ArticleEMBO molecular medicine2014
Heat shock factor 2 is a stress-responsive mediator of neuronal migration defects in models of fetal alcohol syndrome.
Article in EMBO molecular medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
What it found
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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
30 citing papers in PubMed, 49 citations in OpenAlex.
- More than the 'master regulator of cytosolic proteostasis': new roles for HSF1 in promoting tissue health.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2026Review
- Transcriptomic profiling of subpopulations of mouse embryonic subplate neurons.Journal of anatomy · 2026Article
- Heat shock transcription factors in development and disease.Disease models & mechanisms · 2026Review
- Impact of Prenatal Alcohol Exposure on Cerebral Cortex Development.Advances in experimental medicine and biology · 2026Review
- A guide to heat shock factors as multifunctional transcriptional regulators.The FEBS journal · 2025Review
- The function and regulation of heat shock transcription factor inFrontiers in cellular and infection microbiology · 2023Review
- HSF1 and Its Role in Huntington's Disease Pathology.Advances in experimental medicine and biology · 2023Review
- Epigenetic priming of immune/inflammatory pathways activation and abnormal activity of cell cycle pathway in a perinatal model of white matter injury.Cell death & disease · 2022Article
- CBP-HSF2 structural and functional interplay in Rubinstein-Taybi neurodevelopmental disorder.Nature communications · 2022Article
- Heat Shock Transcription Factor 2 Is Significantly Involved in Neurodegenerative Diseases, Inflammatory Bowel Disease, Cancer, Male Infertility, and Fetal Alcohol Spectrum Disorder: The Novel Mechanisms of Several Severe Diseases.International journal of molecular sciences · 2022Review
- HSF2 cooperates with HSF1 to drive a transcriptional program critical for the malignant state.Science advances · 2022Article
- Gambogic acid and gambogenic acid induce a thiol-dependent heat shock response and disrupt the interaction between HSP90 and HSF1 or HSF2.Cell stress & chaperones · 2021Article
- The proteostasis guardian HSF1 directs the transcription of its paralog and interactor HSF2 during proteasome dysfunction.Cellular and molecular life sciences : CMLS · 2021Article
- Review
- Kcnn2 blockade reverses learning deficits in a mouse model of fetal alcohol spectrum disorders.Nature neuroscience · 2020Article
- Cellular stress mechanisms of prenatal maternal stress: Heat shock factors and oxidative stress.Neuroscience letters · 2019Review
- Tailoring of Proteostasis Networks with Heat Shock Factors.Cold Spring Harbor perspectives in biology · 2019Review
- Regulation of heat shock transcription factors and their roles in physiology and disease.Nature reviews. Molecular cell biology · 2018Review
- Alcohol exposure promotes DNA methyltransferase DNMT3A upregulation through reactive oxygen species-dependent mechanisms.Cell stress & chaperones · 2018Article
- Variations in brain defects result from cellular mosaicism in the activation of heat shock signalling.Nature communications · 2017Article
Corrections and comments
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Authors and funding
14 authors at 9 institutions in 3 countries.
Funding
Abstract
Fetal alcohol spectrum disorder (FASD) is a frequent cause of mental retardation. However, the molecular mechanisms underlying brain development defects induced by maternal alcohol consumption during pregnancy are unclear. We used normal and Hsf2-deficient mice and cell systems to uncover a pivotal role for heat shock factor 2 (HSF2) in radial neuronal migration defects in the cortex, a hallmark of fetal alcohol exposure. Upon fetal alcohol exposure, HSF2 is essential for the triggering of HSF1 activation, which is accompanied by distinctive post-translational modifications, and HSF2 steers the formation of atypical alcohol-specific HSF1-HSF2 heterocomplexes. This perturbs the in vivo binding of HSF2 to heat shock elements (HSEs) in genes that control neuronal migration in normal conditions, such as p35 or the MAPs (microtubule-associated proteins, such as Dclk1 and Dcx), and alters their expression. In the absence of HSF2, migration defects as well as alterations in gene expression are reduced. Thus, HSF2, as a sensor for alcohol stress in the fetal brain, acts as a mediator of the neuronal migration defects associated with FASD.
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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.