ReviewEssays in biochemistry2017
mTORC1 as the main gateway to autophagy.
Review in Essays in biochemistry, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 331 papers.
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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
331 citing papers in PubMed, 548 citations in OpenAlex.
- Late isocaloric eating increases hunger, decreases energy expenditure, and modifies metabolic pathways in adults with overweight and obesity.Cell metabolism · 2022Trial
- Time-resolved simultaneous imaging of mitochondrial reactive oxygen species and lysosomal permeabilization to determine organelle-centred cell death.Redox report : communications in free radical research · 2026Article
- The SLC-ome of membrane transport: from molecular discovery to physiology and clinical applications.Physiological reviews · 2026Review
- The Sleeping Giant: Metabolism and Autophagy in the Generation and Survival of Dormant Polyploid Giant Cancer Cells.MedComm · 2026Review
- Proteostasis of organelles in aging and disease.The FEBS journal · 2026Review
- Glucosamine Promotes Autophagy and Attenuates Hepatic Steatosis Via O-GlcNAcylation-Mediated Mechanisms.Journal of biochemical and molecular toxicology · 2026Article
- Global cellular responses to lysosomal damage.Current biology : CB · 2026Review
- Translational resistance to amino acid starvation in breast cancer cells revealed by ribosome profiling.iScience · 2026Article
- pH-mediated activation of the lysosomal arginine sensor SLC38A9.FEBS letters · 2026Article
- TMEM175 rescues post-infarct cardiac dysfunction via mTORC1-lysosomal axis modulation.Acta pharmacologica Sinica · 2026Article
- Article
- Unlocking the aging brain: mTORC1 as a convergent integrator for neurodegeneration and therapeutic intervention.Biogerontology · 2026Review
- Molecular mechanisms and recent advances in cellular senescence.Cell & bioscience · 2026Review
- PINK1 loss in astrocytes triggers inflammatory dysfunction and neuronal death.bioRxiv : the preprint server for biology · 2026Article
- A peptide-induced regression of low-grade malignant breast tumor via activation of autophagy in breast cancer cells.Molecular medicine (Cambridge, Mass.) · 2026Article
- Sleep-circadian modulation of autophagy and glymphatic function: failure of coordinated brain clearance in Parkinson's disease.NPJ Parkinson's disease · 2026Review
- Mechanical Loading Induces the Radial Growth of Myofibrils and Myofibrillogenesis via an mTORC1-Dependent Mechanism.bioRxiv : the preprint server for biology · 2026Article
- Genetically targeted mTORC1 inhibitor reveals transcriptional control by nuclear mTORC1.Nature chemical biology · 2026Article
- Autophagy in cancer nanomedicine: an implication of nanomaterials' impact on the evolutionarily conservative catabolic processes in human tumors.Archives of toxicology · 2026Review
- Molecular and physiological adaptations to low-salinity stress in penaeid shrimp: a focus on Litopenaeus vannamei and Penaeus monodon.Stress biology · 2026Review
271 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Cells and organisms must coordinate their metabolic activity with changes in their environment to ensure their growth only when conditions are favourable. In order to maintain cellular homoeostasis, a tight regulation between the synthesis and degradation of cellular components is essential. At the epicentre of the cellular nutrient sensing is the mechanistic target of rapamycin complex 1 (mTORC1) which connects environmental cues, including nutrient and growth factor availability as well as stress, to metabolic processes in order to preserve cellular homoeostasis. Under nutrient-rich conditions mTORC1 promotes cell growth by stimulating biosynthetic pathways, including synthesis of proteins, lipids and nucleotides, and by inhibiting cellular catabolism through repression of the autophagic pathway. Its close signalling interplay with the energy sensor AMP-activated protein kinase (AMPK) dictates whether the cell actively favours anabolic or catabolic processes. Underlining the role of mTORC1 in the coordination of cellular metabolism, its deregulation is linked to numerous human diseases ranging from metabolic disorders to many cancers. Although mTORC1 can be modulated by a number of different inputs, amino acids represent primordial cues that cannot be compensated for by any other stimuli. The understanding of how amino acids signal to mTORC1 has increased considerably in the last years; however this area of research remains a hot topic in biomedical sciences. The current ideas and models proposed to explain the interrelationship between amino acid sensing, mTORC1 signalling and autophagy is the subject of the present review.
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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.