ArticleEMBO reports2024
Nup358 restricts ER-mitochondria connectivity by modulating mTORC2/Akt/GSK3β signalling.
Article in EMBO reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- Aging-Related Changes in the Injury Response of the Peripheral Nervous System.Neuroscience bulletin · 2026Review
- Neuro-glial lipid imbalance in a Drosophila model of amyotrophic lateral sclerosis 8.Acta neuropathologica communications · 2026Article
- Spatial control of mitochondrial retrograde signaling by nuclear pore-associated contact sites.bioRxiv : the preprint server for biology · 2026Article
- RanBP2-dependent SUMOylation of G3BP2 inhibits formation, and promotes disassembly, of stress granules.Molecular biology of the cell · 2026Article
- PMF proteins mediate mitochondrial fusion in Arabidopsis.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Alzheimer's disease: disrupted communication between the endoplasmic reticulum and mitochondria.Journal of neurology · 2026Review
- STARD3 regulates lysosome positioning and contacts via a GSK3-controlled phosphorylation switch.The EMBO journal · 2026Article
- MAMs-Mediated Calcium Homeostasis in the Pathophysiology of Cardiovascular Diseases: A Mini-Review.Drug design, development and therapy · 2026Review
- Mitochondrial‑endoplasmic reticulum crosstalk: Molecular mechanisms and implications for cardiovascular disease (Review).Molecular medicine reports · 2025Review
- RRP9 promotes prostate cancer metastasis and epithelial-mesenchymal transition through activation of the AKT/GSK3β/β-Catenin signaling pathway.Discover oncology · 2025Article
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Authors and funding
9 authors.
Funding
Abstract
ER-mitochondria contact sites (ERMCSs) regulate processes, including calcium homoeostasis, energy metabolism and autophagy. Previously, it was shown that during growth factor signalling, mTORC2/Akt gets recruited to and stabilizes ERMCSs. Independent studies showed that GSK3β, a well-known Akt substrate, reduces ER-mitochondria connectivity by disrupting the VAPB-PTPIP51 tethering complex. However, the mechanisms that regulate ERMCSs are incompletely understood. Here we find that annulate lamellae (AL), relatively unexplored subdomains of ER enriched with a subset of nucleoporins, are present at ERMCSs. Depletion of Nup358, an AL-resident nucleoporin, results in enhanced mTORC2/Akt activation, GSK3β inhibition and increased ERMCSs. Depletion of Rictor, a mTORC2-specific subunit, or exogenous expression of GSK3β, was sufficient to reverse the ERMCS-phenotype in Nup358-deficient cells. We show that growth factor-mediated activation of mTORC2 requires the VAPB-PTPIP51 complex, whereas, Nup358's association with this tether restricts mTORC2/Akt signalling and ER-mitochondria connectivity. Expression of a Nup358 fragment that is sufficient for interaction with the VAPB-PTPIP51 complex suppresses mTORC2/Akt activation and disrupts ERMCSs. Collectively, our study uncovers a novel role for Nup358 in controlling ERMCSs by modulating the mTORC2/Akt/GSK3β axis.
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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 Socratic graph.