ReviewF1000Research2020
Coordination of Rheb lysosomal membrane interactions with mTORC1 activation.
Review in F1000Research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
23 citing papers in PubMed, 40 citations in OpenAlex.
- Drug resistant epilepsy driven byEpilepsy & behavior reports · 2026Article
- Rheb membrane orientation dynamics and functional consequences elucidated by molecular simulations, single-molecule-FRET and signaling assays.bioRxiv : the preprint server for biology · 2026Article
- mTOR signaling networks: mechanistic insights and translational frontiers in disease therapeutics.Signal transduction and targeted therapy · 2025Review
- Article
- Calmodulin enhances mTORC1 signaling by preventing TSC2-Rheb binding.The Journal of biological chemistry · 2025Article
- Exploring glycolytic enzymes in disease: potential biomarkers and therapeutic targets in neurodegeneration, cancer and parasitic infections.Open biology · 2025Review
- Crosstalk between dysregulated amino acid sensing and glucose and lipid metabolism in colorectal cancer.Frontiers in oncology · 2025Review
- Structural basis for growth factor and nutrient signal integration on the lysosomal membrane by mTORC1.bioRxiv : the preprint server for biology · 2024Article
- Acidity suppresses CD8 + T-cell function by perturbing IL-2, mTORC1, and c-Myc signaling.The EMBO journal · 2024Article
- Lysosomal TBK1 responds to amino acid availability to relieve Rab7-dependent mTORC1 inhibition.The EMBO journal · 2024Article
- The allosteric mechanism of mTOR activation can inform bitopic inhibitor optimization.Chemical science · 2024Article
- Lysosomal TBK1 Responds to Amino Acid Availability to Relieve Rab7-Dependent mTORC1 Inhibition.bioRxiv : the preprint server for biology · 2023Article
- Arf5-mediated regulation of mTORC1 at the plasma membrane.Molecular biology of the cell · 2023Article
- Programmed Cell Death in Diabetic Nephropathy: A Review of Apoptosis, Autophagy, and Necroptosis.Medical science monitor : international medical journal of experimental and clinical research · 2022Review
- Rheb regulates nuclear mTORC1 activity independent of farnesylation.Cell chemical biology · 2022Article
- Review
- Blocking the Farnesyl Pocket of PDEδ Reduces Rheb-Dependent mTORC1 Activation and Survival ofFrontiers in pharmacology · 2022Article
- mTOR Activity and Autophagy in Senescent Cells, a Complex Partnership.International journal of molecular sciences · 2021Review
- A role for BDNF- and NMDAR-induced lysosomal recruitment of mTORC1 in the regulation of neuronal mTORC1 activity.Molecular brain · 2021Article
- Splicing alterations in healthy aging and disease.Wiley interdisciplinary reviews. RNA · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
A complex molecular machinery converges on the surface of lysosomes to ensure that the growth-promoting signaling mediated by mechanistic target of rapamycin complex 1 (mTORC1) is tightly controlled by the availability of nutrients and growth factors. The final step in this activation process is dependent on Rheb, a small GTPase that binds to mTOR and allosterically activates its kinase activity. Here we review the mechanisms that determine the subcellular localization of Rheb (and the closely related RhebL1 protein) as well as the significance of these mechanisms for controlling mTORC1 activation. In particular, we explore how the relatively weak membrane interactions conferred by C-terminal farnesylation are critical for the ability of Rheb to activate mTORC1. In addition to supporting transient membrane interactions, Rheb C-terminal farnesylation also supports an interaction between Rheb and the δ subunit of phosphodiesterase 6 (PDEδ). This interaction provides a potential mechanism for targeting Rheb to membranes that contain Arl2, a small GTPase that triggers the release of prenylated proteins from PDEδ. The minimal membrane targeting conferred by C-terminal farnesylation of Rheb and RhebL1 distinguishes them from other members of the Ras superfamily that possess additional membrane interaction motifs that work with farnesylation for enrichment on the specific subcellular membranes where they engage key effectors. Finally, we highlight diversity in Rheb membrane targeting mechanisms as well as the potential for alternative mTORC1 activation mechanisms across species.
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What OpenQuestion holds
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.