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)

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.
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PMID:Role of 3'-end of viral genome in tumor heteroinduction by the avian sarcoma virus. 629 Mar 99

Chromosome-mediated transfer of murine leukaemia (MuLV) and murine sarcoma (MuSV) virus genetic information to uninfected recipient cells was investigated. Metaphase chromosomes from AKR MuLV-infected SC-1 mouse cells were incubated with NIH/3T3 cells. After several passages (1 to 3 weeks), infectious virions exhibiting reverse transcriptase activity and the characteristic host range of ecotropic, N-tropic AKR virus appeared in the supernatant fluids of the treated cells. Restriction endonuclease analysis of genomic DNA from transfected cells indicated that AKR proviral DNA was associated with the high molecular weight DNA of the host. These results demonstrate that the AKR MuLV genome can be stably transferred to uninfected recipient cells via isolated metaphase chromosomes. Although AKR virions are not able to infect heterologous cells, chromosome-mediated transfection resulted in the establishment of productive AKR MuLV infection in mink cells. Thus, the use of chromosomes to transfer virus genes can circumvent the natural host restriction barrier. In other experiments, it was shown that normal NIH/3T3 cells were transformed after exposure to metaphase chromosomes isolated from an MuSV-infected, non-producer line. Foci were detected 14 to 21 days after chromosome treatment and were shown to contain true viral transformants since transforming virus was produced after superinfection with MuLV.
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PMID:Transfer of murine leukaemia and murine sarcoma virus genetic information by transfection with isolated metaphase chromosomes. 629 50

Closed circular unintegrated DNA of the SEATO strain of gibbon ape leukemia virus (GaLV-S) was isolated from canine thymus fibroblasts after cocultivation with chronically infected bat lung fibroblasts. Restriction endonuclease HindIII cleaves GaLV-S DNA once, thus allowing isolation and cloning of HindIII-digested unintegrated DNA in a permitted form. Two clones isolated in the vector, Charon 21A, were nearly identical by restriction enzyme mapping to each of the two types of GaLV-S previously observed. These two types differ at a single SalI site. Unlike previous maps of GaLV-S proviral DNA, however, both clones lack SstI sites in the long-terminal-repeat units. Both the GaLV-S clones and the major species of GaLV-S proviral DNA contain an EcoRI site in the long-terminal-repeat units. The presence of this EcoRI site and the absence of an SstI site in the GaLV-S long-terminal-repeat units differentiate it from all other known GaLV strains and from the closely related nononcogenic simian sarcoma-associated virus. Heteroduplex comparisons of each of the two clones to clones of simian sarcoma-associated virus show no obvious deletion or substitution loops. This suggests that the ability of GaLV-S to induce myeloid leukemia in gibbon apes in not due to an acquired onc gene.
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PMID:Molecular cloning of circular unintegrated DNA of two types of the SEATO strain of gibbon ape leukemia virus. 629 90

We have molecularly cloned an integrated proviral DNA of Fujinami sarcoma virus (FSV) into a lambda phage vector and further subcloned it into plasmid pBR322. The source of provirus was a quail nonproducer cell clone transformed by FSV. The FSV strain used is temperature sensitive in the maintenance of transformation of avian cells. The recombinant plasmid was shown to contain an entire FSV genome by fingerprinting the hybrids formed with 32P-labeled FSV RNA. This analysis also revealed a previously undetected env-related sequence in FSV which represents the 3' end of the gp85 env gene. A physical map of cloned FSV DNA identifying sites of several restriction enzymes is described. Upon transfection, FSV DNA cloned in pBR322 transformed mouse NIH-3T3 cells, which proved to be temperature sensitive in maintaining transformation. Phosphorylation but not synthesis of p140, the only known gene product of FSV, was also temperature sensitive in these cells. The correlation between transformation and phosphorylation of p140 suggests that phosphorylation of p140 is necessary for transformation of mouse cells, as was shown previously for avian cells. These results provide direct genetic evidence that the mechanisms for maintaining transformation of mammalian and avian cells involve the same FSV gene product, p140. Homology was detected by hybridization between transformation-specific sequences of FSV DNA and certain restriction endonuclease-resistant fragments of cellular DNA of two avian species, chicken and quail. Under the same conditions homology was also detected with DNA of non-avian species, although apparently to a lower degree than with avian cells.
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PMID:DNA clone of avian Fujinami sarcoma virus with temperature-sensitive transforming function in mammalian cells. 629 1

We analyzed 15 recombinant DNA clones of the unintegrated closed circular DNA intermediate of the BALB/c endogenous ecotropic murine leukemia virus WN1802N. Thirteen of these clones had an insert which corresponded to the complete murine leukemia virus genome. Of these, six contained a single long terminal repeat (LTR) and seven contained two LTRs. The viral genomes in nine clones had an LTR of 520 base pairs (bp), one had an LTR of 570 bp, three had an LTR of 600 bp, and one had an LTR of 670 bp. Restriction endonuclease analysis demonstrated that the size variability resides in the U3 region. Seven of eight clones which yielded infectious virus by DNA transfection had the 520-bp LTR, and the other had a 600-bp LTR. More detailed examination of plasmid subclones of three isolates with different-sized LTRs revealed that the approximate position which varies in the U3 region corresponds to the 72-bp repeat region of Moloney sarcoma virus. Possible consequences of these variations are discussed.
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PMID:Analysis of recombinant DNA clones of the endogenous BALB/c murine leukemia virus WN1802N: variation in long terminal repeat length. 629 58

