ArticleScientific reports2015
PERK regulated miR-424(322)-503 cluster fine-tunes activation of IRE1 and ATF6 during Unfolded Protein Response.
Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 43 citations in OpenAlex.
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- NOXA exacerbates endoplasmic-reticulum-stress-induced intervertebral disc degeneration by activating apoptosis and ECM degradation.Cell death discovery · 2025Article
- The significance of calcium ions in cerebral ischemia-reperfusion injury: mechanisms and intervention strategies.Frontiers in molecular biosciences · 2025Review
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- Decoding contextual crosstalk: revealing distinct interactions between non-coding RNAs and unfolded protein response in breast cancer.Cancer cell international · 2024Review
- MicroRNA-322 overexpression reduces neural tube defects in diabetic pregnancies.American journal of obstetrics and gynecology · 2024Article
- UPR-Induced miR-616 Inhibits Human Breast Cancer Cell Growth and Migration by Targeting c-MYC.International journal of molecular sciences · 2023Article
- TGFβ1 regulates HRas-mediated activation of IRE1α through the PERK-RPAP2 axis in keratinocytes.Molecular carcinogenesis · 2022Article
- Preventing unfolded protein response-induced ion channel dysregulation to treat arrhythmias.Trends in molecular medicine · 2022Review
- Sex-Dependent Changes of miRNA Levels in the Hippocampus of Adrenalectomized Rats Following Acute Corticosterone Administration.ACS chemical neuroscience · 2021Article
- The Roles of the Ubiquitin-Proteasome System in the Endoplasmic Reticulum Stress Pathway.International journal of molecular sciences · 2021Review
- Downregulation of miR-17-92 Cluster by PERK Fine-Tunes Unfolded Protein Response Mediated Apoptosis.Life (Basel, Switzerland) · 2021Article
- Network-based analysis implies critical roles of microRNAs in the long-term cellular responses to gold nanoparticles.Nanoscale · 2020Article
- Article
- Review
- PERK-mediated induction of microRNA-483 disrupts cellular ATP homeostasis during the unfolded protein response.The Journal of biological chemistry · 2020Article
- The E3 Ubiquitin Ligase SIAH1 Targets MyD88 for Proteasomal Degradation During Dengue Virus Infection.Frontiers in microbiology · 2020Article
- Expression of activating transcription factor 5 (ATF5) is mediated by microRNA-520b-3p under diverse cellular stress in cancer cells.PloS one · 2020Article
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
The endoplasmic reticulum (ER) responds to changes in intracellular homeostasis through activation of the unfolded protein response (UPR). UPR can facilitate the restoration of cellular homeostasis, via the concerted activation of three ER stress sensors, namely IRE1, PERK and ATF6. Global approaches in several cellular contexts have revealed that UPR regulates the expression of many miRNAs that play an important role in the regulation of life and death decisions during UPR. Here we show that expression of miR-424(322)-503 cluster is downregulated during UPR. IRE1 inhibitor (4 μ8C) and deficiency of XBP1 had no effect on downregulation of miR-424(322)-503 during UPR. Treatment of cells with CCT030312, a selective activator of EIF2AK3/PERK signalling, leads to the downregulation of miR-424(322)-503 expression. The repression of miR-424(322)-503 cluster during conditions of ER stress is compromised in PERK-deficient MEFs. miR-424 regulates the expression of ATF6 via a miR-424 binding site in its 3' UTR and attenuates the ATF6 transcriptional activity during UPR. Further miR-424 had no effect on IRE1-XBP1 axis but enhanced the regulated IRE1-dependent decay (RIDD). Our results suggest that miR-424 constitutes an obligatory fine-tuning mechanism where PERK-mediated downregulation of miR-424(322)-503 cluster regulates optimal activation of IRE1 and ATF6 during conditions of ER stress.
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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.