ArticleCellular and molecular life sciences : CMLS2020
EI24 tethers endoplasmic reticulum and mitochondria to regulate autophagy flux.
Article in Cellular and molecular life sciences : CMLS, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 40 citations in OpenAlex.
- Mitochondria‑endoplasmic reticulum contact site nexus: Molecular integration, disease pathogenesis and therapeutic opportunities (Review).International journal of molecular medicine · 2026Review
- Crosstalk collapse: mitochondria-centric organelle network disruption in ovarian aging.Cell communication and signaling : CCS · 2026Review
- Biological significance, molecular mechanisms and clinical potential of EI24 in cancer.Chinese medical journal · 2026Review
- Microbiota-induced EI24 improves homeostasis but impedes function of alveolar macrophages via metabolic regulation.Nature communications · 2026Article
- Mitochondria-associated membranes in heart failure: from molecular mechanisms to therapeutic targets.Frontiers in physiology · 2026Review
- Hesperidin alleviates pulmonary fibrosis by regulating EI24-mediated autophagy.Future science OA · 2025Article
- Ei24 deficiency in brown adipocytes induces severe hypothermia under cold stress independent of UCP1 activity.Nature communications · 2025Article
- Review
- NSP6 regulates calcium overload-induced autophagic cell death and is regulated by KLHL22-mediated ubiquitination.Journal of advanced research · 2025Article
- Review
- Biophysical characterization of anion channels in mitochondrion-endoplasmic-reticulum contact sites.Biophysical journal · 2025Article
- p53-Mediated Mitochondrial Translocation of EI24 Triggered by ER Stress Plays an Important Role in Arsenic-Induced Liver Damage via Activating Mitochondrial Apoptotic Pathway.Biological trace element research · 2024Article
- Dialogue between mitochondria and endoplasmic reticulum-potential therapeutic targets for age-related cardiovascular diseases.Frontiers in pharmacology · 2024Review
- Shaping cardiac destiny: the role of post-translational modifications on endoplasmic reticulum - mitochondria crosstalk in cardiac remodeling.Frontiers in pharmacology · 2024Review
- SIRT3 ameliorates diabetes-associated cognitive dysfunction via regulating mitochondria-associated ER membranes.Journal of translational medicine · 2023Article
- Downhill running induced DNA damage enhances mitochondrial membrane permeability by facilitating ER-mitochondria signaling.Journal of muscle research and cell motility · 2022Article
- Membrane Contact Sites in Autophagy.Cells · 2022Review
- Mitochondria-ER Tethering in Neurodegenerative Diseases.Cellular and molecular neurobiology · 2022Review
- EI24 promotes cell adaption to ER stress by coordinating IRE1 signaling and calcium homeostasis.EMBO reports · 2022Article
- Olaparib, a PARP-1 inhibitor, protects retinal cells from ocular hypertension-associated oxidative damage.Frontiers in cell and developmental biology · 2022Article
Corrections and comments
- Erratum issued
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Etoposide-induced protein 2.4 (EI24), located on the endoplasmic reticulum (ER) membrane, has been proposed to be an essential autophagy protein. Specific ablation of EI24 in neuronal and liver tissues causes deficiency of autophagy flux. However, the molecular mechanism of the EI24-mediated autophagy process is still poorly understood. Like neurons and hepatic cells, pancreatic β cells are also secretory cells. Pancreatic β cells contain large amounts of ER and continuously synthesize and secrete insulin to maintain blood glucose homeostasis. Yet, the effect of EI24 on autophagy of pancreatic β cells has not been reported. Here, we show that the autophagy process is inhibited in EI24-deficient primary pancreatic β cells. Further mechanistic studies demonstrate that EI24 is enriched at the ER-mitochondria interface and that the C-terminal domain of EI24 is important for the integrity of the mitochondria-associated membrane (MAM) and autophagy flux. Overexpression of EI24, but not the EI24-ΔC mutant, can rescue MAM integrity and decrease the aggregation of p62 and LC3II in the EI24-deficient group. By mass spectrometry-based proteomics following immunoprecipitation, EI24 was found to interact with voltage-dependent anion channel 1 (VDAC1), inositol 1,4,5-trisphosphate receptor (IP3R), and the outer mitochondrial membrane chaperone GRP75. Knockout of EI24 impairs the interaction of IP3R with VDAC1, indicating that these proteins may form a quaternary complex to regulate MAM integrity and the autophagy process.
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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.