[ { "name": "NLRP3", "type": "Pathway/Complex", "description": "Inflammasome sensor driving IL-1β-mediated inflammation, regulated in part by mTOR-dependent immunometabolism.", "description_beginner": "An alarm system inside immune cells. When it senses damage or infection it assembles into a large complex and releases IL-1β, one of the body's strongest inflammation signals. How much fuel the cell is burning - something mTOR helps set - influences how loudly that alarm goes off.", "synonyms": "", "n_linked_studies": 0, "atlas_url": "" }, { "name": "Huntington's disease", "type": "Disease", "description": "Neurodegenerative disease caused by a toxic polyglutamine-expanded protein; cleared via mTOR-inhibition-induced autophagy in animal models.", "description_beginner": "A brain disease caused by a faulty gene that makes a toxic, misshapen protein build up in neurons. In animal studies, drugs that block mTOR help cells clear this toxic protein out.", "synonyms": "", "n_linked_studies": 2, "atlas_url": "" }, { "name": "LARS (leucyl-tRNA synthetase)", "type": "Gene/Protein", "description": "Enzyme that charges tRNA with leucine, proposed as an alternative intracellular leucine sensor acting as a GAP for RagD. Competes with the Sestrin2 model - an unresolved question in the field.", "description_beginner": "An enzyme that loads the amino acid leucine onto its transport molecule (tRNA) so cells can build proteins. Some scientists think it might also work as a second sensor that tells mTORC1 when leucine is available - a rival idea to the more established Sestrin2 sensor, and the two ideas haven't been fully reconciled.", "synonyms": "", "n_linked_studies": 1, "atlas_url": "" }, { "name": "Bisphenol A", "type": "Nutrient/Metabolite", "description": "Ubiquitous environmental plasticiser that disrupts intestinal barrier function and mitochondrial metabolism, perturbing AMPK-mTOR signalling.", "description_beginner": "A chemical used to harden plastics that leaks in small amounts into food and drink. In animal studies it damages the gut lining and the mitochondria (the cell's power plants), which throws off the AMPK-mTOR balance cells use to match growth to available energy.", "synonyms": "", "n_linked_studies": 0, "atlas_url": "" }, { "name": "Pungenin", "type": "Drug", "description": "Phenolic glucoside from Picea wilsonii that promotes hair regrowth via transcriptional regulation of the PI3K/AKT/FoxO/mTOR axis.", "description_beginner": "A plant compound from a spruce tree, reported in lab studies to encourage hair regrowth. It appears to work by switching on the PI3K/AKT growth pathway that feeds into mTOR, telling hair-follicle cells it is time to grow again.", "synonyms": "", "n_linked_studies": 0, "atlas_url": "" }, { "name": "PIK3CA", "type": "Gene/Protein", "description": "Phosphatidylinositol 3-kinase catalytic subunit alpha; its activating mutations (e.g. E545K, H1047R) frequently drive AKT/mTOR pathway hyperactivation in cancer.", "description_beginner": "A gene that makes part of an enzyme (PI3K) sitting just upstream of mTOR. Certain switched-on mutations in this gene are one of the most common ways cancer cells hijack the AKT/mTOR pathway to keep growing.", "synonyms": "", "n_linked_studies": 1, "atlas_url": "" }, { "name": "Lysosome", "type": "Organelle", "description": "The organelle on whose surface mTORC1 is activated. Nutrient signals converge here: mTORC1 must be physically recruited to the lysosomal membrane before Rheb can switch it on.", "description_beginner": "A cell's recycling center and 'sensing station.' mTORC1 doesn't just float around the cell - it has to physically dock on the lysosome's surface before it can be switched on, so this is where a lot of the pathway's decision-making happens.", "synonyms": "", "n_linked_studies": 4, "atlas_url": "https://mtor-atlas.org/organelle/lysosome/" }, { "name": "Mitophagy", "type": "Biological process", "description": "Selective autophagic degradation of damaged or dysfunctional mitochondria; regulated by the AMPK-mTOR-ULK1 axis and implicated in cardiac protection, neurodegeneration, and aging.", "description_beginner": "The process of clearing out damaged mitochondria (the cell's power plants). It's controlled by the AMPK-mTOR-ULK1 signaling chain and may help protect the heart and brain as we age.", "synonyms": "", "n_linked_studies": 1, "atlas_url": "" }, { "name": "PRAS40", "type": "Gene/Protein", "description": "Insulin-regulated inhibitor subunit of mTORC1. Insulin triggers Akt to phosphorylate PRAS40, releasing its brake and switching mTORC1 on.", "description_beginner": "A brake on mTORC1 that insulin can release. When insulin signals arrive, a kinase called Akt tags this protein, which lets go of mTORC1 and allows it to switch on.", "synonyms": "", "n_linked_studies": 1, "atlas_url": "" }, { "name": "TSC1/TSC2", "type": "Gene/Protein", "description": "Tuberin-hamartin tumor suppressor complex; acts as a GTPase-activating protein for Rheb; integrates growth-factor and energy signals to control mTORC1.", "description_beginner": "A two-protein 'off switch' for mTORC1. It works like a brake pedal on the protein Rheb - when a cell lacks nutrients or growth signals, this complex clamps down on Rheb and keeps mTORC1 turned off.", "synonyms": "TSC1; TSC2; TSC1-TSC2; TSC complex; hamartin; tuberin", "n_linked_studies": 9, "atlas_url": "https://mtor-atlas.org/gene/tsc1-tsc2/" }, { "name": "Kynurenic acid", "type": "Nutrient/Metabolite", "description": "A tryptophan metabolite produced by tumor microbiota (e.g. Fusobacterium nucleatum); activates the