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)

The activity of an endonuclease(s) acting on double-stranded, ultraviolet-irradiated, and 2-acetylaminofluorene-bound DNA but not on double-stranded undamaged DNA triples within two hr after partial hepatectomy. Although the activity drops between four and six hr after operation, it remains above levels measured in livers of nonhepatectomized rats until 36 hr after operation. Between 36 and 48 hr after operation, the enzyme activity drops below the levels in liver of nonhepatectomized rats and then rises slowly to reach levels observed in nonhepatectomized animals between 48 hr and seven days after the operation. Studies on the effect of actinomycin on the activity of crude enzyme and on the incorporation of [14C]leucine and [14C]valine on the purified enzyme indicate that the increase in enzyme activity results from de novo synthesis. Eight % of endonucleolytic activity detectable in the crude homogenate is inhibited by an hyperimmune serum prepared against the purified enzyme. By adjusting the time of injection of 2-[14C]acetylaminofluorene with respect to the levels of enzyme activity after partial hepatectomy, an inverse correlation between binding and enzyme activity was demonstrated.
Cancer Res 1981 Jun
PMID:Endonuclease activity on damaged DNA in rat regenerating liver. 626 60

Epstein-Barr viral (EBV) DNA is nearly always detectable in African Burkitt's lymphoma (BL) but is infrequently found in the histologically indistinguishable American BL. We have derived a tumor cell line from a patient with American BL which produces EBV, and we have compared this virus isolate [JLP(c)] with African BL EBV. The American JLP(c) virus immortalizes human umbilical cord lymphocytes in vitro, and its DNA is indistinguishable from African BL EBV DNA by nucleic acid hybridization and preliminary restriction endonuclease cleavage analysis.
Cancer Res 1981 Aug
PMID:Characterization of the Epstein-Barr virus isolated from a cell line derived from a patient with American Burkitt's lymphoma. 626 76

Human papilloma virus (HPV) was isolated from red plaques of a patient (N. F.) with epidermodysplasia verruciformis. Electron microscopic examination showed characteristic particles of papilloma virus as icosahedrons about 45 nm in diameter. DNA was extracted from these particles, and closed-circular DNA (Form I) was purified by centrifugation in CsCl containing ethidium bromide. The molecular weight of the DNA was about 5.0 x 10(6). A physical map of the HPV DNA was constructed using several restriction enzymes. The restriction endonuclease cleavage pattern of the HPV DNA was different from those of other types of HPV reported thus far, suggesting that the isolate was a new, as yet unclassified, HPV.
Cancer Res 1982 Jun
PMID:New human papilloma virus isolated from epidermodysplasia verruciformis lesions. 628 Aug 58

Murine mammary tumor virus (MuMTV) provirus sequences in the DNA from early-occurring (average age 10 mo) and late occurring (age greater than 20 mo) tumors in BALB/cfC3H mice were analyzed by Eco RI restriction endonuclease mapping procedures. All early tumors were MuMTV antigen-positive mammary adenocarcinomas that contained the 0.92- and 4.0-kilo base (kb) exogenous C3H MuMTV-specific Pst I restriction endonuclease fragments. All but 1 of the late mammary adenocarcinomas had MuMTV antigens detected by peroxidase antiperoxidase staining, and all contained the 0.92- and 4.0-kb exogenous virus Pst I fragments. Three late nonmammary tumors lacked both MuMTV antigens and acquired provirus sequences. Greater numbers of MuMTV sequences were detected in both early and late-arising mammary tumors by Eco RI restriction endonuclease mapping than were detected in tissues from uninfected BALB/c mice. However, neither the number nor the location of MuMTV proviruses correlated with tumor latent period.
J Natl Cancer Inst 1982 Jun
PMID:Detection of acquired provirus sequences in mammary tumors from low-expressor, low-risk mice. 628 24

Transformation defective virus was derived by restriction endonuclease cleavage from a clone of the avian sarcoma virus Schmidt-Ruppin strain, strongly oncogenic for rats. The transfection experiments of chicken cells by digested proviral DNA gave rise to transformation defective virus. The td virus was possible to recover in vivo in chickens. The tumors obtained after a long latent period contained the sarcoma virus which was able to transform chicken cells in vitro and to induce tumors in chickens. All viruses, parental, td- and recovered were of D subgroup specificity. The tumor induction experiments in rats have shown that the recovery of viral genome deletion in td mutant by cellular sequences was not enough to regain the oncogenicity for rats. The results stressed the importance of 3-end sequences of the virus genome, probably the sequences in C region for heteroinduction ability of the avian sarcoma virus.
Int J Cancer 1982 Aug 15
PMID:Role of 3'-end of viral genome in tumor heteroinduction by the avian sarcoma virus. 629 Mar 99

