ArticleScience advances2022
Phosphorylation of FAM134C by CK2 controls starvation-induced ER-phagy.
Article in Science advances, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 33 citations in OpenAlex.
- Revisiting Inherited Metabolic Diseases (IMDs) Through the Lens of Selective Autophagy.Journal of inherited metabolic disease · 2026Review
- Remaking an exit: dynamic regulation of ER exit sites by post-translational modifications.Trends in cell biology · 2026Review
- Phosphorylation of OTUB1 promotes autophagy initiation under starvation.Nature communications · 2026Article
- ER-phagy receptors: structural mechanisms in selective ER degradation and disease implications.Acta pharmacologica Sinica · 2026Review
- Article
- Endoplasmic reticulum autophagy in inflammatory diseases.Frontiers in immunology · 2026Review
- Mechanism of autophagy initiation by transmembrane selective autophagy receptors.The EMBO journal · 2025Review
- Reticulophagy receptor FAM134C restrains BMP receptor signaling.The EMBO journal · 2025Article
- ER-phagy Activation by AMFR Attenuates Cardiac Fibrosis Post-Myocardial Infarction via mTORC1 Pathway.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Autophagy, ER-phagy and ER Dynamics During Cell Differentiation.Journal of molecular biology · 2025Review
- The intrinsically disordered regions of organellophagy receptors are interchangeable and control organelle fragmentation, ER-phagy and mitophagy flux.Nature cell biology · 2025Article
- Reticulophagy and viral infection.Autophagy · 2025Review
- FAM134B in Cellular Homeostasis: Bridging Endoplasmic Reticulum-Phagy to Human Diseases.International journal of biological sciences · 2025Review
- Signaling Regulation of FAM134-Dependent ER-Phagy in Cells.Journal of cellular physiology · 2025Review
- Sestrin2 drives ER-phagy in response to protein misfolding.Developmental cell · 2024Article
- Fam134c and Fam134b shape axonal endoplasmic reticulum architecture in vivo.EMBO reports · 2024Article
- Article
- ERK-activated CK-2 triggers blastema formation during appendage regeneration.Science advances · 2024Article
- Combinatorial selective ER-phagy remodels the ER during neurogenesis.Nature cell biology · 2024Article
- Unraveling the Genetic Landscape of Neurological Disorders: Insights into Pathogenesis, Techniques for Variant Identification, and Therapeutic Approaches.International journal of molecular sciences · 2024Review
Corrections and comments
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Authors and funding
20 authors at 7 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Selective degradation of the endoplasmic reticulum (ER) via autophagy (ER-phagy) is initiated by ER-phagy receptors, which facilitate the incorporation of ER fragments into autophagosomes. FAM134 reticulon family proteins (FAM134A, FAM134B, and FAM134C) are ER-phagy receptors with structural similarities and nonredundant functions. Whether they respond differentially to the stimulation of ER-phagy is unknown. Here, we describe an activation mechanism unique to FAM134C during starvation. In fed conditions, FAM134C is phosphorylated by casein kinase 2 (CK2) at critical residues flanking the LIR domain. Phosphorylation of these residues negatively affects binding affinity to the autophagy proteins LC3. During starvation, mTORC1 inhibition limits FAM134C phosphorylation by CK2, hence promoting receptor activation and ER-phagy. Using a novel tool to study ER-phagy in vivo and FAM134C knockout mice, we demonstrated the physiological relevance of FAM134C phosphorylation during starvation-induced ER-phagy in liver lipid metabolism. These data provide a mechanistic insight into ER-phagy regulation and an example of autophagy selectivity during starvation.
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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.