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)

The restriction endonuclease EcoRI has been used to study the inheritance of strain difference in endogenous mouse mammary tumor virus DNA sequences. This enzyme, which cleaves at only one site within the nondefective viral genome, generates DNA fragments containing mouse mammary tumor virus sequences which vary in size according to the locations of EcoRI restriction sites in the flanking mouse sequences, thereby defining unique integration sites of the viral genome. Recombinant inbred strains of mice have been used to study the inheritance of these DNA fragments which hybridize to mouse mammary tumor virus cDNA sequences. The results define 11 segregating units consisting of 1 or 2 fragments. These units were shown to segregate among the recombinant inbred strains, and in some instances linkage was established. Two units were shown to be linked on chromosome 1. Another unit was mapped to chromosome 7, which is presumably identical to the previously defined genetic locus Mtv- 1. One other mouse mammary tumor virus locus was tentatively assigned to chromosome 6. The results are consistent with the view that integration of mouse mammary tumor virus can take place at numerous sites within the genome, and once inserted, these proviruses appear to be relatively stable genetic entities.
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PMID:Genetic mapping of endogenous mouse mammary tumor viruses: locus characterization, segregation, and chromosomal distribution. 627 15

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.
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PMID:Detection of acquired provirus sequences in mammary tumors from low-expressor, low-risk mice. 628 24

Cellular DNA containing integrated murine mammary tumor virus (MuMTV) was isolated from FeI/C6 feline kidney cells and CCL64 mink lung cells infected with milkborne RIII MuMTV. By using restriction enzyme HpaI, intact RIII MuMTV provirus (length, 8.7 kilobases [kb]) was excised from the cellular DNA. Subsequent restriction endonuclease analysis of this HpaI fragment with KpnI, HindIII, EcoRI, BamHI, BglII, PstI, SstI, SalI, and XhoI enabled us to construct a map of the RIII virus genome. A comparison of this map with the maps of the GR and C3H MuMTV's revealed that there are greater sequence differences between the RIII virus and the GR and C3H MuMTV proviruses than there are between the GR and C3H proviruses. The following are features of the restriction map unique to the RIII provirus: the presence of three BamHI and two EcoRI cleavage sites, a HpaI cleavage site in the terminal 3'-5' repeat unit of the provirus, and the absence of an XhoI cleavage site. Another distinguishing feature of the RIII provirus is that the sizes of some of the restriction fragments produced by cleavage of the RIII provirus with PstI are different from the sizes of the fragments obtained by PstI cleavage of the GR and C3H proviruses. Like the GR proviral DNA, the RIII proviral DNA has three SstI (SacI) cleavage sites, whereas the C3H provirus has only two SstI sites. HpaI digestion of MuMTV-infected mink lung cell DNA revealed only one class of provirus (an 8.7-kb fragment); however, we observed several minor classes of RIII proviral DNA in addition to the major class of provirus DNA in infected cat kidney cells. PstI digestion of the HpaI 8.7-kb fragments from both feline and mink cells generated a 3.7-kb DNA fragment identical in size to a PstI-generated fragment that has been found in GR and C3H milkborne virus-infected cells. Although a fragment similar in size to the milkborne 3.7-kb PstI fragment has been found as an endogenous component in many C3H and GR mouse tissues, we did not observe such an endogenous fragment in the RIII mouse strain. Therefore, the 3.7-kb fragment may be useful as a marker for the milkborne RIII MuMTV provirus in RIII mice.
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PMID:Restriction endonuclease mapping of the proviral DNA of the exogenous RIII murine mammary tumor virus. 628 76

We examined the genetic structure, in terms of restriction endonuclease recognition sites, of the milk-transmitted, low-oncogenic mouse mammary tumor virus (MuMTV) of the BALB/cNIV mouse strain. An analysis with EcoRI documented the presence of acquired cNIV proviruses in the mammary tumor DNAs of BALB/cNIV animals. A comparison of tumor DNAs digested with PstI showed that both the cNIV MuMTV and C3Hf MuMTV proviruses lacked the 4.3- and 1.1-kilobase pair fragments characteristic of C3H MuMTV patterns. An examination of mammary tumor and normal, nonmammary tissue DNAs with BamHI supported the idea that the cNIV MuMTV is identical to the C3Hf MuMTV and demonstrated that these two low-oncogenic proviruses are identical to the high-oncogenic C3H MuMTV provirus with respect to a pair of BamHI sites which define a 1.3-kilobase pair fragment. For each of the three MuMTV strains, we also mapped DNAs generated in isolated virions by reverse transcription of their genomic RNAs. Our results showed that cNIV and C3Hf MuMTV are distinct entities by virtue of an additional PstI site within the cNIV long terminal repeat sequence. Another unique feature of cNIV MuMTV revealed by the analysis of virion-generated DNAs was the existence of a family of genomes within the cNIV population. We concluded that cNIV is distinct from its presumptive C3Hf MuMTV predecessor.
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PMID:Identification of a unique mouse mammary tumor virus in the BALB/cNIV mouse strain. 628 94

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

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.
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PMID:Alterations of acquired mouse mammary tumor virus DNA during mammary tumorigenesis in BALB/cfC3H mice. 631 8