The DNA's from two of four methylcholanthrene-induced mouse fibrosarcomas contained transforming genes that were identical in their pattern of restriction endonuclease resistance to inactivation of biologic activity. This transforming gene was identified as the activated homolog of the Kirsten murine sarcoma virus onc gene, v-kis. The finding that a defined carcinogen reproducibly leads to activation of kis as a transforming gene should be of value in elucidating the role of oncogenes in the neoplastic process.
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PMID:Frequent activation of c-kis as a transforming gene in fibrosarcomas induced by methylcholanthrene. 630 39

The avian Fujinami sarcoma virus (FSV) contains a hybrid transforming gene (delta gag-fps) with a 5' 1.3-kb portion derived from the gag gene of avian retroviruses and a 3' 2.8-kb portion (fps) derived from a cellular prototype. A lambda recombinant DNA clone carrying fps sequences within a 16-kb insert of cellular DNA, termed lambda proto-fps clone 12, has been selected from a chicken DNA library for comparison with the viral onc gene. Mapping of endonuclease-resistant proto-fps DNA fragments and hybridization with cloned viral DNA located FSV-related sequences at the 3' end of the insert within a region of about 4.25 kb. Alignment of endonuclease-resistant proto-fps and viral DNA fragments relative to common RNase T1-resistant oligonucleotide sequences of viral RNA, identified by fingerprinting DNA-RNA hybrids, indicated: (i) that proto-fps is colinear with viral fps but is interrupted by 1.75 kb of scattered sequences unrelated to viral fps; (ii) that among the nine endonuclease sites compared, proto-fps and viral fps share one PvuII, one BamHI, and possibly a Kpn1 site at homologous locations, and that they each have unique endonuclease sites and common sites at unique locations; (iii) that within 12 kb upstream from the 5' boundary of overlap with viral fps, proto-fps lacks gag-related sequences; and (iv) that proto-fps clone 12, like several others isolated by us, lacks at the 3' end an equivalent of the 3' 10 to 20% of viral fps. The eight endonuclease site-map coordinates of proto-fps and viral DNA also divided 44 fps oligonucleotides of viral RNA into 9 map segments. We conclude that the onc gene of FSV differs from proto-fps in delta gag and in multiple point mutations, compatible with a transforming function for the viral gene and a normal function for the cellular sequence homolog. Since proto-fps is unrelated to essential virion genes, the onc gene of FSV must have originated from cellular proto-fps by rare, illegitimate recombination.
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PMID:Structural relationship between the chicken DNA locus, proto-fps, and the transforming gene of Fujinami sarcoma virus, delta gag-fps. 631 Aug 87

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

A human transforming gene present in T24 bladder carcinoma cells has been molecularly cloned. The transforming sequences have been located within a 4.6 kilo base pair (kbp) DNA fragment that transforms NIH/3T3 cells with a specific activity of 5 X 10(4) focus-forming units/pmol. Homologous sequences present in normal human DNA have also been molecularly cloned. Comparison of the restriction endonuclease maps of the normal and transforming genes did not reveal any significant differences. These results suggest that subtle molecular changes are responsible for the acquisition of malignant properties by this gene in T24 cells. The T24 oncogene was found to be unrelated to transforming genes present in a variety of human tumors other than bladder carcinomas. In contrast, the T24 oncogene is highly related to the onc genes of the BALB and Harvey strains of murine sarcoma viruses ( MSVs ). Preliminary characterization of the transcriptional and translational products of the T24 oncogene suggests that this gene is transcribed into a 1.2-kbp poly(A)-containing RNA whose translation yields a 23,000-dalton protein antigenically related to the transforming gene products of BALB and Harvey MSVs .
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PMID:Characterization of a human transforming gene isolated from T24 bladder carcinoma cells. 632 52

By the use of recombinant DNA technology and microinjection in cultured cells, the molecular genetic elements involved in the evolution of a retrovirus with the multipotential to infect, transform and replicate in host cell, have been critically examined in this investigation. Recently we have identified and purified the integrated and proviral DNA sequences specific for two rat endogenous helper leukemia viruses, WR- RaLV , originated from a chemically induced wild rat fibrosarcoma, and RHHV , isolated from a chemically induced rat hepatoma, HTC-H1 (1). By using a multidisciplinary approach combining restriction endonuclease analysis, reverse phase V-column chromatography, agarose gel electrophoresis, Southern blot transfer and filter nucleic acid hybridization, we were able to demonstrate that the rat helper leukemia viral DNA sequence was approximately 8.4-8.8 kb. The 8.8 kb RHHV DNA was molecularly cloned via the EK-1 certified vector pBR 322 plasmid into E. coli RRI cells. A successful recombinant clone, 8/32, that carried one entire RHHV 8.8 kb DNA sequence was mapped by restriction endonuclease analyses. Restricted DNA fragments of various sizes throughout the complete RHHV genome were isolated and purified for intranuclear microinjection into normal rat kidney cells. Release of type C infectious helper virus in these microinjected cells was investigated by superinfection on K-NRK, Kirsten sarcoma transformed non-producer cells. Recombination of the helper viral DNA sequence, en toto or of subgenomic sizes, carried in microinjected cells, with the sarcomagenic DNA sequence, carried in K-NRK cells, was also studied by genome-rescue and cell-transformation experiments. Our observations led to the conclusion that all critical genetic elements including the 5' LTR helper DNA sequence, gag, pol, and env genes, encoded for the biological activity of the type C helper virus resided within the 6.0 kb proximal to the 5' terminus of the endogenous rat type C helper virus DNA. They proved vitally essential for the recombination with the Src sequence during the evolution of an infectious, transforming and replication-competent retrovirus.
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PMID:Cloning of the rat endogenous helper leukemia virus DNA sequence and expression of the helper activity encoded by the cloned DNA sequence in normal rat kidney cells by microinjection. 632 7


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