ArticleBiology direct2021
Rab32 uses its effector reticulon 3L to trigger autophagic degradation of mitochondria-associated membrane (MAM) proteins.
Article in Biology direct, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 26 citations in OpenAlex.
- The multifaceted functions of selective autophagy in cancer: molecular basis, consequences, and clinical prospects.Molecular cancer · 2026Review
- Rab32-based vesicles coordinate mitochondria and actin for spindle migration and organelle rearrangement in oocyte meiosis.Journal of advanced research · 2026Article
- p62 limits Salmonella Typhimurium in macrophages through its role in cell signalling.Access microbiology · 2026Article
- Mitochondria-associated membranes in heart failure: from molecular mechanisms to therapeutic targets.Frontiers in physiology · 2026Review
- Subcellular Stress Markers in Epithelial Ovarian Cancer.International journal of molecular sciences · 2025Review
- Integrating pathology genomics and single-cell genomics to identify lactate metabolism-related prognostic features and therapeutic strategies for melanoma.Apoptosis : an international journal on programmed cell death · 2025Article
- Vesicular transport in the autophagic route: RAB GTPases as pivotal regulators of autophagy.The Biochemical journal · 2025Review
- Mitochondrial‑endoplasmic reticulum crosstalk: Molecular mechanisms and implications for cardiovascular disease (Review).Molecular medicine reports · 2025Review
- Review
- Rab32 regulates Golgi structure and cell migration through Protein Kinase A-mediated phosphorylation of Optineurin.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- TMX5/TXNDC15, a natural trapping mutant of the PDI family is a client of the proteostatic factor ERp44.Life science alliance · 2024Article
- High Expression of RAB32 Predicts Adverse Outcomes: A Potential Therapeutic Target for Glioblastoma.Journal of Cancer · 2024Article
- Rab32 promotes glioblastoma migration and invasion via regulation of ERK/Drp1-mediated mitochondrial fission.Cell death & disease · 2023Article
- Dysfunctional mitochondria accumulate in a skeletal muscle knockout model of Smn1, the causal gene of spinal muscular atrophy.Cell death & disease · 2023Article
- ER-phagy: selective autophagy of the endoplasmic reticulum.EMBO reports · 2022Review
- Article
- Nuclear and Cytoplasmatic Players in Mitochondria-Related CNS Disorders: Chromatin Modifications and Subcellular Trafficking.Biomolecules · 2022Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
backgroundRab32 is a small GTPase associated with multiple organelles but is particularly enriched at the endoplasmic reticulum (ER). Here, it controls targeting to mitochondria-ER contacts (MERCs), thus influencing composition of the mitochondria-associated membrane (MAM). Moreover, Rab32 regulates mitochondrial membrane dynamics via its effector dynamin-related protein 1 (Drp1). Rab32 has also been reported to induce autophagy, an essential pathway targeting intracellular components for their degradation. However, no autophagy-specific effectors have been identified for Rab32. Similarly, the identity of the intracellular membrane targeted by this small GTPase and the type of autophagy it induces are not known yet.
resultsTo investigate the target of autophagic degradation mediated by Rab32, we tested a large panel of organellar proteins. We found that a subset of MERC proteins, including the thioredoxin-related transmembrane protein TMX1, are specifically targeted for degradation in a Rab32-dependent manner. We also identified the long isoform of reticulon-3 (RTN3L), a known ER-phagy receptor, as a Rab32 effector.
conclusionsRab32 promotes degradation of mitochondrial-proximal ER membranes through autophagy with the help of RTN3L. We propose to call this type of selective autophagy "MAM-phagy".
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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.