ITGA2-mTOR-CTSV axis to suppress CD8+ T cell function and drive immunotherapy resistance.", "description_beginner": "A breakdown product of the amino acid tryptophan, made by bacteria that live inside some tumors. It switches on a signaling chain (through ITGA2 and mTOR) that weakens the immune system's T cells, helping tumors resist immunotherapy.", "synonyms": "", "n_linked_studies": 1, "atlas_url": "" }, { "name": "Autoimmune cytopenia", "type": "Disease", "description": "Immune-mediated destruction of blood cell lineages (including Evans syndrome and pure red cell aplasia) in which sirolimus is used as a T-cell-directed therapy.", "description_beginner": "A group of conditions in which the immune system attacks and destroys the body's own blood cells. Because rapamycin (sirolimus) calms overactive T cells, it is used as a treatment when the standard drugs do not work.", "synonyms": "", "n_linked_studies": 0, "atlas_url": "" }, { "name": "SGK1", "type": "Gene/Protein", "description": "Serum- and glucocorticoid-regulated kinase 1; a second major AGC kinase phosphorylated and activated by mTORC2 at its hydrophobic motif. Controls ion transport, cell survival, and glucose metabolism. mTORC2→SGK1 signaling is a key output branch of mTORC2 parallel to the mTORC2→Akt axis.", "description_beginner": "A signaling protein activated by mTORC2 (the second mTOR complex). It's a lesser-known cousin of Akt and helps control things like salt/water balance in cells, cell survival, and how cells handle sugar.", "synonyms": "", "n_linked_studies": 0, "atlas_url": "" }, { "name": "Spinal cord injury", "type": "Disease", "description": "Traumatic CNS injury in which AKT/mTOR-driven angiogenesis and neuronal survival are targets for functional recovery.", "description_beginner": "Physical damage to the spinal cord, which the body repairs very poorly. Researchers target the AKT-mTOR pathway here because it controls two things recovery depends on: growing new blood vessels, and whether damaged nerve cells survive at all.", "synonyms": "", "n_linked_studies": 0, "atlas_url": "" }, { "name": "HIF-1α", "type": "Gene/Protein", "description": "Hypoxia-inducible factor 1-alpha, the master transcription factor for metabolic and angiogenic responses to low oxygen, and an mTOR-independent target of rapamycin in aged tissue.", "description_beginner": "The master switch a cell flips when oxygen runs short. It turns on genes that build new blood vessels and that shift the cell to making energy without oxygen. Rapamycin lowers it partly through a route that does not run through mTOR - one of the clues that the drug does more than block a single kinase.", "synonyms": "", "n_linked_studies": 0, "atlas_url": "" }, { "name": "Lung transplant", "type": "Condition", "description": "Clinical setting in which mTOR inhibitors are used as antiproliferative, calcineurin-sparing immunosuppression, notably against chronic lung allograft dysfunction.", "description_beginner": "The situation after a donor lung is implanted, where the immune system has to be held back for life. mTOR inhibitors are used because they block rejection without the kidney damage the usual drugs cause, and may slow the gradual scarring that destroys transplanted lungs.", "synonyms": "", "n_linked_studies": 0, "atlas_url": "" }, { "name": "T cell differentiation", "type": "Biological process", "description": "Process by which immune T cells commit to effector versus regulatory fates; directly controlled by mTOR complex activity.", "description_beginner": "How immune T cells decide what kind of cell to become - an attacking (effector) cell or a peacekeeping (regulatory) cell. mTOR activity is one of the switches that helps make this decision.", "synonyms": "", "n_linked_studies": 1, "atlas_url": "" }, { "name": "eIF4E", "type": "Gene/Protein", "description": "Cap-binding protein that recruits the ribosome to an mRNA. Held hostage by 4E-BP1 until mTORC1 phosphorylates the latter - the rate-limiting step of cap-dependent translation.", "description_beginner": "A protein that grabs onto mRNA and starts the process of building a new protein from it. Normally it's held back by 4E-BP1; mTORC1 releases that hold, which is the key step that turns on protein production.", "synonyms": "", "n_linked_studies": 4, "atlas_url": "https://mtor-atlas.org/gene/eif4e/" }, { "name": "alpha-synuclein (SNCA)", "type": "Gene/Protein", "description": "Presynaptic protein whose misfolded aggregates form Lewy bodies in Parkinson's disease and related synucleinopathies. Cleared primarily by autophagy/chaperone-mediated autophagy; mTORC1 inhibition promotes its clearance while chronic pan-mTOR inhibition risks the mTORC2-dependent synaptic-plasticity cost noted in gap H8.", "description_beginner": "A protein found in nerve endings that can misfold and clump together, forming the toxic 'Lewy bodies' seen in Parkinson's disease. The cell's cleanup system (autophagy) normally clears it out, and turning mTORC1 down can boost that cleanup - though blocking mTOR long-term can also carry a cost for brain-cell signaling.", "synonyms": "", "n_linked_studies": 0, "atlas_url": "" }, { "name": "Torin1", "type": "Drug", "description": "ATP-competitive ('active-site') mTOR inhibitor. Unlike rapamycin, it blocks the kinase active site directly and so fully inhibits BOTH complexes - the tool that revealed rapamycin-resistant functions of mTORC1.", "description_beginner": "A lab-only drug that blocks mTOR directly at its 'engine room' (the active site), so - unlike rapamycin - it shuts down both mTOR complexes completely. It was a key tool