ArticleMolecular and cellular biology2019
Hyperosmotic Stress Induces Unconventional Autophagy Independent of the Ulk1 Complex.
Article in Molecular and cellular biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 18 citations in OpenAlex.
- Chemicals Affecting Autophagy in rCHO Cell Cultures and Their Impacts on Therapeutic Protein Production Processes.Journal of microbiology and biotechnology · 2026Review
- Rapid activation of p62 body-mediated autophagy in human cells under hyperosmotic stress.Communications biology · 2026Article
- Functional Activities of Cohesin Proteins Can Be Altered by Chemical Chaperones.The protein journal · 2025Article
- Morphodynamical adaptation of the endolysosomal system to stress.The FEBS journal · 2025Review
- Inhibition of WNK Kinases in NK Cells Disrupts Cellular Osmoregulation and Control of Tumor Metastasis.Journal of innate immunity · 2024Article
- mAutophagy · 2022Article
- S-adenosylmethionine: A metabolite critical to the regulation of autophagy.Cell proliferation · 2020Review
- Article
- Endocytosis in the adaptation to cellular stress.Cell stress · 2020Review
- Endocytic regulation of cellular ion homeostasis controls lysosome biogenesis.Nature cell biology · 2020Article
- Inhibiting ULK1 kinase decreases autophagy and cell viability in high-grade serous ovarian cancer spheroids.American journal of cancer research · 2020Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Autophagy is considered an adaptive mechanism against hyperosmotic stress. Although the process has been reported to be triggered by the inhibition of mTORC1, the precise downstream mechanisms remain elusive. Here, we demonstrate that hyperosmotic-stress-induced autophagy is different from conventional macroautophagy in mouse embryonic fibroblasts (MEFs) and human T24 cells. Our results indicated that cytoplasmic puncta for the isolation membrane markers WIPI2 and Atg16L increased after hyperosmotic stress. They were found to partially colocalize with puncta for a selective autophagy substrate, SQSTM1/p62, and were shown to be diminished by inhibitors of phosphatidylinositol 3-kinase (PI3K) or by knockdown of human Vps34 (hVps34), a component of PI3K. In addition, flux assays showed that SQSTM1/p62 and NcoA4 were degraded by the lysosomal pathway. Surprisingly, Ulk1, which is essential for starvation-induced macroautophagy, remained inactivated under hyperosmotic stress, which was partially caused by mTOR activity. Accordingly, the Ulk1 complex was not nucleated under hyperosmotic stress. Finally, autophagy proceeded even in MEFs deficient in
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