The mouse mammary tumor virus long terminal repeat (MMTV LTR) has been introduced into cultured murine cells, using the 69% transforming fragment of bovine papilloma virus type 1 (BPV). Transformed cells contain up to 200 copies of the chimeric molecules per diploid genome. The restriction endonuclease map of the acquired recombinants, as well as the physical structure of the DNA, indicates that the LTR-BPV molecules present in these cells occur exclusively as unintegrated, extrachromosomal episome. When a 72-base pair direct repeat "enhancer" element (derived from the Harvey sarcoma retrovirus) was included in the MMTV LTR-BPV chimeric plasmids, DNA acquired through transfection, with a single exception, was integrated or rearranged or both. The transcriptional potential of the episomal MMTV promoter present in these cells was tested in two ways. First, steady-state levels of MMTV-initiated RNA were measured by quantitative S1 mapping. Second, the relative number of transcription complexes initiated in vivo was determined by using a subnuclear fraction highly enriched for MMTV-BPV minichromosomes in an in vitro transcription extension assay. Both approaches showed that the MMTV LTR present in the episomal state was capable of supporting glucocorticoid hormone-regulated transcription. We have therefore demonstrated the hormone response for the first time in a totally defined primary sequence environment. Significant differences both in the basal level of MMTV-initiated transcription and in the extent of glucocorticoid induction were observed in individual cell lines with similar episomal copy numbers. These phenotypic variations suggest that epigenetic structure is an important component of the mechanism of regulation.
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PMID:Glucocorticoid regulation of transcription at an amplified, episomal promoter. 631 79

Endogenous mouse mammary tumor virus (MMTV) proviral copies were characterized in three genetically dissimilar mouse strains: GR, a high-tumor-incidence strain bred in Europe that carries an MMTV proviral copy associated with early mammary tumors; DBA, a high-tumor-incidence laboratory strain bred in the USA with an endogenous copy that is associated with MMTV antigen expression in the milk; and NFS, a recently inbred line of the low-tumor-incidence NIH Swiss mouse. MMTV proviral loci were studied using restriction endonuclease analysis and the Southern transfer procedure in genetic crosses and in somatic cell hybrids. By studying the segregation of MMTV-specific EcoRI, BamHI, and PstI fragments, the organization of these fragments into MMTV proviral loci was determined and it was shown that (1) many homologous proviral loci are present in these three mouse strains, (2) these MMTV proviruses differ in their pattern of internal restriction sites, and (3) the MMTV loci are distributed on multiple chromosomes including 1 and 7.
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PMID:Characterization and chromosomal location of endogenous mouse mammary tumor virus loci in GR, NFS, and DBA mice. 632 May 29

The molecular mechanism of cell death induced by 5-Fluoro-2'-deoxyuridine (FUdR) was investigated. FUdR caused cell death to induce dNTP pool imbalance and following DNA double strand breaks in mouse mammary tumor FM3A cells. We isolated a new endonuclease from FUdR-treated cells, named endonuclease S, that played an important role in FUdR-induced cell death. Cells treated with FUdR showed intracellular acidification before cell death formation. We observed that the endonuclease S in acidic cells may lead the DNA fragmentation. On the other hand, we observed that protease inhibitors (such as TLCK, TPCK, PMSF, p-APMSF, Pefabloc SC and Z-Asp-CH2-DCB) blocked intracellular acidification, DNA fragmentation and FUdR-induced cell death. But the inhibitors did not affect dNTP pool imbalance in the cells. These results suggest that proteases act at the point of downstream of dNTP pool imbalance and upstream of the intracellular acidification.
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PMID:The molecular mechanisms of 5-fluoro-2'-deoxyuridine induced cell death. 958 36

DNA repair takes place in the context of chromatin. Previous studies showed that histones impair base excision repair (BER) of modified bases at both the excision and synthesis steps. We examined BER of uracil in a glucocorticoid response element (GRE) complexed with the glucocorticoid receptor DNA binding domain (GR-DBD). Five substrates were designed, each containing a unique C-->U substitution within the mouse mammary tumor virus promoter, one located within each GRE half-site and the others located outside the GRE. To examine distinct steps of BER, DNA cleavage by uracil-DNA glycosylase and Ape1 endonuclease was used to assess initiation, dCTP incorporation by DNA polymerase (pol) beta was used to measure repair synthesis, and DNA ligase I was used to seal the nick. For uracil sites within the GRE, there was a reduced rate of uracil-DNA glycosylase/Ape1 activity following GR-DBD binding. Cleavage in the right half-site, with higher GR-DBD binding affinity, was reduced approximately 5-fold, whereas cleavage in the left half-site was reduced approximately 3.8-fold. Conversely, uracil-directed cleavage outside the GRE was unaffected by GR-DBD binding. Surprisingly, there was no reduction in the rate of pol beta synthesis or DNA ligase activity on any of the fragments bound to GR-DBD. Indeed, we observed a small increase ( approximately 1.5-2.2-fold) in the rate of pol beta synthesis at uracil residues in both the GRE and one site six nucleotides downstream. These results highlight the potential for both positive and negative impacts of DNA-transcription factor binding on the rate of BER.
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PMID:Base excision repair in a glucocorticoid response element: effect of glucocorticoid receptor binding. 2062 60


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