ArticleGenes & development2015
NLK phosphorylates Raptor to mediate stress-induced mTORC1 inhibition.
Article in Genes & development, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
34 citing papers in PubMed, 56 citations in OpenAlex.
- SIRT1 Exon 2-Encoded IDR Gates CREB-Dependent Transcriptional Timing During Fasting.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- Development of a SIN1 Targeting Inhibitor as a Novel Therapeutic Approach for the Treatment of Malignancies.Molecular cancer therapeutics · 2026Article
- Evolutionary analysis through structural modeling of FAM222 proteins reveals a novel disordered conserved domain in vertebrates that interacts with NLK.Scientific reports · 2025Article
- Crosstalk of Nemo-Like Kinase (NLK) and Yes-Associated Protein (YAP) Phosphorylation in Endometrial Epithelial Cells.Development & reproduction · 2025Article
- Nemo-like kinase disrupts nuclear import and drives TDP43 mislocalization in ALS.The Journal of clinical investigation · 2025Article
- Article
- MAPK Signaling in the Interplay Between Oxidative Stress and Autophagy.Antioxidants (Basel, Switzerland) · 2025Review
- From Molecular Therapies to Lysosomal Transplantation and Targeted Drug Strategies: Present Applications, Limitations, and Future Prospects of Lysosomal Medications.Biomolecules · 2025Review
- Targeting a chemo-induced adaptive signaling circuit confers therapeutic vulnerabilities in pancreatic cancer.Cell discovery · 2024Article
- High glucose induces an early and transient cytoprotective autophagy in retinal Müller cells.Endocrine · 2022Article
- Targeting lysosomes in human disease: from basic research to clinical applications.Signal transduction and targeted therapy · 2021Review
- Regulation and metabolic functions of mTORC1 and mTORC2.Physiological reviews · 2021Review
- Therapeutic Targeting of Nemo-like Kinase in Primary and Acquired Endocrine-resistant Breast Cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2021Article
- mTORC1 Crosstalk With Stress Granules in Aging and Age-Related Diseases.Frontiers in aging · 2021Review
- Exosome-transferred long non-coding RNA ASMTL-AS1 contributes to malignant phenotypes in residual hepatocellular carcinoma after insufficient radiofrequency ablation.Cell proliferation · 2020Article
- Regulation of mTORC1 by Upstream Stimuli.Genes · 2020Review
- Diamond Blackfan anemia is mediated by hyperactive Nemo-like kinase.Nature communications · 2020Article
- Multiple distinct pathways lead to hyperubiquitylated insoluble TDP-43 protein independent of its translocation into stress granules.The Journal of biological chemistry · 2020Article
- Dietary resveratrol supplementation inhibits heat stress-induced high-activated innate immunity and inflammatory response in spleen of yellow-feather broilers.Poultry science · 2019Article
- TBK1 Limits mTORC1 by Promoting Phosphorylation of Raptor Ser877.Scientific reports · 2019Article
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 2 countries.
Funding
Abstract
The mechanistic target of rapamycin (mTOR) is a central cell growth controller and forms two distinct complexes: mTORC1 and mTORC2. mTORC1 integrates a wide range of upstream signals, both positive and negative, to regulate cell growth. Although mTORC1 activation by positive signals, such as growth factors and nutrients, has been extensively investigated, the mechanism of mTORC1 regulation by stress signals is less understood. In this study, we identified the Nemo-like kinase (NLK) as an mTORC1 regulator in mediating the osmotic and oxidative stress signals. NLK inhibits mTORC1 lysosomal localization and thereby suppresses mTORC1 activation. Mechanistically, NLK phosphorylates Raptor on S863 to disrupt its interaction with the Rag GTPase, which is important for mTORC1 lysosomal recruitment. Cells with Nlk deletion or knock-in of the Raptor S863 phosphorylation mutants are defective in the rapid mTORC1 inhibition upon osmotic stress. Our study reveals a function of NLK in stress-induced mTORC1 modulation and the underlying biochemical mechanism of NLK in mTORC1 inhibition in stress response.
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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.