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

Previously we have demonstrated the existence of stable transcripts from the noncoding strand of a rearranged c-myc gene in murine plasmacytomas in which the oncogene has translocated to an immunoglobulin constant-region gene element (M. Dean, R. B. Kent, and G. E. Sonenshein, Nature [London] 305:443-446, 1983). The resulting RNAs are chimeric, containing c-myc antisense and immunoglobulin sense sequences. A normal unrearranged murine c-myc gene is transcribed in the antisense orientation throughout much of the gene; however, stable transcripts have not been detected. In this study, using Northern (RNA) blot, S1 nuclease, and primer extension analyses, we have mapped the 5' end of the stable chimeric transcripts to a site 175 bp from the start of exon 3, within intron 2 of the c-myc gene. In vitro transcription assays with constructs containing this site and 400 bp upstream, in the antisense orientation, and nuclear extracts from plasmacytoma cells, as well as a number of cell lines with normal unrearranged c-myc genes, indicated that this promoter was functional. This finding was confirmed in transient transfection assays using the antisense promoter linked to the chloramphenicol acetyltransferase reporter gene. These results suggest that a normal promoter of antisense transcription is used following c-myc gene translocation.
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PMID:An antisense promoter of the murine c-myc gene is localized within intron 2. 154 13

The 5'-terminal sequence of the kappa light-chain gene expressed in MPC11 plasmacytoma cells was definitively determined by analysis of both the kappa mRNA and the gene from which it is transcribed. The distance between the cap site and the translation initiation codon is only 3 nucleotides, and in a minor variant only 2 nucleotides, considerably less than that found in other species of nucleus-derived mRNA. S1 nuclease protection experiments with MPC11 nuclear RNA indicate that the cap sites are coincident with the transcriptional start sites, suggesting that the 5'-terminal heterogeneity is caused by imprecision in transcriptional initiation. A comparison of the 5'-terminal structure of the MPC11 V kappa gene with that of several other V genes indicates that the length of the first exon, which is composed of the 5' untranslated region which is composed of the 5' untranslated region and a sequence encoding most of the signal peptide, is highly conserved. Within this set of examples, the 5' untranslated region varies from 3 to 33 nucleotides, and the signal-peptide-coding block from 46 to 76 nucleotides. This analysis has also provided insight into the genetic origins for two anomalous properties of the MPC11 light chain.
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PMID:Functional significance and evolutionary development of the 5'-terminal regions of immunoglobulin variable-region genes. 628 67

We have investigated whether the translocated and the untranslocated human c-myc oncogenes of Burkitt lymphoma cells are equally or differentially expressed in host mouse B cells. The human c-myc mRNA levels in somatic cell hybrids between mouse plasmacytoma cells and Burkitt lymphoma cells with either the t(8;14) or the t(2;8) chromosome translocation were determined by using the nuclease S1 protection procedure. Although both the human parental lines and the hybrid cells carrying the translocated c-muc oncogene expressed high levels of human specific c-myc transcripts, the hybrid cells carrying the untranslocated c-myc gene on normal chromosome 8 did not contain human specific c-myc mRNA. These results suggest that the translocated human c-myc oncogene has escaped the normal transcriptional control to which the untranslocated c-myc gene remains subjected. This interpretation is also supported by the finding that the expression of the c-myc genes of lymphoblastoid cells and of HL-60 promyelocytic leukemia cells are repressed when they are transferred into a mouse plasmacytoma background. The ability of the translocated c-myc oncogene to escape the normal transcriptional control occurring in B cells may be important for the expression of B cell neoplasia in mouse and man. We have also transferred the Burkitt 14q+ chromosome carrying a translocated c-myc oncogene into mouse LM-TK- fibroblasts and studied the levels of human c-myc transcripts in the hybrids. Because the levels of human c-myc transcripts in the fibroblast hybrids are dramatically decreased in comparison to the plasmacytoma hybrids, we conclude that the levels of transcripts of the translocated c-myc oncogene depend on the differentiated state of the cells harboring the translocated chromosome.
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PMID:Differential expression of the normal and of the translocated human c-myc oncogenes in B cells. 630 54