Evidence map›Paper›PMID 8537118›Full record

ArticleImmunogenetics1996

The function of the octamer-binding site in the DRA promoter.

C F Voliva, N Jabrane-Ferrat, B M Peterlin

Abstract readComparative Study
PubMed Publisher
In one paragraph

Article in Immunogenetics, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

2 citing papers in PubMed.

  1. Article
  2. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors.

C F VolivaSearle Research and Development, Monsanto Company, St. Louis, MO 63198, USA.
N Jabrane-Ferrat
B M Peterlin

Funding

REGULATION OF HUMAN IMMUNODEFICIENCY VIRUS GENER01AI025109 · NIAID · UNIVERSITY OF CALIFORNIA DAVIS · PI LUCIW, PAUL A · 1987 to 1989
–
NIAID NIH HHS R01-AI25109
6 · The paper itself

Abstract

The octamer binding site, which is located immediately upstream of the poorly conserved DRA TATA sequence, is important for high levels of expression of this human major histocompatibility class II gene in B cells. In this study, we demonstrate that the substitution of the DRA TATA sequence with the TATA box from the adenovirus E1b promoter removes the requirement for the octamer binding site for high levels of expression from the DRA promoter. Since only the TATA box from the E1b but not the DRA promoters binds the TATA binding protein, we conclude that the octamer binding site helps to recruit TBP to the DRA promoter.

Indexed as

Promoter Regions, GeneticAdenovirus E1B ProteinsBase SequenceBinding SitesBurkitt LymphomaDNA-Binding ProteinsDNA, RecombinantHeLa CellsHLA-DR alpha-ChainsHLA-DR AntigensHumansMolecular Sequence DataOctamer Transcription Factor-2Regulatory Sequences, Nucleic AcidTATA BoxTATA-Box Binding ProteinAdenovirus E1B ProteinsDNA-Binding ProteinsDNA, RecombinantHLA-DR alpha-ChainsHLA-DR AntigensOctamer Transcription Factor-2POU2F2 protein, humanTATA-Box Binding ProteinTranscription FactorsTranscription Factor TFIID

Identifiers

PMID8537118

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.