ArticleThe EMBO journal2023
TECPR1 is activated by damage-induced sphingomyelin exposure to mediate noncanonical autophagy.
Article in The EMBO journal, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.
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Who cites it
53 citing papers in PubMed, 64 citations in OpenAlex.
- Canonical and noncanonical autophagy in immunity.Immunity · 2026Review
- A role for CASM in the repair of damaged Golgi architecture.Autophagy · 2026Article
- RNF213-dependent lytic destruction ofProceedings of the National Academy of Sciences of the United States of America · 2026Article
- Sorting of lysosomal enzyme and autophagy are regulated by the GGA1-induced TGN lipid scrambling.Science advances · 2026Article
- Astrocytes mobilize a broader repertoire of lysosomal repair mechanisms than neurons.iScience · 2026Article
- Article
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- Lipid-manager autophagy proteins ATG2 and ATG9 regulate extracellular vesicle secretion via amphisome biogenesis and cell lipidome modulation.Nature communications · 2026Article
- Contradictory Effects on Hepatocytes in ASMD.International journal of molecular sciences · 2026Review
- Ca²⁺ leakage is a conserved signal for non-canonical ATG8/LC3 lipidation and membrane repair.The EMBO journal · 2026Article
- Full length TECPR1 displays 'cis' Dysferlin domain architecture.bioRxiv : the preprint server for biology · 2026Article
- Crosstalk between protein lipidation and ubiquitination in tumor biology.Apoptosis : an international journal on programmed cell death · 2026Review
- EVA1A-Mediated Signaling Networks in Physiological and Pathological Contexts: Dual Roles in Autophagy and Apoptosis.Cell biochemistry and biophysics · 2026Review
- Membrane atg8ylation and autophagy in protection against Mycobacterium tuberculosis.Journal of immunology (Baltimore, Md. : 1950) · 2026Review
- The ATG8 E3-like ligases sense lysosomal damage and initiate ESCRT-mediated membrane repair.The EMBO journal · 2026Article
- Lysosomal membrane homeostasis and its importance in physiology and disease.Nature reviews. Molecular cell biology · 2026Review
- Repair of damaged lysosomes by TECPR1-mediated membrane tubulation during energy crisis.Cell research · 2026Article
- Pneumolysin-dependent and independent non-canonical autophagy processes mediate host defense against pneumococcal infection.Autophagy · 2025Article
- JIP4 and RILPL1 utilize opposing motor force to dynamically regulate lysosomal tubulation.The Journal of cell biology · 2025Article
- BLTP3A is associated with membranes of the late endocytic pathway and is an effector of CASM.The EMBO journal · 2025Article
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Authors and funding
11 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cells use noncanonical autophagy, also called conjugation of ATG8 to single membranes (CASM), to label damaged intracellular compartments with ubiquitin-like ATG8 family proteins in order to signal danger caused by pathogens or toxic compounds. CASM relies on E3 complexes to sense membrane damage, but so far, only the mechanism to activate ATG16L1-containing E3 complexes, associated with proton gradient loss, has been described. Here, we show that TECPR1-containing E3 complexes are key mediators of CASM in cells treated with a variety of pharmacological drugs, including clinically relevant nanoparticles, transfection reagents, antihistamines, lysosomotropic compounds, and detergents. Interestingly, TECPR1 retains E3 activity when ATG16L1 CASM activity is obstructed by the Salmonella Typhimurium pathogenicity factor SopF. Mechanistically, TECPR1 is recruited by damage-induced sphingomyelin (SM) exposure using two DysF domains, resulting in its activation and ATG8 lipidation. In vitro assays using purified human TECPR1-ATG5-ATG12 complex show direct activation of its E3 activity by SM, whereas SM has no effect on ATG16L1-ATG5-ATG12. We conclude that TECPR1 is a key activator of CASM downstream of SM exposure.
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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.