Evidence map›Paper›PMID 2474756›Full record

ArticleMolecular and cellular biology1989

E1a transactivation of the human HSP70 promoter is mediated through the basal transcriptional complex.

G T Williams, T K McClanahan, R I Morimoto

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 1989. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed
6.6field-weighted citation impact, top 2% of its field
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

52 citing papers in PubMed, 144 citations in OpenAlex.

  1. Article
  2. Down-regulation of heat shock protein HSP90ab1 in radiation-damaged lung cells other than mast cells.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2014
    Article
  3. Article
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  5. Induction of heat shock proteins by hyperthermia and noise overstimulation in hsf1 -/- mice.Journal of the Association for Research in Otolaryngology : JARO · 2012
    Article
  6. Article
  7. The induction levels of heat shock protein 70 differentiate the vulnerabilities to mutant huntingtin among neuronal subtypes.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2007
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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 at 1 institution in 1 country.

G T WilliamsDepartment of Biochemistry, Molecular Biology, and Cellular Biology, Northwestern University, Evanston, Illinois 60208.
T K McClanahan
R I Morimoto
Northwestern University · US

Funding

CARCINOGENESIS TRAINING PROGRAMT32CA009560 · NCI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI Kathleen Janee Green · 1986 to 2026
$8.4M
CHARACTERIZATION OF THE HUMAN HSP70 GENE FAMILYF32GM011877 · NIGMS · NORTHWESTERN UNIVERSITY · PI MCCLANAHAN, TERRILL K · 1987 to 1988
–
NCI NIH HHS CA 09560NIGMS NIH HHS GM 11877
6 · The paper itself

Abstract

We have examined the promoter sequence requirements for E1a transactivation of the human HSP70 gene by using a transient cotransfection assay. A 5' deletion study has defined a basal transcription unit extending to -74 relative to the transcription initiation site which was fully E1a responsive. Further deletion, abolishing a CCAAT element at -67, drastically reduced basal and E1a-induced expression. A linker-scanner analysis has identified four functional elements within the basal transcription unit which may interact with CTF, SP1, TFIID, and an ATF/AP1-like factor. Sequences between -100 and -188 can partially compensate for mutations in these elements. No mutation specifically abolished E1a inducibility. Any reduction in absolute E1a-induced levels was accompanied by a corresponding reduction in absolute basal levels, thereby maintaining a constant relative fold induction. We conclude that E1a transactivation of the human HSP70 promoter does not require any single basal transcription element. We also examined an HSP70 promoter fragment, containing the CCAAT element at -67 and the purine-rich element at -54, out of its normal context by fusing it upstream of a transcriptionally inactive herpes simplex virus thymidine kinase deletion construct containing only the TATA box. The resulting chimeric promoter was fully E1a responsive. Mutagenesis of this promoter fusion demonstrated that the CCAAT element was essential for detectable basal and E1a-induced expression. Mutations in the purine-rich element resulted in an approximately 10-fold elevation in basal levels and rendered the promoter nonresponsive to E1a.

Indexed as

Gene Expression RegulationPromoter Regions, GeneticAdenovirus Early ProteinsBase SequenceCells, CulturedChimeraChromosome DeletionCloning, MolecularDNAGenetic VectorsHeat-Shock ProteinsHumansMolecular Sequence DataOncogene Proteins, ViralRNATranscription FactorsAdenovirus Early ProteinsDNAHeat-Shock ProteinsOncogene Proteins, ViralRNATranscription Factors

Identifiers

PMID2474756
PMCPMC362330
OpenAlexW2126613339

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.