for discovering what rapamycin-resistant mTOR functions look like.", "synonyms": "", "n_linked_studies": 1, "atlas_url": "" }, { "name": "Growth hormone / IGF-1 axis", "type": "Pathway/Complex", "description": "Upstream growth-signaling axis; reduced activity (as in Ames dwarf mice) is one of the most robust lifespan-extending interventions known in mammals, acting upstream of PI3K/Akt/mTOR.", "description_beginner": "A hormone signaling chain (growth hormone leads to IGF-1) that sits upstream of mTOR. Turning this axis down - as seen in naturally long-lived dwarf mice - is one of the most reliable ways scientists know to extend lifespan in mammals.", "synonyms": "", "n_linked_studies": 2, "atlas_url": "" }, { "name": "Cardiac aging", "type": "Outcome", "description": "Age-related decline in heart function (hypertrophy, stiffening, reduced contractility). Late-life rapamycin partially reverses it in mice.", "description_beginner": "The gradual decline in heart function with age - thicker heart muscle, stiffer walls, weaker pumping. In mice, giving rapamycin late in life partly reverses these changes.", "synonyms": "", "n_linked_studies": 1, "atlas_url": "" }, { "name": "Curcumin", "type": "Drug", "description": "Turmeric-derived polyphenol widely marketed for anti-aging effects; showed no lifespan effect in ITP testing.", "description_beginner": "The active compound in turmeric, widely sold as an anti-aging supplement. In a rigorous mouse lifespan study, it didn't actually extend lifespan.", "synonyms": "", "n_linked_studies": 1, "atlas_url": "" }, { "name": "Melittin", "type": "Drug", "description": "The main bioactive component of bee venom; suppresses PI3K/Akt/mTOR pathway and activates autophagy, showing anti-inflammatory effects in psoriasis models.", "description_beginner": "The main active ingredient in bee venom. In animal studies it dials down the PI3K/Akt/mTOR pathway and switches on autophagy (cellular self-cleaning), which calmed inflammation in a mouse model of the skin disease psoriasis.", "synonyms": "", "n_linked_studies": 1, "atlas_url": "" }, { "name": "PP242", "type": "Drug", "description": "An ATP-competitive mTOR kinase inhibitor (a 'TORKinib'); like Torin1, inhibits both mTORC1 and mTORC2 and blocks outputs that rapamycin leaves intact.", "description_beginner": "A lab tool drug, similar to Torin1, that blocks mTOR's active site directly. Like Torin1, it shuts down both mTOR complexes, unlike rapamycin which mainly hits one.", "synonyms": "", "n_linked_studies": 1, "atlas_url": "" }, { "name": "Longevity", "type": "Outcome", "description": "Lifespan extension; the key outcome tracked across mTOR-targeting interventions.", "description_beginner": "How long an organism lives - the single outcome most often measured across every mTOR-targeting intervention in this Atlas.", "synonyms": "", "n_linked_studies": 36, "atlas_url": "https://mtor-atlas.org/outcome/longevity/" }, { "name": "MCT oil", "type": "Drug", "description": "Medium-chain triglyceride oil; tested by the ITP as a metabolic/longevity intervention with no significant lifespan effect.", "description_beginner": "An oil made of medium-length fat molecules, tested as a metabolic/longevity supplement. It showed no meaningful effect on lifespan in formal testing.", "synonyms": "", "n_linked_studies": 1, "atlas_url": "" }, { "name": "Leucine/BCAA restriction", "type": "Intervention", "description": "Restriction of branched-chain amino acids (leucine, isoleucine, valine); modulates mTORC1 via the Sestrin2 sensor.", "description_beginner": "Cutting back on branched-chain amino acids - leucine, isoleucine and valine - from the diet. Leucine is one of the main nutrients that switches mTORC1 on, largely through the Sestrin2 sensor, so restricting it is one way researchers try to dial the pathway down.", "synonyms": "", "n_linked_studies": 1, "atlas_url": "" }, { "name": "IRS1 / IRS2", "type": "Gene/Protein", "description": "Insulin receptor substrate proteins 1 and 2; scaffold adaptors that couple the insulin/IGF-1 receptor to PI3K–Akt signaling. S6K1 (activated by mTORC1) phosphorylates and destabilizes IRS1/2, creating a negative feedback loop. Rapamycin blocks mTORC1/S6K1, relieving IRS1 inhibition and allowing paradoxical Akt re-activation — a critical consideration in the clinical use of rapalogs.", "description_beginner": "Adaptor proteins that relay signals from the insulin/IGF-1 receptor into the cell. mTORC1's downstream partner S6K1 tags them for breakdown as a feedback brake - part of why blocking mTOR can, paradoxically, make some insulin signaling more active.", "synonyms": "", "n_linked_studies": 0, "atlas_url": "" }, { "name": "Muscle growth", "type": "Biological process", "description": "mTORC1-dependent process of skeletal muscle fiber enlargement (hypertrophy); driven by growth factors and exercise, blocked by rapamycin.", "description_beginner": "The process by which muscle fibers get bigger (hypertrophy), driven by exercise and growth signals and requiring mTORC1 activity. Blocking mTORC1 blocks this growth response.", "synonyms": "", "n_linked_studies": 3, "atlas_url": "https://mtor-atlas.org/process/muscle-growth/" }, { "name": "Cognition", "type": "Outcome", "description": "Learning, memory and related brain function. mTOR inhibition can enhance cognition in young mice and blunt age-related cognitive decline.", "description_beginner": "Learning, memory, and related brain function. Turning mTOR down can sharpen thinking in young mice and may soften age-related mental decline, though the same drugs also carry real risks for