaI, but many viruses exhibited other group B hemagglutinins, a property of the fiber protein. Further analysis of DNAs from 40 of these isolates, mapped by using the enzymes BamHI, HpaI, and PstI, revealed a total of 14 genomic variants from the Ad35 prototype. Seven of these genomic types, with either Ad7 or Ad11 hemagglutinin, had corresponding restriction site differences within the fiber gene, a result consistent with recombination events with other group B adenoviruses.
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PMID:Molecular epidemiology of adenovirus type 35 infections in immunocompromised hosts. 303 89

Adenovirus 2 mRNAs synthesized in productive infection were assigned to specific regions of the genome by hybridization to unique fragments of viral DNA. Radioactive viral RNA synthesized early or late in infection was first fractionated by polyacrylamide gel electrophoresis. Eluted RNAs were then tested for complementary hybrid formation with each of the six fragments of adenovirus 2 DNA generated by cleavage with endonuclease R.R1. Early RNA species migrating as 13S, 19S, and 20S RNAs were identified as transcription products of fragments A, B, and D, respectively. In addition to the 13S RNA transcribed from A fragment DNA, 13S RNA also hybridized to the D and E fragment DNAs; 11S RNA annealed to both A and B fragments. The RNA that hybridized to fragment C DNA was heterogeneous in size. Viral RNA synthesized late in infection included 27S, 24S, 19S, and 11S size classes, all of which annealed to A fragment DNA. Additional RNA migrating as 24S hybridized to E and C fragment DNA, and 23S RNA annealed to F fragment DNA. The results of the hybridizations of size fractionated RNAs with viral DNA fragments enabled formation of a partial map of viral mRNAs with respect to the adenovirus 2 genome. Some of the viral RNAs may represent transcripts which overlap R1 cleavage sites, because in at least three instances hybridization revealed viral RNAs which have the same electrophoretic mobility and anneal to fragments that are contiguous on the genome.
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PMID:Localization of adenovirus 2 messenger RNA's to segments of the viral genome defined by endonuclease R-R1. 461 May 67

The construction of recombinant M13 phages containing adenovirus DNA inserts was undertaken to provide strand-specific hybridization probes for analyses of adenovirus type 2 RNA transcripts. A library of molecular probes was constructed by cloning restriction endonuclease fragments of adenovirus types 2 and 5 DNA in the duplex replicative form DNA of the single-stranded bacteriophage vectors, M13mp7, M13mp8, and M13mp9 (Messing, J., and Vieira, J. (1982) Gene 19,269-276). Adenovirus DNA segments from early, intermediate, and late gene regions, accounting for at least 95% of the adenovirus chromosome, have been cloned in both possible orientations using these M13 derivatives as vectors. DNA cloned into these vectors can readily be obtained in a circular single-stranded form directly from mature phage particles. The cloned DNA fragments have been oriented and further characterized by restriction endonuclease mapping and hybridization with 32P-labeled adenovirus DNA. The polarity and fidelity of the adenovirus DNA in the recombinant phages has been confirmed by hybridization with labeled adenovirus 2 early and late mRNA. Restriction endonuclease analyses of M13 clones containing adenovirus DNA inserts spanning genome coordinates 31.7-56.9 have indicated that the relative locations of some restriction coordinates located within this region do not correspond to the mapped restriction sites in the DNA of adenovirus 2. Potential uses for these M13 clones in studies of adenovirus gene expression are discussed.
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PMID:Construction of a cloned library of adenovirus DNA fragments in bacteriophage M13. 630 66

Thirty-five stool specimens, collected over a 14-week period from pediatric gastroenteritis patients and shown to contain adenovirus by electron microscopy, were inoculated onto 293 and HeLa cells. Virus isolates were characterized by serum neutralization and restriction endonuclease cleavage analysis of viral DNA from infected cells. Adenovirus was isolated upon primary inoculation of 293 cells from all 35 specimens shown to contain adenovirus by electron microscopy. Fastidious adenoviruses 40 and 41 (Ad40 and Ad41) were found in 17 (49%) of the stool specimens, and 4 of these specimens contained a conventional species (Ad1, Ad1, Ad18, Ad31) as well as Ad40. This was first manifest by the observation that four of the isolates which initially grew only in 293 cells acquired the capacity to grow in HeLa cells upon subsequent passage. In each case, the conventional species was undetectable by DNA analysis in the original inoculum but was selected in 293 cells and became the only one detectable by the second passage. Four other specimens, containing Ad1 or Ad31 alone, failed to grow initially in HeLa cells but did grow in 293 cells. The results of this study demonstrate therefore that (i) 293 cells are more sensitive than HeLa cells for the isolation of conventional as well as fastidious enteric adenovirus species and (ii) identification of viruses from patient specimens should involve minimal passage of the virus in cell culture, as a single passage can result in misdiagnosis of the virus associated with the infection.
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PMID:Diagnosis of fastidious enteric adenoviruses 40 and 41 in stool specimens. 649 Aug 23

Adenovirus uncouples DNA replication from polyamine biosynthesis and causes chromosome aberrations in rodent cells. Addition of polyamines protected infected cells from this chromosome damage. Spermine was the only individual polyamine which protected. The diamine oxidase inhibitor aminoguanidine also protected. Neither compound detectably reduced synthesis of viral early proteins. The protective effects of spermine and aminoguanidine were not additive. Maximal protection was obtained when the compounds were added 4.5 h before mitosis, but significant protection was observed up to 1.25 h before mitosis. This suggests that the compounds act in G2. In vitro, spermine bound strongly to DNA and protected it from mild endonuclease attack, but aminoguanidine did neither. We propose that viral infection causes a deficiency in spermine during a critical period G2, possibly accompanied by an increase in endonuclease activity. The resulting chromosome damage can be prevented by adding exogenous spermine, or by inhibiting the oxidative degradation of endogenous spermine.
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PMID:Spermine and aminoguanidine protect cells from chromosome aberrations induced by adenovirus during the G2 phase of the cell cycle. 707 55


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