Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.1.30.2 (endonuclease)
 18,621 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Plaque-purified viable simian virus 40 deletion mutants containing deletions between map positions 0.54 and 0.59 induced tumors in 21--92% of LSH hamsters inoculated during the first 24 hr of life. HinfI restriction endonuclease digestion patterns of the genomes of virions rescued from the tumor cells and the distribution of simian virus 40 early proteins in these cells associated tumor induction with the inoculated mutants. These results imply that the DNA sequences comprising that portion of the early simian virus 40 genome between map positions 0.54 and 0.59 are not essential for simian virus 40 oncogenicity.
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PMID:Oncogenicity of simian virus 40 deletion mutants that induce altered 17-kilodalton t-proteins. 22 94

Human papovavirus JC virus was adapted to growth in human embryonic kidney (HEK) cells. After eight passages, the HEK-adapted JC virus produced high virus yields and was capable of forming plaques in HEK monolayer cultures. Eleven plaque-purified stocks were prepared and characterized. Biologically, the plaque-purified virus induced tumor and viral antigens in HEK cells earlier and in a higher percentage of cells than uncloned virus. Cytopathic changes were also evident sooner and were more extensive. The DNA from uncloned as well as plaque-purified isolates was analyzed by restriction endonuclease cleavage followed by gel electrophoresis. The DNA from uncloned HEK-adapted virus was heterogeneous. Plaque-purified virus isolates yielded DNA which, although much less heterogeneous than the uncloned stock, still consisted of two or more species of viral DNA.
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PMID:Characterization of JC papovavirus adapted to growth in human embryonic kidney cells. 625 88

A lymphocytic leukemia induced by the oncogenic DNA simian virus 40 (SV40) in an inbred LSH/SsLak Syrian golden hamster was evoked to produce infectious SV40 by fusion of the leukemia cells with grivet monkey kidney (GMK) cells and by exposure of the leukemia cells to the chemical inducers mitomycin C and cycloheximide. Plaque-purified viable substrains of the rescued SV40 when studied by restriction endonuclease digestion of viral DNA were found to contain small deletions within the Hind III restriction fragment C. These deletions lay near the viral origin of DNA replication. Ten plaque-purified substrains of the rescued virus identified by immunofluorescence as being SV40 were found, when compared to the wild-type SV40, to replicate slowly and to form small plaques. Although these substrains transformed NIH/3T3 cells as efficiently as the wild-type SV40 in tissue culture, they were generally less oncogenic in vivo--7 of the 10 failed to induce tumors. The 3 oncogenic SV40-rescued substrains were not found to exhibit "lymphocytotropism," i.e., the capacity to infect and neoplastically transform preferentially hamster lymphocytes. Thus the hamster lymphocytic leukemia originally induced by the wild-type SV40 was most likely a chance-stochastic event rather than the result of tropism-determinism mediated by the virus, as is usually the case with leukemogenic RNA viruses.
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PMID:Biologic properties of viable deletion mutants of simian virus 40 (SV40) rescued from the cells of an SV40-induced hamster lymphocytic leukemia. 631 36

The thymidine kinase (TK) of herpesviruses, in contrast to cellular TKs, phosphorylates a variety of substrates including antiherpetic nucleoside analogues. This study reports the identification and DNA sequence of the simian varicella virus (SVV) TK gene. A 32P-labeled varicella zoster virus (VZV) TK DNA probe hybridized to the HindIII B subclone of the SVV BamHI B restriction endonuclease (RE) fragment, indicating the presence of a SVV DNA sequence homologous to the VZV TK gene. DNA sequence analysis of the SVV HindIII B subclone revealed a 1014 base pair (bp) open reading frame (ORF) encoding a 337 amino acid polypeptide homologous to herpesvirus TKs. The predicted SVV and VZV TK polypeptides share 51.3% identity, and alignment of the putative protein sequence of several TK homologues suggests the position of a conserved nucleotide binding site and a nucleoside (substrate) binding site in the SVV TK. Identification of the 5' end of the SVV TK transcript by primer extension analysis allowed a comparison of the SVV and VZV TK promoter regions indicating extensive conservation of the DNA sequence and transcription factor binding sites. Plaque reduction assays demonstrate that the SVV TK is active based on the susceptibility of SVV to acyclovir treatment and that SVV is less sensitive to acyclovir than VZV and herpes simplex virus (HSV-1) in infected Vero cells. Identification of the SVV TK ORF will facilitate studies that examine the role of viral TKs in pathogenesis and antiviral sensitivity and provides a potential insertion site for the expression of foreign genes.
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PMID:Identification and analysis of the simian varicella virus thymidine kinase gene. 862 50

