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 p110gag-myc protein coded for by the retrovirus MC29 was purified 3,000-fold from MC29-Q8 transformed cells by immuno-affinity chromatography using IgG specific for the N-terminal region of the gag protein. Interaction of the protein with DNA fragments was studied by filter binding assay. DNA fragments were obtained from a MC29 DNA clone by restriction endonuclease treatment. Besides the complete DNA provirus the clone contained flanking cellular sequences into which the provirus had integrated. The DNA fragments which were retained by the p110gag-myc protein were eluted from the filter and analyzed by agarose gel electrophoresis. Preferential binding of a DNA fragment originating from the flanking cellular sequences was detected. The protein did not preferentially bind to the viral LTR promoter/enhancer region as suggested by an autoregulatory model, which can therefore no longer be substantiated.
J Cancer Res Clin Oncol 1986
PMID:Interaction of the oncogene protein myc with specific DNA fragments. 377 28

We determined a complete nucleotide sequence of an activated form of the c-H-ras-1 proto-oncogene cloned from the human cell line (QG56), using the DNA transfection technique and NIH3T3 cells as recipients. This cell line was established from a squamous-cell lung carcinoma of a Japanese patient, and the activated gene had 2 nucleotide substitutions. One substitution of a thymidine for an adenosine was found at position 1069 of the 2898 nucleotide sequence in a restriction endonuclease (SacI) fragment, which corresponds to the second base of the 61st codon of the gene encoding P21 protein. This nucleotide replacement was assumed to be responsible for the transforming activity. Another substitution of a guanosine for an adenosine which was detected at position 746 in the first intron was thought to be a genetic polymorphism unassociated with the transforming activity. Comparison of the various lengths of restricted fragments suggested that the activity was markedly influenced by certain sequences flanking the c-H-ras-1 gene.
Int J Cancer 1985 Jun 15
PMID:Isolation and characterization of an activated C-H-ras-1 gene from a squamous-cell lung carcinoma cell line. 400 2

Human T-cell leukemia virus (HTLV) is a family of related human T-lymphotropic retroviruses closely linked with certain human T-cell malignancies and associated with many cases of acquired immunodeficiency syndrome (AIDS). We isolated and molecularly cloned HTLV from patients with both types of clinical disorders and found by restriction endonuclease mapping and core and envelope protein analysis that at least two evolutionarily divergent viral subgroups exist, HTLV-I and HTLV-II. Previous studies have failed to detect significant nucleotide sequence homology between HTLV-I and HTLV-II even though these different members of the HTLV family share certain biologic properties such as T-cell tropism and transformation. To further test these viruses for conserved regions in their genomes, we examined hybridization between HTLV-I and HTLV-II by using Southern blotting and heteroduplex mapping at different melting points. These two techniques produced similar results, showing that HTLV-I and HTLV-II proviruses have, in fact, strongly conserved nucleotide sequences in the pX region and lesser although still substantial homology in the LTR, gag, pol, and env regions. These data provide experimental evidence that HTLV-II, like HTLV-I, contains pX sequences. Although the function of pX is unknown, its conservation in evolutionarily divergent human T-lymphotropic viruses implies a biologically important function. It is possible, but unproven, that pX could encode proteins involved in T-cell tropism, cell transformation, immune suppression, or other biologic actions characteristic of the HTLV family.
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PMID:Genomes of evolutionarily divergent members of the human T-cell leukemia virus family (HTLV-I and HTLV-II) are highly conserved, especially in pX. 608 32

Site-specific methylation of the human c-myc oncogene was investigated in a set of cultured human tumor cell lines and normal human fibroblast strains. As previously reported, all of the tumor cell lines in contrast to normal cells were hypomethylated to various degrees in their total genomic DNA. The presence of methylation in specific regions of the c-myc gene was analyzed by use of the restriction endonuclease isoschizomers MspI and HpaII, which recognize the sequence 5'-CCGG-3' (CCGG = DNA sequence of 2 cytosine bases followed by 2 guanine bases) but differ in their abilities to cleave at the internal cytosine residue when it is methylated. The first exon, first intervening sequence, and the second exon were hypomethylated in all cell types, regardless of whether the cells were normal or oncogenically transformed and regardless of the degree of total genomic methylation of the cell. However, the solitary CCGG site in the third exon was fully methylated in normal cell strains. In contrast, in 3 of 5 tumor cell lines measured, this site was hypomethylated. This is the first demonstration of a site-specific DNA methylation defect in a cellular oncogene. Some possible implications relating disruption of DNA methylation to oncogene control and oncogenesis are discussed.
J Natl Cancer Inst 1984 Nov
PMID:Hypomethylation of DNA in human cancer cells: a site-specific change in the c-myc oncogene. 609 64

Retroviruses cause a wide variety of diseases in avian and mammalian species. Human acquired immune deficiency syndrome (AIDS) leads to collapse of the immune system and death by a wide variety of opportunistic infections; unusual forms of cancer are associated with this syndrome. Retroviruses have been recovered from tissues of AIDS patients and from patients with related conditions. These similar newly-isolated viruses are lymphadenopathy-associated virus (LAV), human T-cell lymphotropic virus (HTLV-III) and AIDS-associated retrovirus (ARV-2). We have identified a RNA genome of approximately 9 kilobases (kb) in virions purified from the culture medium of a human T-cell tumour line infected with ARV-2. A cDNA probe made from viral RNA detected circular DNA molecules and proviral forms in infected cells. We prepared a library of infected cell DNA. Recombinant phage included those with a 9.5-kb proviral DNA and viral DNA permuted with respect to the single EcoRI site. Comparison of three ARV isolates from different AIDS patients revealed polymorphism of restriction endonuclease sites.
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PMID:Molecular cloning of AIDS-associated retrovirus. 609 18