C3H/Sm mice have lost the exogenous milk-borne mouse mammary tumor virus (MMTV) characteristic of the C3H strain and have a very low (1.5%) incidence of spontaneous mammary tumors, yet they are highly susceptible to mammary carcinogenesis by either chemical carcinogens or infection with the milk-borne virus. We have analyzed the MMTV proviral DNA content of normal tissues and of spontaneous, virus-induced, and chemically induced mammary tumors by restriction endonuclease digestion and Southern blot analysis. Although the results clearly showed additional MMTV sequences in the virus-induced tumor which are not present in normal liver DNA, none of the spontaneous or chemically induced tumors could be shown to contain either newly acquired exogenous or amplified endogenous MMTV sequences. Interestingly, mammary tumors arising in C3H/Sm mice treated simultaneously with infectious MMTV (C3H) and dimethylbenz[a]anthracene (DMBA) possessed new exogenous MMTV DNA even though no quantitative change in tumor production was observed when these mice were compared with C3H/Sm mice treated with DMBA alone (Smith et al., Int. J. Cancer 26:373-379, 1980). Our data indicate that the endogenous MMTV proviral units are extensively methylated in normal tissues, such as livers and normal nonlactating mammary glands. In the absence of MMTV (C3H), we found that in the rare, spontaneously occurring C3H/Sm mammary tumors, certain endogenous MMTV sequences were specifically hypomethylated. Hypomethylation of endogenous MMTV sequences was also noted in the chemically induced mammary tumors, even though radioimmune competition assays for MMTV gp52 and p28 are negative (Smith et al., Int. J. Cancer 27:81-86, 1981). Our results support the conclusion that amplification of endogenous MMTV sequences is not intrinsic to C3H/Sm mouse mammary tumors arising spontaneously or after induction by chemicals. On the other hand, integration of exogenous MMTV DNA into the genome was a constant feature of mammary tumors developing in MMTV (C3H)-infected C3H/Sm mice, even when DMBA was used as the carcinogen. Hypomethylation of some endogenous MMTV sequences is characteristic of C3H/Sm mammary tumors, whether spontaneous or induced by chemicals, which suggests that these sequences are located in actively transcribing regions of the tumor cell genome.
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PMID:Mouse mammary tumor virus proviral sequences congenital to C3H/Sm mice are differentially hypomethylated in chemically induced, virus-induced, and spontaneous mammary tumors. 629 67

A bifunctional intercalator may intercalate with DNA in at least two ways. Both intercalating moieties may intercalate with the same DNA molecule (type I, intramolecular cross-linking) or with two separate DNA molecules (type II, intermolecular cross-linking). Production of type I is often assumed. Type II biintercalation has been suggested, but no direct evidence has been reported. In the present study, endonuclease-restricted PM2 phage or pBR322 plasmid DNA fragments were treated with the bifunctional intercalative antitumor antibiotics, luzopeptin A (BBM-928A) and echinomycin, and analyzed by agarose gel electrophoresis. Luzopeptin A treatment produced additional DNA bands which were the products of type II biintercalation. The types of restriction fragments involved were identified. Maximal type II biintercalation occurred at a luzopeptin A/DNA range of 0.14 to 0.18, at which more than 50% of the total DNA molecules were involved. Type II products were converted gradually to type I products upon prolonged incubation at 37 degrees, probably due to the tendency for intermolecular bonds to disrupt. Echinomycin treatment failed to produce type II products, probably because of a DNA-binding affinity weaker than that of luzopeptin A. Thus, it is possible to use the present gel system to demonstrate the type II biintercalation for strong biintercalators, but milder systems are needed for weak biintercalators.
Cancer Res 1983 Jun
PMID:Intermolecular cross-linking of DNA through bifunctional intercalation of an antitumor antibiotic, luzopeptin A (BBM-928A). 630 66

Recombinant DNA technology has already had a major impact on our understanding of microbiology, cell biology, and genetic diseases and it will certainly have extensive applications in laboratory medicine. The techniques of restriction endonuclease analysis of DNA, nucleic acid hybridization after electrophoretic separation of nucleic acid fragments, and molecular cloning of bacterial, viral, and human genes are already being used in epidemiologic studies and the prenatal diagnosis of certain genetic diseases, such as sickle cell anemia and the thalassemias. New insights into genes that may be involved in human cancer are being developed and may lead to improved methods for diagnosis and classification of tumors.
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PMID:Recombinant DNA technology and laboratory medicine. 631 Nov 40

The patterns of the milk-transmitted (exogenous) mouse mammary tumor virus (MuMTV) DNA restriction endonuclease fragments in the nodule and tumor stages of BALB/cfC3H mouse mammary neoplasia were compared with the use of the Southern blot analysis. Acquired MuMTV restriction fragments were detected in DNA from hyperplastic alveolar nodules (HAN), from primary hyperplastic outgrowths (HPO), from families of transplanted HPO, from tumors from HPO, and from serially transplanted tumors. The restriction fragment patterns suggested that the HAN were composed of clonal dominant populations. Transplantation of subdivisions of individual HAN resulted in HPO with DNA restriction patterns suggesting that HAN also contained two or more subpopulations. In all cases, HAN subpopulations shared MuMTV restriction fragments suggesting a common origin. Forty-seven tumors arising from HPO shared MuMTV restriction fragments with the HPO. Most but not all tumors had additional acquired MuMTV restriction fragments not detected in the progenitor HPO, indicating that they were composed of a distinct subpopulation that originated from the HPO. The restriction fragment pattern in some tumor lines was remarkably stable through many transplant generations. Some tumors had no major additional restriction fragments, suggesting that major rearrangements of MuMTV DNA are not required for tumorigenesis.
J Natl Cancer Inst 1983 Nov
PMID:Alterations of acquired mouse mammary tumor virus DNA during mammary tumorigenesis in BALB/cfC3H mice. 631 8

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.
J Natl Cancer Inst 1983 Dec
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


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