Evidence map›Paper›PMID 9501096›Full record

ArticleThe EMBO journal1998

Disruption of the HSF3 gene results in the severe reduction of heat shock gene expression and loss of thermotolerance.

M Tanabe, Y Kawazoe, S Takeda, R I Morimoto, K Nagata, A Nakai

Open access · bronzeAbstract read
In one paragraph

Article in The EMBO journal, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
3.0field-weighted citation impact, top 8% 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

37 citing papers in PubMed, 118 citations in OpenAlex.

  1. Adaptation to heat stress by diversification of the vertebrate heat shock transcription factor family.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2026
    Review
  2. Article
  3. Review
  4. Article
  5. The Function of Heat Shock Transcription Factors in Sex Differentiation inAnimals : an open access journal from MDPI · 2025
    Article
  6. Article
  7. Review
  8. Role of Heat Shock Factors in Stress-Induced Transcription: An Update.Methods in molecular biology (Clifton, N.J.) · 2023
    Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Tailoring of Proteostasis Networks with Heat Shock Factors.Cold Spring Harbor perspectives in biology · 2019
    Review
  14. Sexual Dimorphism and Aging Differentially Regulate Adaptive Homeostasis.The journals of gerontology. Series A, Biological sciences and medical sciences · 2018
    Article
  15. Role of Heat Shock Factors in Stress-Induced Transcription.Methods in molecular biology (Clifton, N.J.) · 2018
    Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. 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

6 authors at 1 institution in 1 country.

M TanabeDepartment of Cell Biology, Chest Disease Research Institute, Faculty of Medicine, Kyoto University, Sakyo-ku, Kyoto 606-01, Japan.
Y Kawazoe
S Takeda
R I Morimoto
K Nagata
A Nakai
Kyoto University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The vertebrate genome encodes a family of heat shock factors (HSFs 1-4) of which the DNA-binding and transcriptional activities of HSF1 and HSF3 are activated upon heat shock. HSF1 has the properties of a classical HSF and exhibits rapid activation of DNA-binding and transcriptional activity upon exposure to conditions of heat shock and other stresses, whereas HSF3 typically is activated at higher temperatures and with distinct delayed kinetics. To address the role of HSF3 in the heat shock response, null cells lacking the HSF3 gene were constructed by disruption of the resident gene by somatic recombination in an avian lymphoid cell line. Null cells lacking HSF3, yet expressing normal levels of HSF1, exhibited a severe reduction in the heat shock response, as measured by inducible expression of heat shock genes, and did not exhibit thermotolerance. At intermediate heat shock temperatures, where HSF1 oligomerizes to an active trimer in wild-type cells, HSF1 remained as an inert monomer in the HSF3 null cell line. HSF3 null cells were restored to a nearly normal heat shock-responsive state by reintroduction of an exogenous HSF3 gene. These results reveal that HSF3 has a dominant role in the regulation of the heat shock response and directly influences HSF1 activity.

Indexed as

Avian ProteinsAnimalsB-LymphocytesCell LineChickensDNA-Binding ProteinsGene Expression RegulationGene TargetingHeat-Shock ProteinsHeat-Shock ResponseHeat Shock Transcription FactorsHot TemperatureMaleProtein ConformationRNA, MessengerSequence DeletionAvian ProteinsDNA-Binding ProteinsHeat-Shock ProteinsHeat Shock Transcription FactorsHSF3 protein, Gallus gallusRNA, MessengerTrans-ActivatorsTranscription Factors

Identifiers

PMID9501096
PMCPMC1170522
OpenAlexW1973510010

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.