The fragmentation of Hind III- and Pst I-digested PM2 DNA and of Hind III-digested pBR322 DNA by bleomycin A2 and B2 and talisomycins A, B, S2b, and S10b was investigated. As observed by electrophoresis on agarose gels, the ethidium bromide staining band patterns produced following incubation of the various restriction endonuclease-digested DNAs with the compounds were different for the bleomycin analogs and for the talisomycin analogs. Quantitation of the degree of fragmentation of various segments of linear PM2 DNA by either bleomycin A2 or talisomycin A indicated that certain segments of the PM2 genome serve as better substrates than other segments for double-strand fragmentation by either of the two antitumor antibiotics. These results show that in this system bleomycin and talisomycin analog treatment of linear PM2 or pBR322 DNA resulted in breakage of DNA, producing different-length DNA fragments, and demonstrate the importance of the two amino acids and the 4-amino-4,6-dideoxy-L-talose sugar, which are located near the bithiazole in talisomycin but absent in the bleomycin structure in conferring a different site-specificity for DNA fragmentation to talisomycin than to bleomycin.
Cancer Chemother Pharmacol 1982
PMID:Structure-activity relationships involved in the site-specific fragmentation of linear duplex DNAs by talisomycin and bleomycin analogs. 617 26

The 5-methylcytosine (m5C) content of DNAs from Morris hepatomas of varying growth rates and from normal liver was analyzed. DNA methylation in all hepatomas studied was found to be 20-45% less than in normal liver. This result was confirmed independently by restriction endonuclease (Hpa II and Msp I) analysis. While these results agreed with recent literature data suggesting hypomethylation of DNA from some neoplastic sources, no correlation was observed between the extent of DNA hypomethylation and the growth rates of the tumors.
Cancer Lett 1983 Jun
PMID:DNA hypomethylation in Morris hepatomas. 619 2

By centrifuging total cellular DNA derived from human genital warts (condylomata acuminata) in CsCl-ethidium bromide gradients, supercoiled DNA was isolated. The molecular weight of this DNA was determined by agarose gel electrophoresis and amounted to 5.1 X 10(4). This DNA isolated from an individual genital wart was annealed to fractions of aqueous supernatants of the same wart after prior centrifugation of this material in CsCl density gradients. Annealing was observed at a density of approximately 1.32 g/ml corresponding to the expected density of papilloma virus particles. Since such particles were also observed in the same preparation by electron microscopy, it was concluded that the supercoiled DNA molecules were derived from papilloma virus nucleocapsids. Positive hybridization was found with six additional preparations from individual genital warts. Therefore, it seems that the isolated DNA prevails in condylomata acuminata. The DNA is different from the other five types of human papilloma viruses described thus far in regard to its restriction endonuclease cleavage patterns. The virus analyzed is tentatively designated as human papilloma virus type 6 (HPV 6).
Int J Cancer 1980 May 15
PMID:Partial characterization of viral DNA from human genital warts (Condylomata acuminata). 624 10

Cyclobutyl pyrimidine dimers have been detected in the DNA of human skin following in vivo irradiation with suberythemal doses of ultraviolet (UV) radiation from FS-20 sun lamp fluorescent tubes. Dimers were assayed by treatment of extracted DNA with Micrococcus luteus UV-specific endonuclease, alkaline agarose electrophoresis, and ethidium bromide staining. This technique, in contrast to conventional dimer assays, can be used with nonradioactive DNA and is optimal at low UV light doses. M. luteus endonuclease-sensitive sites were determined after exposure of untanned skin in two volunteers to UV light (0.97, 1.94, or 3.88 X 10(3) J/sq m; lambda, 290 to 360 nm). At 20 min postirradiation (dose, 1.94 X 10(3) J/sq m), fewer M. luteus endonuclease-sensitive sites were found in the DNA than immediately after the irradiation. Even fewer endonuclease-sensitive sites were found at 20 min when the UV-irradiated skin was subsequently irradiated with visible light than when the area was kept in the dark. These data suggest that some dimer disappearance by excision repair occurs within 20 min of UV irradiation and that photoreactivation of dimers can make a contribution to the total repair process.
Cancer Res 1980 Sep
PMID:Pyrimidine dimer formation and repair in human skin. 625 56

We have studied repair of ultraviolet light (UV)-induced damage in a strain of Bloom's syndrome cells which we have shown to be defective in host cell reactivation of UV-irradiated herpes simplex virus. Excision repair was monitored by following loss of sensitivity of DNA in permeabilized cells to digestion by the Micrococcus luteus UV endonuclease preparation. The Bloom's syndrome fibroblasts apparently removed endonuclease-sensitive sites from the DNA slightly less efficiently than did normal strains. After 24 hr, 38% of the sites remained in the Bloom's syndrome cells in comparison with 16% in normal fibroblasts. DNA newly synthesized in UV-irradiated Bloom's syndrome cells sedimented less far into alkaline sucrose gradients than did DNA from similarly treated normal cells. In other respects, including the effect of caffeine exposure, DNA synthesis in Bloom's syndrome cells was indistinguishable from that in normal cells. We were therefore able to detect only minor defects in the repair of UV-induced damage in Bloom's syndrome fibroblasts. This is consistent with the normal survival exhibited by these cells. The defect in excision repair may, however, be sufficient to allow the cellular repair capacity to become saturated at high infecting multiplicities of UV-irradiated herpes simplex virus.
Cancer Res 1981 Mar
PMID:Excision of ultraviolet damage and the effect of irradiation on DNA synthesis in a strain of Bloom's syndrome fibroblasts. 625 83


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