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)

We have examined the epidermal growth factor (EGF) receptor gene for structural alterations in fresh human tumors. DNA samples from 92 patients with solid tumors (lung cancer, 37; breast cancer, 24; head and neck cancer, 17; other tumors, 14) were analyzed and compared with those from 22 leukemia patients and 14 individuals without malignant neoplasms. When DNA samples were digested with HindIII restriction endonuclease, Southern blot analysis demonstrated 3 distinct polymorphic bands (9.8, 11, and 12 kilobases) after hybridization to the HER-A64-1 probe and another 2 distinct polymorphic bands (4.9 and 5.2 kilobases) after hybridization to the HER-A64-3 probe. Pedigree analysis of 43 members of a single family and comparative analysis of tumor and normal DNA samples from the same patients demonstrated that the variations in fragment size observed were due to 2 independent restriction fragment length polymorphisms in the region of the EGF receptor gene. Amplification of the EGF receptor gene was detected in 3 cases of breast cancer, but not in other tumors studied. We conclude that the human EGF receptor gene has multiple restriction fragment length polymorphisms and that in fresh human tumor samples rearrangement and amplification of the gene occur infrequently, if ever, within the region encompassed by the 2 complementary DNA probes used.
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PMID:Multiple restriction fragment length polymorphisms of the human epidermal growth factor receptor gene. 289 88

Enhanced expression of the human SIS/PDGF-2 gene has been reported in a number of human cell lines, sarcomas, and glioblastomas. We have analyzed the SIS/PDGF-2 gene for structural alterations in fresh human tumors. DNA samples from 79 patients with solid tumors (63 mesenchymal tumors, 12 lung carcinomas, 4 breast carcinomas) were examined and compared with DNA samples from 50 leukemia patients and 14 unrelated individuals without malignant neoplasms. When DNA samples were digested with a HindIII restriction endonuclease, Southern blot analysis demonstrated two distinct bands (21kb and 18kb) after hybridization to the SIS/PDGF-2 gene probe. A pedigree analysis of a 43-member family indicated that these allelic variants segregated in a Mendelian fashion. There was, however, tumor specific allele loss in 18% of the mesenchymal tumors analyzed, which may indicate a common etiology for this tumor type.
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PMID:Reduction to homozygosity at the SIS/PDGF-2 locus in human mesenchymal tumors. 290 34

3-Methylcholanthrene-induced T-cell thymic lymphomas in RF mice were examined for involvement of murine leukemia virus (MuLV)-related sequences in leukemogenesis. Both the expression of MuLV-related RNA species and the organization of endogenous MuLV proviral DNA were analyzed. Of 27 primary tumors examined, only 5 exhibited elevated MuLV-related RNA species homologous to xenotropic specific env DNA. None of these RNA species hybridized with ecotropic p15E DNA sequences. Only two of these five tumors contained MuLV-like RNA species that hybridized with ecotropic MuLV long terminal repeat sequences, despite the probe's ability to detect both ecotropic MuLV and mink cell focus-inducing viral RNA. No muLV resembling mink cell focus-inducing virus whose expression could be correlated with lymphomagenesis was detected in either preleukemic thymocytes, primary 3-methylcholanthrene-induced thymic tumors, tumors passaged in vivo, or cell lines derived from tumors. Restriction endonuclease analysis of DNA from both primary tumors and cell lines failed to reveal either proviral DNA with recombinant env genes or rearrangement of endogenous MuLV proviruses. Therefore, chemically induced lymphomagenesis in RF mice appears different from the spontaneous lymphomagenic process in AKR mice with respect to the involvement of endogenous MuLV sequences.
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PMID:Comparison of endogenous murine leukemia virus proviral organization and RNA expression in 3-methylcholanthrene-induced and spontaneous thymic lymphomas in RF and AKR mice. 298 67

