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)

Adenovirus 40 (Ad40) is defective for growth in tissue culture but is complemented when the Ad2/5 or Ad12 E1B 55K protein is supplied in trans. Ad40 E1B mRNA has not been detected in E1-transformed cells, or at early times in lytically infected cells. In cells constitutively expressing the E1B region of Ad2, Ad40 E1B mRNAs are detected at late times in infection, after the onset of DNA replication. We have determined the Ad40 E1B transcription map from RNA produced at late times in infected KB16 cells, using S1 nuclease, primer extension, PCR-cDNA analysis, and Northern blotting. E1B transcripts corresponding to Ad2 14 S, 22 S, and 9 S mRNAs were identified but no 13 S mRNA equivalent was detected, a pattern similar to that seen in the Ad12 transcription map. The coding potential for E1B 19K, 55K, and 15K proteins and for ppIX is retained in the Ad40 transcripts. In addition we find novel E1A-E1B cotranscript counterparts of the 14 S and 22 S mRNAs. These contain the first 40 codons of the E1A first exon linked to a site 4-5 nt downstream of the E1B cap site, retaining all the coding potential of the E1B mRNAs. No new open reading frames are created by the junction, and the E1A ORF terminates with one codon added after the junction. Each E1A-E1B cotranscript is present in abundance comparable to that of its authentic E1B counterpart. The E1A-E1B junction is unusual in that it does not conform to splice consensus sequences and thus may not be generated by a conventional splicing mechanism.
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PMID:Enteric adenovirus type 40:E1B transcription map and identification of novel E1A-E1B cotranscripts in lytically infected cells. 182 50

The human immunodeficiency virus (HIV) type 1 long terminal repeat (LTR) is the site of activation of the HIV tat protein. However, additional transactivators, such as the adenovirus E1A and herpesvirus ICPO proteins, have also been shown to be capable of activating the HIV LTR. Analysis of adenovirus mutants indicated that complete transactivation of the HIV LTR was dependent on both the E1A and E1B proteins. To determine which regions of the HIV LTR were important for complete E1A/E1B activation, a variety of oligonucleotide-directed mutations in HIV transcriptional regulatory domains were assayed both in vivo and in vitro. S1 nuclease analysis of RNA prepared after transfection of these HIV constructs into HeLa cells infected with wild-type adenovirus indicated that the enhancer, SP1, TATA, and a portion of the transactivation-responsive element were each required for complete E1A/E1B-mediated activation of the HIV LTR. These same promoter elements were required for both basal and E1A/E1B-induced levels of transcription in in vitro transcription reactions performed with cellular extracts prepared from cells infected with dl434, an E1A/E1B deletion mutant, or wild-type adenovirus. No mutations were found that reduced only E1A/E1B-induced expression without proportionally reducing basal levels of transcription, suggesting that E1A/E1B-mediated induction of the HIV LTR requires multiple promoter elements which are also required for basal transcriptional levels. Unlike activation by the tat protein, there was not a rigid dependence on maintenance of the transactivation-responsive stem base pairing for E1A/E1B-mediated activation either in vivo or in vitro, indicating that activation occurs by a mechanism distinct from that of tat induction.
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PMID:Multiple transcriptional regulatory domains in the human immunodeficiency virus type 1 long terminal repeat are involved in basal and E1A/E1B-induced promoter activity. 252 78

Mouse adenovirus type 1 (MAV-1) genomic DNA from 8.9 to 13.7 map units was sequenced and the early region 1 (E1) transcription map was determined by S1 nuclease, primer extension, and Northern analyses, and cDNA sequencing. The E1 transcription map of MAV-1 had marked dissimilarities from the conserved transcription maps of primate adenovirus E1s. One major E1A and two E1B mRNAs were identified in overlapping transcription units. The single E1A mRNA was composed of three exons; the last exon was coincident with the last exon of the E1B mRNAs. While human adenovirus type 2 (Ad2) utilizes alternate splice donors for the first E1A mRNA exon, MAV-1 does not. Thus, no protein is predicted that would correspond to the Ad2 243 amino acid protein, although MAV-1 can encode a protein similar to the Ad2 289 amino acid protein (A. O. Ball, M. E. Williams, and K. R. Spindler, 1988, J. Virol. 62, 3947-3957). Two spliced E1B mRNAs differed from each other in an intron near the 5' end of the smaller E1B mRNA. This smaller mRNA could encode only the 55K E1B protein, while the larger mRNA could encode both the 21K and 55K E1B proteins.
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PMID:Genome organization of mouse adenovirus type 1 early region 1: a novel transcription map. 254 28

The nonpermissive interaction of hamster cells with human adenovirus type 12 (Ad12) is characterized by a total block of Ad12 DNA replication and late transcription, whereas most of the early functions of Ad12 DNA can be transcribed. Ad2 can replicate in hamster cells. The replication and late transcription defects of Ad12 DNA can be complemented to a certain extent by the E1B functions of Ad2 DNA. This complementation fails, however, to lead to the synthesis of the late Ad12 proteins and to the assembly of infectious virions. It will now be demonstrated that the Ad12 L1 (late genes of group 1) and virus-associated (VA) RNAs are not transcribed in hamster cells. Synthesis of these RNAs in productively infected human cells or Ad2-infected hamster cells is readily detectable by S1 nuclease protection experiments and Northern (RNA) blotting. Similarly, the Ad2-transformed hamster cell line BHK-Ad2E1 fails to complement L1 and VA RNA syntheses after superinfection with Ad12. However, Ad12 infection of the Ad5-transformed hamster cell line BHK297-C131 leads to the transcription of the Ad12 L1 and VA segments. This difference in complementation by the two transformed hamster cell lines might be accounted for by functions in the segment of Ad5 DNA extending between map units 30 and 40 and persisting in the Ad5-transformed hamster cells or by hamster host cell functions which might be operative in cell line BHK297-C131 but not in BHK-Ad2E1 or BHK-21 hamster cells.
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PMID:Defect of adenovirus type 12 replication in hamster cells: absence of transcription of viral virus-associated and L1 RNAs. 274 38

The mRNAs from early region 1 (E1) and pIX of bovine adenovirus type 3 (BAV-3) have been studied by Northern blot, S1 nuclease, and cDNA analysis and transcriptional maps for the regions were constructed. The transcriptional map for the E1 region of BAV-3 is different from those of mouse and human adenoviruses for which transcriptional maps for the regions have been constructed. The E1A region of BAV-3 is located between 0.8 and 10.5 map units and several different transcripts are produced from the region using alternative splice donor sites. The transcripts from the E1A region overlap with those of E1B and pIX. In BAV-3, the E1B region maps between 4.2 and 10.5 map units and encodes two major mRNA species. The mRNAs of E1B region differ from each other in that the smaller mRNA coding for the 157R protein has a large intron removed from a region corresponding to the coding region of E1B 420R protein. As in HAVs, the E1B 420R protein of BAV-3 could be translated only by internal initiation from the larger bicistronic mRNA as there are no transcripts produced exclusively for the production of 420R protein. The transcriptional unit of pIX is transcribed from an independent promoter and encodes a structural component of the adenovirus capsid. To identify and characterize the proteins produced from the region, antibodies were raised in rabbits that recognized specific proteins in Western blot and immunoprecipitation assays.
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PMID:Characterization of early region 1 and pIX of bovine adenovirus-3. 991 88