The purpose of this study was to investigate whether there was an intrafamilial similarity of mutans streptococcal strains in some Swedish families using chromosomal DNA fingerprinting. Plaque samples were obtained from buccal and occlusal surfaces of 25 three-year-old children, their mothers and 18 fathers. The colonization levels of mutants streptococci were estimated with the "Strip mutans" test, and caries experience was scored by decayed, missing and filled teeth or decayed, extracted and filled teeth. Interviews about medical history, diet regimes, breastfeeding and care of the child were performed. In 11 families isolates of mutans streptococci were detected in all three individuals. These isolates were serotyped by immunofluorescent technique and genotyped using the restriction endonuclease Hae III. The results showed that 5 children harbored mutans streptococci genotypes different from their parents. Six children showed genotypes identical to their mothers. None of the children harbored genotypes similar to their fathers, even though two thirds of the fathers had high or very high mutans streptococci levels. No matching of genotypes was observed within the 11 parental pairs. Mothers as primary caregivers with high "Strip mutans" scores were more often observed in the group with identical genotypes within the mother-child pairs, the "matching group", than in the "no-matching group". These data indicate that the fathers and the children had not acquired each others' strains of mutans streptococci nor had the spouses. The results suggest that the children acquired mutans streptococci both from outside and inside the family.
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PMID:Genotyping shows different strains of mutans streptococci between father and child and within parental pairs in Swedish families. 980 18

Terminase, the DNA packaging enzyme of bacteriophage lambda, is a heteromultimer of gpNu1 and gpA subunits. In an earlier investigation, a lethal mutation changing gpA residue 497 from lysine to aspartic acid (K497D) was found to cause a mild change in the high-affinity ATPase that resides in gpA and a severe defect in the endonuclease activity of terminase. The K497D terminase efficiently sponsored packaging of mature lambda DNA into proheads. In the present work, K497D terminase was found to have a severe defect in the cohesive end separation, or helicase, activity. Plaque-forming pseudorevertants of lambda A K497D were found to carry mutations in A that suppressed the lethality of the A K497D mutation. The two suppressor mutations identified, A E515G and A E515K, affected residue 515, which is located near the putative P-loop of gpA. A codon substitution study of codon 515 showed that hydrophobic and basic residues suppress the K497D defect, but hydrophilic and acidic residues do not. The E515G change was demonstrated to reverse the endonuclease and helicase defects caused by the K497D change. Moreover, the gpA K497D E515G enzyme was found to have kinetic constants for the high-affinity ATPase center similar to those of the wild type enzyme, and the endonuclease activity of the K497D E515G enzyme was stimulated by ATP to an extent similar to the ATP stimulation of the endonuclease activity of the wild type enzyme.
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PMID:Endonuclease and helicase activities of bacteriophage lambda terminase: changing nearby residue 515 restores activity to the gpA K497D mutant enzyme. 1106 51