Analysis of total feline DNA by genomic blot hybridization, using the viral oncogene of Abelson murine leukemia virus as a specific probe, has led to the identification of multiple v-abl homologous genetic sequences in the cat genome. Upon restriction endonuclease BamHI digestion, the combined size of the v-abl homologous DNA fragments was about 31 kbp. To characterize these sequences further, four independent v-abl homologous cosmid clones with overlapping cellular inserts have been isolated from a gene library of cat lung genomic DNA. These inserts represent a contiguous region of cellular DNA sequences of 56 kbp in length. Within this region of the feline genome, the v-abl homologous sequences are discontinuously dispersed over a region of about 34 kbp. They represent the complete feline v-abl cellular homolog and are colinear with the viral v-abl oncogene. Nine regions of highly repetitive DNA sequences have been mapped in close proximity to v-abl homologous sequences. These results establish the presence of only a single c-abl proto-oncogene in the cat genome and present its genetic organization.
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PMID:Characterization of the feline c-abl proto-oncogene. 298 4

In order to test if trans-acting regulatory factors specific for globin genes of the adult and embryonic stages of development exist in erythroid cells, transcriptionally active embryonic and adult globin genes on the same chromosome were transferred by cell fusion from the human leukemia cell K562 into phenotypically adult mouse erythroleukemia cells. Restriction-fragment-length polymorphisms of the K562 zeta (embryonic) globin genes were used to establish that all three copies of human chromosome 16 present in the K562 cell showed the same pattern of human globin gene expression after transfer to the mouse erythroleukemia cell. Adult (alpha) but not embryonic (zeta) human globin mRNA was detected in all nine of the independently derived mouse erythroleukemia hybrid cells, each of which contained human chromosome 16. Restriction endonuclease studies of the K562 alpha- and zeta-globin genes after transfer into the mouse erythroleukemia cell showed no evidence of rearrangements or deletions that could explain this loss of zeta-globin gene expression. These data suggest that regulation of globin gene expression in these erythroleukemia cells involves trans-acting regulatory factors specific for the adult and embryonic stages of development.
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PMID:Regulatory factors specific for adult and embryonic globin genes may govern their expression in erythroleukemia cells. 298 42

A 2.3 kb cDNA was cloned from human T-cell leukaemia virus [HTLV(MT-2)] virion RNA using a vector system, as plasmid pHTLV 707. The restriction endonuclease map of pHTLV 707 revealed that the insert contained the 5' half of the env gene and a portion of the pX region of HTLV, corresponding to the subgenomic RNA derived from 32S defective HTLV. Nucleotide sequence analysis of pHTLV 707 indicated that the clone contained an open reading frame for a 60K mol. wt. protein including the upstream and entire pX IV region. A rabbit antibody raised against a synthetic decapeptide deduced from the nucleotide sequence at the carboxyl terminus of the pX IV region immunoprecipitated gp68, and also 80K and 40K proteins.
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PMID:Molecular cloning of cDNA encoding gp68 of adult T-cell leukaemia-associated antigen: evidence for expression of the pX IV region of human T-cell leukaemia virus. 299 47

Rat thymic lymphomas induced by Moloney murine leukemia virus carry DNA rearrangements due to provirus integration in at least five independent cellular DNA domains (Mlvi-1, Mlvi-2, Mlvi-3, RMoInt-1, and c-myc). We had previously shown that rearrangements in more than one of these domains could occur in the same tumor. In this report we extend these findings by showing that, with one exception, tumors containing provirus insertions in Mlvi-1 always contained provirus insertions in a second locus, Mlvi-2. To determine whether both events occurred in the same population of tumor cells, we examined the clonal nature of these tumors by taking advantage of allelic polymorphisms that occur naturally in both Mlvi-1 and Mlvi-2. Tumors with provirus insertions in both Mlvi-1 and Mlvi-2 arising in rats heterozygous at one of these loci were identified. DNA from these tumors was analyzed by restriction endonuclease digestion and hybridization to DNA probes derived from both Mlvi-1 and Mlvi-2. Thus, we determined the clonal nature of three thymomas and showed that in these tumors both insertion events occurred in the same population of tumor cells. The concomitant appearance of provirus insertions in Mlvi-1 and Mlvi-2 suggests a synergism of these two events that may be important in tumor induction and progression.
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PMID:Concerted DNA rearrangements in Moloney murine leukemia virus-induced thymomas: a potential synergistic relationship in oncogenesis. 299 54

