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Updated: Jul 16, 2026

Measuring Endoplasmic Reticulum Stress and Unfolded Protein Response in HIV-1 Infected T-Cells and Analyzing its Role in HIV-1 Replication
Published on: June 14, 2024
Transcriptional activation of ATF6 by endoplasmic reticulum stressors
Takushi Namba1, Tomoaki Ishihara, Ken-ichiro Tanaka
1Graduate School of Medical and Pharmaceutical Sciences, Kumamoto University, Kumamoto 862-0973, Japan.
Abstract:
Previous studies have shown that modification of activating transcription factor 6 (ATF6) protein is important for the endoplasmic reticulum (ER) stress response; ER stressors stimulate the degradation of ATF6 by Site-1 protease (S1P) and Site-2 protease (S2P) into p50-ATF6, which acts as a transcription factor. In the current study, we found that all of the ER stressors tested (such as thapsigargin) up-regulate ATF6 mRNA expression. As thapsigargin did not affect the stability of the ATF6 mRNA, it was concluded that this up-regulation is due to transcriptional activation of ATF6. An inhibitor of S1P suppressed this up-regulation of ATF6 mRNA expression and putative ATF6-binding elements in the promoter of ATF6 were identified, suggesting that p50-ATF6 positively regulates the gene expression of ATF6. Since cells over-expressing ATF6 showed an enhanced ER stress response, we propose that up-regulation of ATF6 mRNA expression is involved in enhancing the ER stress response.
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