The purpose of this study was to investigate whether there was transmission between adults in Chinese families using chromosomal DNA fingerprinting. Plaque samples were obtained from buccal and occlusal surfaces of 11 married couples. The colonization levels of mutans streptococci were estimated as colony-forming units per milliliter, and caries experience was scored by decayed, missing and filled teeth. Information about medical history, diet regimes and age at marriage was obtained. The isolates were serotyped by biochemical test and genotyped using the restriction endonuclease HaeIII. The procedure was repeated after 3 months. The results showed that 1 couple had the same genotype of mutans streptococcus at the first examination, but this could not be repeated for the husband who had lost his mutans streptococci at the second examination. On the contrary, another couple that did not have the same mutans streptococcal genotype at the beginning had the same genotype after 3 months. No matching of genotypes was observed within 8 couples. In 1 male, no mutans streptococci were detected, therefore that couple was not considered. These data indicate that spouses had a chance to be infected by strains of mutans streptococci from another person. The results suggest that there may be transmission between adults in Chinese families, but it may be difficult for mutans streptococci to colonize another mouth permanently.
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PMID:Transmission of mutans streptococci in adults within a Chinese population. 1206 67

The aim of this study was to clarify the distribution and persistence of mutans streptococci on different tooth sites in the same oral cavity. Thirteen subjects, aged 20-40 years, were examined. Salivary levels of mutans streptococci, caries prevalence, oral hygiene habits and status of tooth surfaces sampled were recorded. Plaque samples were obtained from four sites, the mesial and buccal surfaces of the first permanent molar on the right side of the lower jaw (46m and 46b), the distal surface of the first permanent premolar (24d) and the mesial surface of the second permanent premolar (25m) on the left side of the upper jaw, using sterile toothpicks on two occasions at 4-7-month intervals. The samples were cultivated on site-specific Strip mutans. Up to 10 colonies/site were isolated when present and genotyped by random amplified polymorphic DNA (RAPD) analysis, after species identification with PCR. Genotyping was also performed by restriction endonuclease analysis (REA) on 148 isolates, and results were consistent with the RAPD results. Most mutans streptococcus-positive samples were obtained from 46m. Within each individual, the same genotype occurred on at least two sites on all but one sampling occasion. A maximum of seven different genotypes were found in an individual. For a particular tooth site, four genotypes occurred simultaneously and taking both sampling occasions together the maximum was six different types. The same genotypes/types were found again after 4-7 months on 25 sites in 12 subjects. Fifteen sites were mutans streptococcus-positive on only one sampling occasion. The results indicate that several different genotypes of mutans streptococci colonize a tooth site, and that the same genotype colonizes several sites in the same oral cavity. Persistence of genotypes on a site for several months and interindividual differences in the occurrence of genotypes were also found.
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PMID:Tracing genotypes of mutans streptococci on tooth sites by random amplified polymorphic DNA (RAPD) analysis. 1258 55

The purposes of this study were to determine the age at the initial acquisition of mutans streptococci (MS) and to determine the transmission of MS among children at day nursery by describing the occurrence of genotypes prepared by chromosomal DNA fingerprinting of the bacteria using restriction endonuclease EcoRI and HaeIII. The samples were 39 children (23 boys and 16 girls) aged 0-5 years old, 14 pairs of parents and 6 nursery caretakers of a day nursery in Hiroshima city, Japan. The children had no dental caries throughout the experiment. Plaque samples of the children were taken using toothbrushes at 1 month intervals for 30 months. The initial acquisition of MS occurred between the ages of 8 months and 52 months with a mean age of 24.2 months. The cumulative probability of initial acquisition of MS increased rapidly at the age of 12 to 25 months after 10 to 20 primary teeth had erupted. Transmission of MS was found between child and mother (33.3%), child and father (8.3%) and child and others including amongst the children (58.4%), but no evidence of MS transmission from nursery caretakers was found. Two children acquired MS from intra- and extra-familial transmission. This study suggests that the child's environment also plays a role in the initial acquisition and transmission of MS, in addition to the oral condition of the children.
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PMID:Initial acquisition and transmission of mutans streptococci in children at day nursery. 1261 13