ArticleEMBO reports2021
Role of FAM134 paralogues in endoplasmic reticulum remodeling, ER-phagy, and Collagen quality control.
Article in EMBO reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers.
What it found
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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.
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Who cites it
69 citing papers in PubMed, 111 citations in OpenAlex.
- Revisiting Inherited Metabolic Diseases (IMDs) Through the Lens of Selective Autophagy.Journal of inherited metabolic disease · 2026Review
- Intracellular lipopolysaccharide binds RETREG1/FAM134B to regulate ER remodeling upon bacterial infection.Autophagy · 2026Article
- FAM134B-mediated ER-phagy degrades APP and suppresses Alzheimer's disease pathology.The EMBO journal · 2026Article
- ER-phagy receptors: structural mechanisms in selective ER degradation and disease implications.Acta pharmacologica Sinica · 2026Review
- RETREG1-Mediated Reticulophagy is Essential for Dendritic Cell Maturation and Function in Sepsis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Article
- Sepsis alters NK cell transcriptional programs for stress, actin remodeling, and intracellular trafficking.Cellular & molecular biology letters · 2026Article
- FAM134B controls collagen I dynamics in hepatic stellate cell-driven fibrosis.American journal of physiology. Gastrointestinal and liver physiology · 2026Article
- ER membrane receptors engage core autophagy machinery to initiate ER-phagy.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Deep Proteome Profiling of Rat Dorsal Striatal Synaptoneurosomes Following Methamphetamine Exposure.ACS chemical neuroscience · 2026Article
- The role of ER-associated degradation and ER-phagy in health and disease.Signal transduction and targeted therapy · 2026Review
- Endoplasmic reticulum autophagy in inflammatory diseases.Frontiers in immunology · 2026Review
- From homeostasis to pathology, organelle-specific autophagy in skeletal muscle: a PRISMA-ScR scoping review.Frontiers in physiology · 2026Review
- LC3 and GABARAP independent autophagy of misfolded procollagen in mouse osteoblasts.Autophagy · 2025Article
- Reticulophagy receptor FAM134C restrains BMP receptor signaling.The EMBO journal · 2025Article
- Mechanism of autophagy initiation by transmembrane selective autophagy receptors.The EMBO journal · 2025Review
- Article
- Murine leukemia virus glycoGag antagonizes SERINC5 via ER-phagy receptor RETREG1.PLoS pathogens · 2025Article
- Autophagy, ER-phagy and ER Dynamics During Cell Differentiation.Journal of molecular biology · 2025Review
- LAPTM4B as a key regulator in the copper-induced endoplasmic reticulum-lysosome interplay disorder in duck liver and the protective role of baicalin.Journal of animal science and biotechnology · 2025Article
9 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
17 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Degradation of the endoplasmic reticulum (ER) via selective autophagy (ER-phagy) is vital for cellular homeostasis. We identify FAM134A/RETREG2 and FAM134C/RETREG3 as ER-phagy receptors, which predominantly exist in an inactive state under basal conditions. Upon autophagy induction and ER stress signal, they can induce significant ER fragmentation and subsequent lysosomal degradation. FAM134A, FAM134B/RETREG1, and FAM134C are essential for maintaining ER morphology in a LC3-interacting region (LIR)-dependent manner. Overexpression of any FAM134 paralogue has the capacity to significantly augment the general ER-phagy flux upon starvation or ER-stress. Global proteomic analysis of FAM134 overexpressing and knockout cell lines reveals several protein clusters that are distinctly regulated by each of the FAM134 paralogues as well as a cluster of commonly regulated ER-resident proteins. Utilizing pro-Collagen I, as a shared ER-phagy substrate, we observe that FAM134A acts in a LIR-independent manner and compensates for the loss of FAM134B and FAM134C, respectively. FAM134C instead is unable to compensate for the loss of its paralogues. Taken together, our data show that FAM134 paralogues contribute to common and unique ER-phagy pathways.
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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.