ArticleJournal of virology1995
Repression in vitro, by human adenovirus E1A protein domains, of basal or Tat-activated transcription of the human immunodeficiency virus type 1 long terminal repeat.
Article in Journal of virology, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
15 citing papers in PubMed, 19 citations in OpenAlex.
- Article
- Article
- The adenovirus E1A N-terminal repression domain represses transcription from a chromatin template in vitro.Virology · 2012Article
- Article
- The transcription-repression domain of the adenovirus E1A oncoprotein targets p300 at the promoter.Oncogene · 2008Article
- Adenovirus E1A proteins are closely associated with chromatin in productively infected and transformed cells.Virology · 2008Article
- Interaction of Adenovirus E1A with the HHV8 Promoter of Latent Genes: E1A Proteins are Able to Activate the HHV-8 LANAp in MV3 Reporter Cells.The open virology journal · 2008Article
- Adenovirus E1A N-terminal amino acid sequence requirements for repression of transcription in vitro and in vivo correlate with those required for E1A interference with TBP-TATA complex formation.Journal of virology · 2002Article
- Transcriptional cofactor CA150 regulates RNA polymerase II elongation in a TATA-box-dependent manner.Molecular and cellular biology · 1999Article
- HIV transcriptional activation by the accessory protein, VPR, is mediated by the p300 co-activator.Proceedings of the National Academy of Sciences of the United States of America · 1998Article
- The adenovirus E1A repression domain disrupts the interaction between the TATA binding protein and the TATA box in a manner reversible by TFIIB.Molecular and cellular biology · 1997Article
- Distinct domains of adenovirus E1A interact with specific cellular factors to differentially modulate human immunodeficiency virus transcription.Journal of virology · 1997Article
- Role of p300-family proteins in E1A oncogene induction of cytolytic susceptibility and tumor cell rejection.Proceedings of the National Academy of Sciences of the United States of America · 1996Article
- Transcription factor TFIID is a direct functional target of the adenovirus E1A transcription-repression domain.Proceedings of the National Academy of Sciences of the United States of America · 1995Article
- Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Human adenovirus E1A proteins can repress the expression of several viral and cellular genes. By using a cell-free transcription system, we demonstrated that the gene product of the E1A 12S mRNA, the 243-residue protein E1A243R, inhibits basal transcription from the human immunodeficiency virus type 1 (HIV-1) long terminal repeat (LTR). The HIV-1 transactivator protein Tat greatly stimulates transcription from the viral promoter in vitro. However, E1A243R can repress Tat-activated transcription in vitro. Strong repression of both basal and Tat-activated transcriptions requires only E1A N-terminal amino acid residues 1 to 80. Deletion analysis showed that E1A N-terminal amino acids 4 to 25 are essential for repression, whereas amino acid residues 30 to 49 and 70 to 80 are dispensable. Transcriptional repression by E1A in the cell-free transcription system is promoter specific, since under identical conditions, transcription of the adenovirus major late promoter and the Rous sarcoma virus LTR promoter was unaffected. The repression of transcription by small E1A peptides in vitro provides an assay for investigation of molecular mechanisms governing E1A-mediated repression of both basal and Tat-activated transcriptions of the HIV-1 LTR promoter.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.