ArticleAutophagy2016
Functional characterization of EI24-induced autophagy in the degradation of RING-domain E3 ligases.
Article in Autophagy, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.
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
25 citing papers in PubMed, 1 synthesis or guideline pooled it, 35 citations in OpenAlex.
- Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition)Autophagy · 2021Guideline
- Biological significance, molecular mechanisms and clinical potential of EI24 in cancer.Chinese medical journal · 2026Review
- Ei24 deficiency in brown adipocytes induces severe hypothermia under cold stress independent of UCP1 activity.Nature communications · 2025Article
- Reciprocal stabilization of CtBP and TRIM28 represses autophagy to promote metastasis.Nature structural & molecular biology · 2025Article
- A Novel Function of NaFASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Etoposide-induced protein 2.4 homolog promotes argininosuccinate synthase 1 and cancer cell survival upon arginine deprivation.Cellular & molecular biology letters · 2025Article
- EI24 binds to IGF1R, enhancing glucose homeostasis and fostering healthy aging in male mice.Frontiers in aging · 2025Article
- Gene Expression Dysregulation in Whole Blood of Patients withInternational journal of molecular sciences · 2024Article
- 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
- Algal rhodopsins encoding diverse signal sequence holds potential for expansion of organelle optogenetics.Biophysics and physicobiology · 2023Article
- Review
- Article
- The roles and targeting options of TRIM family proteins in tumor.Frontiers in pharmacology · 2022Review
- Autophagy augments the self-renewal of lung cancer stem cells by the degradation of ubiquitinated p53.Cell death & disease · 2021Article
- The central regulator p62 between ubiquitin proteasome system and autophagy and its role in the mitophagy and Parkinson's disease.BMB reports · 2020Review
- Altered myogenesis and premature senescence underlie human TRIM32-related myopathy.Acta neuropathologica communications · 2019Article
- EI24, as a Component of Autophagy, Is Involved in Pancreatic Cell Proliferation.Frontiers in oncology · 2019Article
- DNA damage triggers tubular endoplasmic reticulum extension to promote apoptosis by facilitating ER-mitochondria signaling.Cell research · 2018Article
- Etoposide-induced protein 2.4 functions as a regulator of the calcium ATPase and protects pancreatic β-cell survival.The Journal of biological chemistry · 2018Article
- Crosstalk Between Mammalian Autophagy and the Ubiquitin-Proteasome System.Frontiers in cell and developmental biology · 2018Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Historically, the ubiquitin-proteasome system (UPS) and autophagy pathways were believed to be independent; however, recent data indicate that these pathways engage in crosstalk. To date, the players mediating this crosstalk have been elusive. Here, we show experimentally that EI24 (EI24, autophagy associated transmembrane protein), a key component of basal macroautophagy/autophagy, degrades 14 physiologically important E3 ligases with a RING (really interesting new gene) domain, whereas 5 other ligases were not degraded. Based on the degradation results, we built a statistical model that predicts the RING E3 ligases targeted by EI24 using partial least squares discriminant analysis. Of 381 RING E3 ligases examined computationally, our model predicted 161 EI24 targets. Those targets are primarily involved in transcription, proteolysis, cellular bioenergetics, and apoptosis and regulated by TP53 and MTOR signaling. Collectively, our work demonstrates that EI24 is an essential player in UPS-autophagy crosstalk via degradation of RING E3 ligases. These results indicate a paradigm shift regarding the fate of E3 ligases.
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.