brain-cell signaling.", "synonyms": "", "n_linked_studies": 1, "atlas_url": "" }, { "name": "Atg5", "type": "Gene/Protein", "description": "Core gene required for autophagosome formation; overexpressing it in mice is sufficient to extend lifespan on its own.", "description_beginner": "A core gene needed to build the membrane sacs (autophagosomes) that carry out cellular cleanup. Simply making mice produce more of it - without any drug - was enough to extend their lifespan.", "synonyms": "", "n_linked_studies": 1, "atlas_url": "" }, { "name": "PXR (NR1I2)", "type": "Gene/Protein", "description": "Pregnane X receptor, a xenobiotic-sensing nuclear receptor whose activation drives liver growth via the AKT-mTOR pathway.", "description_beginner": "A sensor in liver cells that detects foreign chemicals and drugs and switches on the genes needed to break them down. Turning it on also makes the liver grow, and that growth instruction is carried by the AKT-mTOR pathway.", "synonyms": "", "n_linked_studies": 0, "atlas_url": "" }, { "name": "KICSTOR", "type": "Pathway/Complex", "description": "A lysosomal scaffold complex (composed of KAPTIN, ITFG2, C12orf66, and SZT2) that recruits GATOR1 to the lysosomal surface. Required for amino-acid-deprivation-dependent suppression of mTORC1; without KICSTOR, GATOR1 cannot reach the Rag GTPases and mTORC1 remains inappropriately active during starvation.", "description_beginner": "A docking complex on the lysosome that helps station the GATOR1 'brake' where it can reach and switch off mTORC1. Without it, GATOR1 can't do its job, so mTORC1 stays on even when nutrients are scarce.", "synonyms": "", "n_linked_studies": 0, "atlas_url": "" }, { "name": "Lymphangioleiomyomatosis", "type": "Disease", "description": "LAM - a rare progressive cystic lung disease in women driven by inappropriate mTOR activation; sirolimus stabilizes lung function (MILES trial).", "description_beginner": "LAM - a rare lung disease, almost always in women, in which mTOR gets stuck in the 'on' position and slowly destroys healthy lung tissue with cysts. The mTOR-blocking drug sirolimus is a proven treatment that keeps lung function from declining further.", "synonyms": "", "n_linked_studies": 2, "atlas_url": "" }, { "name": "v-ATPase", "type": "Gene/Protein", "description": "Vacuolar H+-ATPase; senses lysosomal amino acids from the inside and relays the signal to Ragulator-Rag to activate mTORC1.", "description_beginner": "A proton pump on the lysosome that helps sense how many amino acids are inside, then passes that information along to the Ragulator-Rag system to help switch mTORC1 on.", "synonyms": "", "n_linked_studies": 1, "atlas_url": "" }, { "name": "P-glycoprotein (ABCB1)", "type": "Gene/Protein", "description": "Multidrug resistance efflux transporter encoded by ABCB1; selectively upregulated at the translational level by mTOR-eIF4A signaling under oxidative stress.", "description_beginner": "A pump on the cell surface that expels foreign chemicals, including many drugs - a major cause of drug resistance. Under oxidative stress, mTOR signaling can boost how much of this pump gets made.", "synonyms": "", "n_linked_studies": 1, "atlas_url": "" }, { "name": "ULK1", "type": "Gene/Protein", "description": "Initiator of autophagy; target of mTORC1 inhibition and AMPK activation.", "description_beginner": "The kick-starter protein for autophagy (cellular cleanup). mTORC1 normally holds it back; when mTORC1 is switched off (or AMPK switches on), it's released and cleanup begins.", "synonyms": "", "n_linked_studies": 5, "atlas_url": "https://mtor-atlas.org/gene/ulk1/" }, { "name": "ITGA2 (Integrin alpha-2)", "type": "Gene/Protein", "description": "Integrin subunit alpha-2; found to mediate kynurenic acid-driven mTOR activation in the ITGA2-mTOR-CTSV immunotherapy resistance axis in gastric cancer.", "description_beginner": "A cell-surface protein (part of an integrin receptor) that picks up the kynurenic acid signal from tumor bacteria and passes it on to activate mTOR - part of a chain that helps gastric cancer resist immunotherapy.", "synonyms": "", "n_linked_studies": 1, "atlas_url": "" }, { "name": "TFEB", "type": "Gene/Protein", "description": "Master transcription factor for lysosome biogenesis and autophagy. mTORC1 phosphorylates TFEB to trap it in the cytosol; when mTORC1 is off, TFEB enters the nucleus and turns on the cell's recycling program.", "description_beginner": "The master control switch for making new lysosomes and ramping up cellular cleanup. mTORC1 normally keeps it locked out of the nucleus; once mTORC1 turns off, it moves in and switches on the cell's recycling genes.", "synonyms": "", "n_linked_studies": 4, "atlas_url": "https://mtor-atlas.org/gene/tfeb/" }, { "name": "Cisplatin", "type": "Drug", "description": "Platinum-based chemotherapeutic whose tolerance is modulated by mTOR-dependent cytoprotective autophagy.", "description_beginner": "A platinum-based chemotherapy drug that kills cancer cells by damaging their DNA. Cells can survive it by switching on autophagy - digesting their own parts for spare material - and because mTOR controls autophagy, blocking or boosting mTOR changes how well the drug works.", "synonyms": "", "n_linked_studies": 0, "atlas_url": "" }, { "name": "SIN1 / MAPKAP1", "type": "Gene/Protein", "description": "Essential structural subunit of mTORC2 (stress-activated protein kinase-interacting protein 1). Required for mTORC2 assembly and integrity; controls the substrate specificity of mTORC2 toward Akt and other AGC kinases. Prolonged rapamycin treatment can disrupt