ArticleMolecular and cellular biochemistry2015
Single-prolonged stress activates the transcription factor ATF6α branch of the unfolded protein response in rat neurons of dorsal raphe nucleus.
Article in Molecular and cellular biochemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Transcriptional changes across tissue and time provide molecular insights into a therapeutic window of opportunity following traumatic stress exposure.Translational psychiatry · 2025Article
- Downregulation of miR156-TargetedFrontiers in plant science · 2022Article
- TLR4/MyD88/NF-κB-Mediated Inflammation Contributes to Cardiac Dysfunction in Rats of PTSD.Cellular and molecular neurobiology · 2020Article
- The nuclear transportation routes of membrane-bound transcription factors.Cell communication and signaling : CCS · 2018Review
- Molecular Mechanisms of IRE1α-ASK1 Pathway Reactions to Unfolded Protein Response in DRN Neurons of Post-Traumatic Stress Disorder Rats.Journal of molecular neuroscience : MN · 2017Article
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In our previous studies, we have found that endoplasmic reticulum (ER) stress is associated with post-traumatic stress disorder (PTSD), however, the activation of ER stress sensors in PTSD remains unclear. ATF6 alpha (ATF6α) is an ER-membrane-bound transcription factor and functions as a critical sensor and regulator of ER stress in mammalian cells. The goal of this study is to detect whether there is activation of the transcription factor ATF6α branch of the unfolded protein response in the dorsal raphe nucleus neurons of the rats exposed to single-prolonged stress (SPS), which is a model employed extensively in PTSD study. Our results have demonstrated that SPS activated the ER transmembrane protein ATF6α via its cleavage; and induced the up-regulation of the downstream targets of ATF6α, the mRNA of XBP1 and GRP94. To the best of our knowledge, this is the first study to investigate the relationship between the ATF6α pathways and PTSD, and our results show that SPS activates the ATF6α branch of the ER stress response, which may be contributed to the pathogenesis of PTSD.
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