ReviewJournal of cellular physiology2025
Signaling Regulation of FAM134-Dependent ER-Phagy in Cells.
Review in Journal of cellular physiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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
3 citing papers in PubMed.
- Identification of potential biomarkers and therapeutic targets for liver cirrhosis based on Mendelian randomization and machine learning.Biochemistry and biophysics reports · 2026Article
- RETRACTED: Plant rhabdovirus glycoprotein activates unfolded protein response-mediated antiviral ER-phagy in insect vectors.PLoS pathogens · 2026Article
- LC3 and GABARAP independent autophagy of misfolded procollagen in mouse osteoblasts.Autophagy · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
Abstract
The endoplasmic reticulum (ER) is a pivotal organelle responsible for protein and lipid synthesis, calcium homeostasis, and protein quality control within eukaryotic cells. To maintain cellular health, damaged or excess portions of the ER must be selectively degraded via a process known as selective autophagy, or ER-phagy. This specificity is driven by a network of protein receptors and regulatory mechanisms. In this review, we explore the molecular mechanisms governing ER-phagy, with a focus on the FAM134 family of ER-resident ER-phagy receptors. We discuss the molecular pathways and Posttranslational modifications that regulate receptor activation and clustering, and how these modifications fine-tune ER-phagy in response to stress. This review provides a concise understanding of how ER-phagy contributes to cellular homeostasis and highlights the need for further studies in models where ER stress and autophagy are dysregulated.
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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.