SIN1-containing mTORC2, explaining chronic-rapamycin-induced impairment of Akt signaling.", "description_beginner": "A structural building block that mTORC2 (the second mTOR complex) needs in order to assemble and work properly. Long-term rapamycin use can eventually break apart mTORC2 that contains it, part of why chronic rapamycin can dull Akt signaling.", "synonyms": "SIN1; mSIN1; MAPKAP1", "n_linked_studies": 0, "atlas_url": "" }, { "name": "Rapamycin", "type": "Drug", "description": "Sirolimus; mTORC1 inhibitor (and, with chronic dosing, mTORC2 too); immunosuppressant; extends lifespan in mice.", "description_beginner": "Also called sirolimus. The original mTOR-blocking drug (mainly hits mTORC1, and mTORC2 too with long-term use). Used to prevent organ-transplant rejection, and the single most reliable drug known for extending lifespan in mice.", "synonyms": "Sirolimus; RAPA; AY-22989\n\nPozn.: Sirolimus je mezinárodní nechráněný název (INN) téže látky — v klinických studiích převažuje, v základním výzkumu 'rapamycin'.", "n_linked_studies": 38, "atlas_url": "https://mtor-atlas.org/drug/rapamycin/" }, { "name": "Oxaloacetic acid", "type": "Drug", "description": "Metabolic intermediate marketed as a longevity supplement; no lifespan effect found in ITP testing.", "description_beginner": "A natural metabolic molecule sold as a longevity supplement. Formal mouse testing found no lifespan benefit.", "synonyms": "", "n_linked_studies": 1, "atlas_url": "" }, { "name": "Forsythoside A", "type": "Drug", "description": "Phenylethanoid glycoside from Forsythiae Fructus that binds ASCL1 and blocks a downstream CCNB1/mTOR axis.", "description_beginner": "A compound from forsythia fruit, long used in traditional medicine. In lab work it sticks to the ASCL1 protein and shuts down a signalling chain that runs from there through CCNB1 to mTOR.", "synonyms": "", "n_linked_studies": 0, "atlas_url": "" }, { "name": "FoxO", "type": "Gene/Protein", "description": "Forkhead box O transcription factors (FOXO1/3/4) that act as key downstream targets of mTORC1/Akt signalling; phosphorylation by Akt excludes them from the nucleus, while mTORC1 inhibition promotes nuclear translocation and transcription of stress-response and longevity genes.", "description_beginner": "A family of 'stress-response' gene switches that Akt normally keeps locked out of the nucleus. When mTORC1/Akt signaling drops, they move into the nucleus and turn on genes linked to stress resistance and longevity.", "synonyms": "", "n_linked_studies": 3, "atlas_url": "https://mtor-atlas.org/gene/foxo/" }, { "name": "Mitochondrial biogenesis", "type": "Biological process", "description": "Production of new mitochondria and their oxidative machinery. mTORC1 drives it via a YY1-PGC-1alpha transcriptional program, linking growth signaling to energy production.", "description_beginner": "Building new mitochondria - a cell's power plants. mTORC1 drives this process through a genetic program, linking growth signals directly to how much energy-making machinery a cell has.", "synonyms": "", "n_linked_studies": 1, "atlas_url": "" }, { "name": "Renal cell carcinoma (RCC)", "type": "Disease", "description": "Cancer of the kidney; target indication for everolimus treatment in clinical practice.", "description_beginner": "The most common form of kidney cancer. It's an approved use for the mTOR-blocking drug everolimus in clinical practice.", "synonyms": "", "n_linked_studies": 3, "atlas_url": "https://mtor-atlas.org/disease/renal-cell-carcinoma-rcc/" }, { "name": "eIF4A", "type": "Gene/Protein", "description": "ATP-dependent RNA helicase that unwinds 5' mRNA secondary structures; activated downstream of mTORC1 to promote selective cap-dependent translation initiation.", "description_beginner": "A protein 'motor' that unwinds tangled sections of mRNA so the cell's protein-building machinery can read through them. mTORC1 activity switches this motor on to help build proteins faster.", "synonyms": "", "n_linked_studies": 1, "atlas_url": "" }, { "name": "Rictor", "type": "Gene/Protein", "description": "Defining subunit of mTORC2 (Rapamycin-Insensitive Companion of mTOR); routes mTOR toward Akt and the cytoskeleton rather than S6K1/4E-BP1.", "description_beginner": "The defining building block of mTORC2 (the second mTOR complex) - without it, you don't have mTORC2. It steers mTOR signaling toward Akt and the cell's internal skeleton rather than toward growth/protein-building.", "synonyms": "rictor; RICTOR; AVO3", "n_linked_studies": 3, "atlas_url": "https://mtor-atlas.org/gene/rictor/" }, { "name": "Prostate cancer", "type": "Disease", "description": "Cancer in which oncogenic mTOR signaling reprograms the cell's translation to drive proliferation, invasion and metastasis.", "description_beginner": "A cancer in which mTOR signaling gets hijacked to rev up a tumor's protein-building machinery, helping it grow, invade nearby tissue, and spread.", "synonyms": "", "n_linked_studies": 1, "atlas_url": "" }, { "name": "mLST8", "type": "Gene/Protein", "description": "mLST8 (GbetaL) - a shared subunit of BOTH mTOR complexes. Especially required for mTORC2 to assemble and signal to Akt; largely dispensable for mTORC1.", "description_beginner": "A small building block shared by both mTOR complexes, but it matters much more for mTORC2 - without it, mTORC2 can't properly assemble and signal to Akt, while mTORC1 mostly works fine without it.", "synonyms": "", "n_linked_studies": 2, "atlas_url": "" }, { "name": "Ferroptosis", "type": "Biological process", "description": "Iron-dependent, lipid-peroxidation-driven