Evidence map›Paper›PMID 12391166›Full record

ArticleMolecular and cellular biology2002

Heat shock transcription factor 2 is not essential for embryonic development, fertility, or adult cognitive and psychomotor function in mice.

D Randy McMillan, Elisabeth Christians, Michael Forster, XianZhong Xiao, Patrice Connell, Jean-Christophe Plumier, XiaoXia Zuo, James Richardson, Sylvia Morgan, Ivor J Benjamin

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

34 citing papers in PubMed, 76 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. Review
  3. Article
  4. Review
  5. Tailoring of Proteostasis Networks with Heat Shock Factors.Cold Spring Harbor perspectives in biology · 2019
    Review
  6. Article
  7. Review
  8. Targeted Deletion of Hsf1, 2, and 4 Genes in Mice.Methods in molecular biology (Clifton, N.J.) · 2018
    Article
  9. Article
  10. Article
  11. Article
  12. HSF1: Guardian of Proteostasis in Cancer.Trends in cell biology · 2016
    Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  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

10 authors at 4 institutions in 1 country.

D Randy McMillanDepartments of Internal Medicine. Pediatrics. Pathology. Division of Cell and Molecular Biology, The University of Texas Southwestern Medical Center at Dallas, Dallas, Texas 75235, USA.
Elisabeth Christians
Michael Forster
XianZhong Xiao
Patrice Connell
Jean-Christophe Plumier
XiaoXia Zuo
James Richardson
Sylvia Morgan
Ivor J Benjamin
Harvard University · USPediatrics and Genetics · USThe University of Texas Southwestern Medical Center · USUniversity of North Texas · US

Funding

MECHANISMS FOR CARDIOPROTECTION IN HSF1 KNOCKOUT MICER01HL060667 · NHLBI · UNIVERSITY OF TEXAS SW MED CTR/DALLAS · PI BENJAMIN, IVOR J · 1998 to 2001
$670k
NHLBI NIH HHS R01-HL60667-03PHS HHS K14
6 · The paper itself

Abstract

Members of the heat shock factor (HSF) family are evolutionarily conserved regulators that share a highly homologous DNA-binding domain. In mammals, HSF1 is the main factor controlling the stress-inducible expression of Hsp genes while the functions of HSF2 and HSF4 are less clear. Based on its developmental profile of expression, it was hypothesized that HSF2 may play an essential role in brain and heart development, spermatogenesis, and erythroid differentiation. To directly assess this hypothesis and better understand the underlying mechanisms that require HSF2, we generated Hsf2 knockout mice. Here, we report that Hsf2(-/-) mice are viable and fertile and exhibit normal life span and behavioral functions. We conclude that HSF2, most probably because its physiological roles are integrated into a redundant network of gene regulation and function, is dispensable for normal development, fertility, and postnatal psychomotor function.

Indexed as

CognitionEmbryonic and Fetal DevelopmentFertilityPsychomotor PerformanceAcetylcysteineAnimalsBehavior, AnimalBrainCysteine Proteinase InhibitorsFibroblastsGene Expression Regulation, DevelopmentalHeat-Shock ProteinsMaleMiceMice, Inbred StrainsMice, KnockoutAcetylcysteineCysteine Proteinase InhibitorsHeat-Shock ProteinsHSF2 protein, humanlactacystinTranscription Factors

Identifiers

PMID12391166
PMCPMC134743
OpenAlexW2147187641

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.