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Updated: May 6, 2026

Co-immunoprecipitation Assay Using Endogenous Nuclear Proteins from Cells Cultured Under Hypoxic Conditions
Published on: August 2, 2018
The proto-oncogene JUN is a target of the heat shock transcription factor HSF1
Maki Sawai1, Yukio Ishikawa, Azumi Ota
1Department of Clinical Laboratory Science, Kanazawa University Graduate School of Medical Science, Ishikawa, Japan.
Abstract:
The transcription factor activator protein-1 (AP-1) participates in many aspects of cell physiology, such as cellular proliferation, transformation, and death. AP-1 is a dimeric complex that primarily contains Jun and Fos family members. Here, we report that JUN is a target of heat shock transcription factor HSF1. HSF1 is the master regulator of genes encoding molecular chaperones, and is involved in cellular processes such as the stress response, cell differentiation, aging and carcinogenesis. In HeLa cells, JUN transcription was rapidly induced by heat treatment. We found that HSF1 bound to the JUN promoter and was necessary for its efficient response to heat shock. In heat-shocked cells, c-Jun-mediated gene expression was induced slowly following accumulation of c-Jun protein. Forced expression of active HSF1 in cells resulted in an increase in c-Jun expression and activation of c-Jun target genes. These results show that HSF1 regulates JUN expression, thereby modulating AP-1 activity.
Insights
Heat shock transcription factor HSF1 regulates JUN gene expression, impacting activator protein-1 (AP-1) activity. This study reveals HSF1
Area of Science:
- Molecular Biology
- Cellular Stress Response
Background:
- The transcription factor activator protein-1 (AP-1) regulates key cellular processes.
- AP-1 is a dimeric complex mainly composed of Jun and Fos proteins.
- Heat shock transcription factor 1 (HSF1) controls the expression of molecular chaperones and is involved in stress response, aging, and carcinogenesis.
Purpose of the Study:
- To investigate the regulatory relationship between HSF1 and JUN, a component of AP-1.
- To elucidate the role of HSF1 in modulating AP-1 activity.
Main Methods:
- Analysis of JUN transcription in HeLa cells under heat treatment.
- Chromatin immunoprecipitation to assess HSF1 binding to the JUN promoter.
- Examination of c-Jun expression and activity following HSF1 modulation.
Main Results:
- JUN transcription is rapidly induced by heat shock in HeLa cells.
- HSF1 directly binds to the JUN promoter and is essential for heat-induced JUN expression.
- Forced expression of active HSF1 increases c-Jun levels and activates c-Jun target genes.
Conclusions:
- HSF1 acts as a regulator of JUN gene expression.
- HSF1 influences AP-1 activity by controlling JUN levels, particularly under heat stress conditions.
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