regulated cell death that is modulated by mTOR signalling and autophagy.", "description_beginner": "A distinct way for a cell to die: iron inside the cell sets off a chain reaction that shreds the fatty membranes holding it together. It is not the tidy, programmed suicide most cells use, and both mTOR signalling and autophagy change how easily it happens.", "synonyms": "", "n_linked_studies": 0, "atlas_url": "" }, { "name": "SLC7A5 (LAT1)", "type": "Gene/Protein", "description": "Large neutral amino acid transporter 1, which imports leucine and is a key upstream input into mTORC1 nutrient sensing.", "description_beginner": "A doorway in the cell membrane that carries large amino acids, leucine among them, into the cell. Since mTORC1 measures leucine to judge whether there is enough raw material to grow, this transporter is one of the taps feeding that decision.", "synonyms": "", "n_linked_studies": 0, "atlas_url": "" }, { "name": "Placental nutrient sensing", "type": "Biological process", "description": "Placental mTORC1-dependent regulation of amino acid transport and mitochondrial respiration that sets fetal growth trajectory.", "description_beginner": "How the placenta decides how much nourishment to pass from mother to fetus. mTORC1 inside placental cells reads the mother's nutrient supply and adjusts the amino-acid transporters accordingly, which helps set how big the baby grows.", "synonyms": "", "n_linked_studies": 0, "atlas_url": "" }, { "name": "LC3B (MAP1LC3B)", "type": "Gene/Protein", "description": "Key autophagosome membrane marker; lipidation of LC3B (LC3-II) is induced when mTOR is inhibited and marks autophagy induction.", "description_beginner": "A protein that gets attached to the membrane of autophagosomes (cellular cleanup sacs) - scientists use it as a marker to see autophagy happening. It shows up more when mTOR is blocked.", "synonyms": "", "n_linked_studies": 1, "atlas_url": "" }, { "name": "Raptor", "type": "Gene/Protein", "description": "Defining subunit of mTORC1; scaffold that presents substrates (S6K1, 4E-BP1) to mTOR. Its presence is what makes a complex 'mTORC1'.", "description_beginner": "The defining building block of mTORC1 - it's what makes an mTOR complex 'mTORC1' rather than mTORC2. It acts as a scaffold that presents mTORC1's targets (like S6K1 and 4E-BP1) to the mTOR enzyme.", "synonyms": "raptor; RPTOR; KOG1", "n_linked_studies": 7, "atlas_url": "https://mtor-atlas.org/gene/raptor/" }, { "name": "Astragaloside IV", "type": "Drug", "description": "Bioactive saponin from Astragalus membranaceus that inhibits mTOR to activate TFEB-mediated autophagy, protecting against tacrolimus-induced nephrotoxicity.", "description_beginner": "A compound from the astragalus root. It blocks mTOR to switch on TFEB-driven cellular cleanup, which in animal studies helped protect kidneys from a drug-induced toxicity.", "synonyms": "", "n_linked_studies": 1, "atlas_url": "" }, { "name": "mTOR", "type": "Gene/Protein", "description": "Serine/threonine kinase; central regulator of cell growth and metabolism; direct target of rapamycin.", "description_beginner": "The central enzyme this whole Atlas is about - short for 'mechanistic target of rapamycin.' It's a master switch that senses nutrients and growth signals and decides whether a cell should grow, build new proteins, and skip its cleanup routines, or hold back and recycle.", "synonyms": "MTOR; mechanistic target of rapamycin; mammalian target of rapamycin; FRAP1; TOR; dTOR\n\nPozn.: TOR (kvasinky, Drosophila) je ortholog, ne synonymum v úzkém smyslu. Veden tu záměrně, aby zakládající práce (HEI1991, VEZ1975) byly dohledatelné pod mTOR.", "n_linked_studies": 63, "atlas_url": "https://mtor-atlas.org/gene/mtor/" }, { "name": "5'TOP mRNA", "type": "Biological process", "description": "Class of mRNAs with a 5' terminal oligopyrimidine tract encoding ribosomal proteins and translation factors; their translation is a canonical output of mTORC1 signaling.", "description_beginner": "A group of messenger RNAs (the templates cells read to build proteins) that mostly encode the protein-building machinery itself. Turning their translation on is one of mTORC1's classic, best-established jobs.", "synonyms": "", "n_linked_studies": 2, "atlas_url": "" }, { "name": "Lipid synthesis", "type": "Biological process", "description": "De novo synthesis of fatty acids and cholesterol via SREBP. A growing cell needs membrane as much as it needs protein; both mTOR complexes feed this.", "description_beginner": "Building new fats and cholesterol from scratch, mainly through a genetic switch called SREBP. A growing cell needs new membranes just as much as new proteins, and both mTOR complexes help fuel this.", "synonyms": "", "n_linked_studies": 4, "atlas_url": "https://mtor-atlas.org/process/lipid-synthesis/" }, { "name": "Corilagin", "type": "Drug", "description": "Natural ellagitannin with anti-inflammatory activity that inhibits PI3K/AKT/mTOR and NF-κB signalling and restores autophagy.", "description_beginner": "A plant compound (a tannin) found in several medicinal herbs. In lab studies it calms inflammation by blocking both PI3K/AKT/mTOR and NF-κB signalling, and it restores autophagy, the cell's recycling process.", "synonyms": "", "n_linked_studies": 0, "atlas_url": "" }, { "name": "Arginine", "type": "Nutrient/Metabolite", "description": "Essential amino acid sensed by two separate routes: cytosolic arginine binds CASTOR1, and lysosomal arginine is read by the transporter-like protein SLC38A9.", "description_beginner": "An essential amino acid the cell senses