Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.1.30.1 (S1 nuclease)
 3,660 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

T-cell lymphomas induced by Moloney murine leukemia virus frequently have proviruses integrated at the Mlvi-4 and Mlvi-1 loci, which map approximately 30 and 270 kilobases 3' of the promoter region of the Myc protooncogene, respectively. Provirus insertion in these loci is responsible for the activation of adjacent genes. To determine whether Myc expression was also affected by these provirus insertions, we constructed T-cell hybrids between two rat thymic lymphomas containing a provirus in Mlvi-4 or Mlvi-1 and the murine T-cell lymphoma line BW5147. These hybrids segregated the provirus-containing rearranged alleles from the normal nonrearranged alleles of Mlvi-4 and Mlvi-1, and they carried an intact copy of rat Myc. Using an S1 nuclease protection assay, we observed that the expression of the rat Myc cosegregated with the rearranged Mlvi-4 or Mlvi-1 locus. However, provirus insertion in these loci had no effect on promoter utilization or on the expression of the murine Myc locus. We conclude that provirus insertion exerts a long-range cis effect on the expression of Myc. Therefore, provirus integration in a single locus may affect the expression of multiple genes, some of which may be located a long distance from the site of integration.
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PMID:Long-distance activation of the Myc protooncogene by provirus insertion in Mlvi-1 or Mlvi-4 in rat T-cell lymphomas. 168 53

Specific chromosomal aberrations are associated with specific types of cancer (for review see ref. 1). The distinctiveness of each association has led to the belief that these chromosomal aberrations are clues to oncogenic events or to the state of differentiation in the malignant cell type. Malignancies of T lymphocytes demonstrate such an association characterized most frequently by structural translocations or inversions of chromosomes 7 and 14 (refs 7-9). Analyses of these chromosomally marked tumours at the molecular level may therefore provide insight into the aetiology of the cancers as well as the mechanisms by which chromosomes break and rejoin. Here we report such an analysis of the tumour cell line SUP-T1 derived from a patient with childhood T-cell lymphoma carrying an inversion of one chromosome 14 between bands q11.2 and q32.3, that is, inv(14) (q11.2; q32.2). These are the same chromosomal bands to which the T-cell receptor alpha-chain (14q11.2) and the immunoglobulin heavy-chain locus (14q32.3) have been assigned. Our analysis reveals that this morphological inversion of chromosome 14 was mediated by a site-specific recombination event between an immunoglobulin heavy-chain variable region (Ig VH) and a T-cell receptor (TCR) alpha-chain joining segment (TCR J alpha). S1 nuclease analysis shows that this hybrid gene is transcribed into poly(A)+ RNA.
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PMID:A chromosome 14 inversion in a T-cell lymphoma is caused by site-specific recombination between immunoglobulin and T-cell receptor loci. 300 4

A region of the Herpesvirus saimiri genome that is not essential for replication of the virus has recently been shown to be required for its oncogenicity in New World primates. We have examined the RNAs derived from this region of the genome in permissively infected cells. Two polyadenylated RNAs, of 4.9 and 2.3 kilobases, were the major species coded for by this region of the genome. These two RNAs, as well as a much less abundant RNA of 6.5 kilobases, were specifically altered in two different nononcogenic deletion mutants of H. saimiri. The 4.9- and 2.3-kilobase RNAs were mapped by S1 nuclease and exonuclease VII digestion of DNA-RNA hybrids. The transcripts were found to be spliced, overlapping, and transcribed from right to left on the genetic map, with their 3' termini each ca. 150 base pairs from the left border between the unique and repetitive DNA regions. These RNAs were not detected at immediate early times after infection. The possible role of these RNAs in the origin of the malignant T-cell lymphoma caused by this virus is discussed.
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PMID:Mapping of RNA transcribed from a region of the Herpesvirus saimiri genome required for oncogenicity. 609 74