Envelope gp70s were isolated from the thymotropic recombinant viruses related to Moloney murine leukemia virus (RM-M-MuLVs) which were generated by the inoculation of two strains of ecotropic M-MuLV (strain 1869 and temperature-sensitive mutant-1) into BALB/c or CFW/D mice. Chymotrypsin oligopeptide maps of parental ecotropic MuLV, RM-M-MuLV, and inducible xenotropic MuLV showed each of the above virus types had a distinctly characteristic peptide map. The majority of RM-M-MuLV gp70 molecules examined showed a high degree of peptide homology. Data from restriction endonuclease mapping demonstrated that the newly acquired sequences in each of the RM-M-MuLVs were very related and encompassed both the polymerase and the envelope genes. The source of the sequences acquired by the RM-M-MuLV was from endogenous nonecotropic and nonxenotropic proviruses. This suggested that the family of endogenous proviruses which combined with the parental ecotropic virus was either specifically selected or was much more available than other endogenous proviruses. Although slight variations of envelope-specific sequences and peptides existed among various RM-M-MuLV isolates; within a single thymoma, individual clones of tumor cells yielded RM-M-MuLV gp70s which were identical to each other. These findings are discussed within the context of the leukemogenic potential of RM-MuLVs.
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PMID:Thymotropic envelope gene recombinants of Moloney leukemia virus have highly conserved envelope structures. 299 79

The DNA sequence of the gag and pol regions of a provirus cloned from a bovine tumor is presented. In order to confirm these results the sequence of portions of a second clone, derived from a virus-producing cell line, was also determined. The gag gene was found to consist of 1179 nucleotides, which probably encode only three proteins: an N-terminal protein of 109 amino acids, a major core protein (p24) of 215 amino acids, and a nucleic acid binding protein (p12) of 69 residues. An open reading frame, whose translated product showed clear homology to the avian and murine proteases, was found beginning immediately upstream of the 3' end of gag. Following this protease region, a third long open reading frame, encoding 852 amino acids, showed clear homology to both avian and murine pol genes. The mechanism of translation of the protease and pol gene products cannot be predicted with certainty. Like Moloney murine leukemia virus (M-MuLV), BLV has a termination signal at the 3' end of gag, but unlike M-MuLV the protease is in a different reading frame. Like Rous sarcoma virus (RSV), BLV has a termination signal at the 3' end of the protease region and the reverse transcriptase is in a different (i.e., the third) reading frame. Possible translation mechanisms are discussed. Finally, the BLV gag and pol gene products are highly related to those of the human T-cell leukemia virus (HTLV); relatedness varied from 37% amino acid identities within the N terminal gag protein to 54% within the nucleic acid binding protein. Highly significant homology with both murine and avian type-C proteins was found within p24, p12, and the putative protease, reverse transcriptase, and endonuclease. Based on this homology, the BLV-HTLV family of viruses appears about equally distantly related to murine and avian type-C viruses.
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PMID:The gag and pol genes of bovine leukemia virus: nucleotide sequence and analysis. 299 90

The induction of thymic lymphomas by Moloney murine leukemia virus in the rat is linked to provirus integration in at least four independent cellular DNA regions (Mlvi-1, Mlvi-2, Mlvi-3, and c-myc). Because sequences homologous to at least three of these regions (Mlvi-1, Mlvi-2, and c-myc) map to chromosome 15 in the mouse, the question was raised whether they are closely linked in the rat genome and whether provirus integration in any one of these regions affects the same functional domain in rat DNA. In this study, we identified the chromosomal map location of Mlvi-1, Mlvi-2, and Mlvi-3 in the rat by using mouse-rat somatic cell hybrids that lose the rat chromosomes. The results showed that Mlvi-1 maps similarly to c-myc to chromosome 7, and Mlvi-2 maps to chromosome 2. Mlvi-3 probably maps to chromosome 15. We conclude that Mlvi-1, Mlvi-2, and Mlvi-3 are separate and independent genetic loci. Although Mlvi-1 and c-myc map to the same chromosome, they are not related, as determined by hybridization and restriction endonuclease mapping. The chromosomal map location of Mlvi-1 to chromosome 7 and Mlvi-2 to chromosome 2 is interesting, since chromosomal aberrations involving these two chromosomes are reproducibly observed in rat neoplasias induced by a variety of agents.
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PMID:Cellular DNA regions involved in the induction of rat thymic lymphomas (Mlvi-1, Mlvi-2, Mlvi-3, and c-myc) represent independent loci as determined by their chromosomal map location in the rat. 299 46


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