through two separate paths - a sensor inside the cell (CASTOR1) reads free-floating arginine, while a transporter-like protein on the lysosome (SLC38A9) reads arginine stored inside the lysosome.", "synonyms": "", "n_linked_studies": 5, "atlas_url": "https://mtor-atlas.org/nutrient/arginine/" }, { "name": "Macrophage polarization", "type": "Biological process", "description": "The M1/M2 phenotypic switch in macrophages, an immunometabolic decision governed substantially by PI3K/AKT/mTOR signalling.", "description_beginner": "Macrophages are immune cells that can take on opposite jobs: attacking invaders (M1) or cleaning up and repairing tissue (M2). Which one they become depends heavily on how they burn fuel, and PI3K/AKT/mTOR signalling is a main controller of that choice.", "synonyms": "", "n_linked_studies": 0, "atlas_url": "" }, { "name": "FGF21", "type": "Gene/Protein", "description": "Fibroblast growth factor 21, a metabolic hormone that activates AMPK/mTOR signaling to regulate glucose metabolism and wound healing.", "description_beginner": "A hormone released mostly by the liver that helps regulate blood sugar and metabolism. It works partly by activating the AMPK/mTOR signaling chain, and has also been shown to help wounds heal.", "synonyms": "", "n_linked_studies": 1, "atlas_url": "" }, { "name": "Atrial fibrillation", "type": "Disease", "description": "The most common age-related cardiac arrhythmia, driven by atrial electrical and structural remodelling.", "description_beginner": "The most common irregular heartbeat, and one that becomes far more likely with age. The heart's upper chambers change electrically and become scarred, so instead of a clean beat they quiver out of rhythm.", "synonyms": "", "n_linked_studies": 0, "atlas_url": "" }, { "name": "Lung cancer (NSCLC/LUAD)", "type": "Disease", "description": "Non-small cell lung cancer including lung adenocarcinoma, in which PI3K-AKT-mTOR and mTORC2 signalling are frequently dysregulated.", "description_beginner": "The most common form of lung cancer, including the adenocarcinoma subtype. The PI3K-AKT-mTOR growth pathway is often stuck in the 'on' position in these tumours, which is why mTOR is studied as a target here.", "synonyms": "", "n_linked_studies": 0, "atlas_url": "" }, { "name": "GATOR2", "type": "Pathway/Complex", "description": "Positive arm that inhibits GATOR1; the target through which amino acid sensors (Sestrin2, CASTOR1) relay their signal to mTORC1.", "description_beginner": "A relay switch that reactivates mTORC1. Amino-acid sensors like Sestrin2 and CASTOR1 work by inhibiting it (when nutrients are scarce) or releasing it (when nutrients return), and it in turn keeps GATOR1 - mTORC1's main brake - in check.", "synonyms": "", "n_linked_studies": 2, "atlas_url": "" }, { "name": "Integrated stress response", "type": "Pathway/Complex", "description": "Conserved response to unfolded protein, amino-acid and other stresses. Reaches mTORC1 by routes independent of both TSC and AMPK.", "description_beginner": "The cell's general-purpose alarm system for problems like misfolded proteins or amino-acid shortage. It can reach and suppress mTORC1 through routes that don't go through the two other main brakes, TSC or AMPK.", "synonyms": "", "n_linked_studies": 1, "atlas_url": "" }, { "name": "Simvastatin", "type": "Drug", "description": "Cholesterol-lowering statin; tested as a candidate longevity drug in the same ITP cohort as rapamycin but showed no lifespan effect.", "description_beginner": "A cholesterol-lowering statin drug that was tested alongside rapamycin in the same large mouse longevity study. Unlike rapamycin, it showed no effect on lifespan.", "synonyms": "", "n_linked_studies": 1, "atlas_url": "" }, { "name": "Parkinson's disease", "type": "Disease", "description": "Neurodegenerative disease marked by loss of dopaminergic neurons and accumulation of misfolded alpha-synuclein (Lewy bodies). mTORC1 hyperactivity suppresses the autophagy that would clear alpha-synuclein aggregates; rapamycin enhances their autophagic clearance in animal models. Relevant to gap H8 (brain-penetrant mTOR inhibition for aggregate clearance).", "description_beginner": "A brain disease caused by loss of dopamine-producing neurons and buildup of a misfolded protein (alpha-synuclein) into Lewy bodies. Overactive mTORC1 blocks the cellular cleanup that would normally clear this protein out; rapamycin can restore that clearance in animal models.", "synonyms": "", "n_linked_studies": 0, "atlas_url": "" }, { "name": "Everolimus", "type": "Drug", "description": "Rapamycin analog (RAD001); used in oncology and tested for immune function in older adults.", "description_beginner": "A modified version of rapamycin. Used in cancer treatment and also studied for boosting immune responses in older adults.", "synonyms": "", "n_linked_studies": 14, "atlas_url": "https://mtor-atlas.org/drug/everolimus/" }, { "name": "Acarbose", "type": "Drug", "description": "Alpha-glucosidase inhibitor (diabetes drug) that slows carbohydrate absorption; found by the ITP to extend mouse lifespan, especially in males.", "description_beginner": "A diabetes drug that slows carbohydrate absorption in the gut. In a large mouse study it extended lifespan, especially in males, working mostly through a route separate from mTOR.", "synonyms": "", "n_linked_studies": 1, "atlas_url": "" }, { "name": "Grb10", "type": "Gene/Protein", "description": "mTORC1 substrate that, once phosphorylated, damps insulin/IGF-1 receptor signalling - one arm of the negative feedback that makes mTOR inhibitors paradoxically