ArticleMolecular endocrinology (Baltimore, Md.)2016
miR-204 Targets PERK and Regulates UPR Signaling and β-Cell Apoptosis.
Article in Molecular endocrinology (Baltimore, Md.), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
34 citing papers in PubMed, 56 citations in OpenAlex.
- MiR-204-5p mediates PERK inhibition to suppress growth and induce apoptosis in ovarian cancer through the eIF2α/ATF-4/CHOP pathway.Scientific reports · 2025Article
- Article
- Importance of unfolded protein response modulation on diabetes management: a systematic review.Journal of diabetes and metabolic disorders · 2024Review
- Decoding contextual crosstalk: revealing distinct interactions between non-coding RNAs and unfolded protein response in breast cancer.Cancer cell international · 2024Review
- miRNAs in the Beta Cell-Friends or Foes?Endocrinology · 2023Review
- Role of ceramides in diabetic foot ulcers (Review).International journal of molecular medicine · 2023Review
- The Association between the Differential Expression of lncRNA and Type 2 Diabetes Mellitus in People with Hypertriglyceridemia.International journal of molecular sciences · 2023Article
- ER stress: an emerging regulator in GVHD development.Frontiers in immunology · 2023Review
- Crocin attenuates endoplasmic reticulum stress in methylglyoxal-induced diabetic nephropathy in male mice: MicroRNAs alterations and glyoxalase 1-Nrf2 signaling pathways.Iranian journal of basic medical sciences · 2022Article
- Epigenetics and endoplasmic reticulum in podocytopathy during diabetic nephropathy progression.Frontiers in immunology · 2022Review
- Living Dangerously: Protective and Harmful ER Stress Responses in Pancreatic β-Cells.Diabetes · 2021Review
- Article
- Machine learning workflows identify a microRNA signature of insulin transcription in human tissues.iScience · 2021Article
- The role of microRNAs in cell death pathways.Yeungnam University journal of medicine · 2021Article
- Human Glucagon Expression Is under the Control of miR-320a.Endocrinology · 2021Article
- Molecular Mechanisms of Nutrient-Mediated Regulation of MicroRNAs in Pancreatic β-cells.Frontiers in endocrinology · 2021Review
- PERK Signaling Controls Myoblast Differentiation by Regulating MicroRNA Networks.Frontiers in cell and developmental biology · 2021Article
- Article
- The ER Stress/UPR Axis in Chronic Obstructive Pulmonary Disease and Idiopathic Pulmonary Fibrosis.Life (Basel, Switzerland) · 2020Review
- Genetic deletion of miR-204 improves glycemic control despite obesity in db/db mice.Biochemical and biophysical research communications · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Endoplasmic reticulum (ER) stress plays an important role in the pathogenesis of diabetes and the associated β-cell apoptosis. Although microRNAs (miRNAs) have been widely studied in various diseases including diabetes, the role of miRNAs in ER stress and β-cell apoptosis has only started to be elucidated. We recently showed that diabetes increases β-cell miR-204 and have now discovered that miR-204 directly targets the 3'untranslated region of protein kinase R-like ER kinase (PERK), 1 of the 3 ER transmembrane sensors and a key factor of the unfolded protein response (UPR). In addition, by using primary human islets, mouse islets, and INS-1 β-cells, we found that miR-204 decreased PERK expression as well as its downstream factors, activating transcription factor 4 and CCAAT enhancer-binding protein homologous protein, whereas it had no effect on the other 2 ER transmembrane sensors, activating transcription factor 6 and inositol-requiring enzyme-1α. Interestingly, we discovered that miR-204 also inhibited PERK signaling in the context of ER stress, and this exacerbated ER stress-induced β-cell apoptosis. This effect could be mimicked by PERK inhibitors supporting the notion that the miR-204-mediated inhibition of PERK and UPR signaling was conferring these detrimental effects on cell survival. Taken together, we have identified PERK as a novel target of miR-204 and show that miR-204 inhibits PERK signaling and increases ER stress-induced cell death, revealing for the first time a link between this miRNA and UPR.
Indexed as
Identifiers
What OpenQuestion holds
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.