raise upstream Akt activity.", "description_beginner": "A protein that mTORC1 activates as part of a feedback loop - once switched on, it dials down signaling from the insulin/IGF-1 receptor. It's one reason mTOR inhibitors can paradoxically boost upstream Akt activity.", "synonyms": "", "n_linked_studies": 2, "atlas_url": "" }, { "name": "PTEN", "type": "Gene/Protein", "description": "Phosphatase that erases PIP3 and so shuts down the PI3K arm. One of the most frequently lost tumour suppressors in human cancer, and the commonest way this pathway gets stuck on.", "description_beginner": "A tumor-suppressing enzyme that erases the 'go' signal generated by PI3K, shutting that branch of the pathway down. It's one of the genes most frequently lost in human cancer, and losing it is a common way this pathway gets stuck switched on.", "synonyms": "", "n_linked_studies": 2, "atlas_url": "" }, { "name": "PDCD4", "type": "Gene/Protein", "description": "Translation inhibitor that blocks the eIF4A helicase. S6K1 marks it for degradation, giving mTORC1 a second, 4E-BP-independent route to raising protein synthesis.", "description_beginner": "A protein that blocks the translation helper eIF4A. mTORC1's downstream partner S6K1 tags it for destruction, giving the pathway a second way - separate from 4E-BP1 - to boost protein production.", "synonyms": "", "n_linked_studies": 1, "atlas_url": "" }, { "name": "Immune function", "type": "Outcome", "description": "Function of the immune system, especially vaccine response; improved by low-dose everolimus in older adults.", "description_beginner": "How well the immune system works, especially how strongly it responds to vaccines. Low-dose everolimus has improved this in older adults in some clinical trials.", "synonyms": "", "n_linked_studies": 5, "atlas_url": "https://mtor-atlas.org/outcome/immune-function/" }, { "name": "Glutamine", "type": "Nutrient/Metabolite", "description": "Most abundant free amino acid; activates mTORC1 partly through glutaminolysis and, in some settings, through a Rag-independent Arf1 route - one of the clearest examples that 'amino acid sensing' is not a single mechanism.", "description_beginner": "The most abundant free amino acid in the body. It switches on mTORC1 partly by being broken down for fuel and, in some cell types, through a completely separate route that skips the usual Rag-GTPase sensors - a reminder that 'amino acid sensing' isn't just one single mechanism.", "synonyms": "", "n_linked_studies": 2, "atlas_url": "" }, { "name": "MRPS17", "type": "Gene/Protein", "description": "Mitochondrial ribosomal protein S17, upregulated in lung adenocarcinoma where it activates PI3K-AKT-mTOR signalling.", "description_beginner": "A building block of the ribosomes inside mitochondria - the little machines that make proteins for the cell's power plants. It is present at unusually high levels in lung adenocarcinoma, where it switches on PI3K-AKT-mTOR growth signalling.", "synonyms": "", "n_linked_studies": 0, "atlas_url": "" }, { "name": "ErbB3 (HER3)", "type": "Gene/Protein", "description": "Receptor tyrosine kinase that is one of the most potent upstream activators of PI3K/AKT/mTOR signalling.", "description_beginner": "A receiver sitting on the cell surface that catches growth signals from outside. It is one of the strongest known switches for the PI3K/AKT/mTOR pathway, which is why tumours so often exploit it.", "synonyms": "", "n_linked_studies": 0, "atlas_url": "" }, { "name": "Breast cancer", "type": "Disease", "description": "Hormone-receptor-positive advanced breast cancer becomes resistant to endocrine therapy partly by activating mTOR; adding the rapalog everolimus re-sensitizes it (BOLERO-2).", "description_beginner": "Hormone-driven advanced breast cancer can become resistant to standard hormone therapy partly by switching on mTOR signaling as a workaround. Adding the mTOR-blocking drug everolimus can make the cancer sensitive to hormone therapy again.", "synonyms": "", "n_linked_studies": 3, "atlas_url": "https://mtor-atlas.org/disease/breast-cancer/" }, { "name": "Pancreatic neuroendocrine tumor", "type": "Disease", "description": "Pancreatic neuroendocrine tumor - a cancer where mTOR drives growth; everolimus more than doubled progression-free survival (RADIANT-3), an FDA-approved indication.", "description_beginner": "A type of pancreatic cancer driven partly by mTOR signaling. Everolimus more than doubled the time before the tumor progressed in a major clinical trial, and it's now an approved treatment.", "synonyms": "", "n_linked_studies": 1, "atlas_url": "" }, { "name": "USP7", "type": "Gene/Protein", "description": "Ubiquitin-specific protease 7, a deubiquitinase that modulates the TSC1/mTOR axis and promotes renal fibrosis via stabilization of KDM5B.", "description_beginner": "An enzyme that removes a 'degrade-me' tag (ubiquitin) from other proteins, protecting them from being broken down. By stabilizing one such protein (KDM5B), it silences TSC1 and activates mTOR - a chain that promotes kidney scarring (fibrosis) in mouse models of kidney disease.", "synonyms": "", "n_linked_studies": 1, "atlas_url": "" }, { "name": "Metformin", "type": "Drug", "description": "Antidiabetic biguanide; activates AMPK (ZHO2001) and inhibits mTORC1. How much of its action actually runs through AMPK is disputed: metformin still suppresses hepatic gluconeogenesis in AMPK-null and LKB1-null mouse liver (FOR2010) and still inhibits mTORC1 in AMPK-null cells, via the Rag GTPases (KAL2010). Frequently discussed as a geroprotector alongside rapamycin.", "description_beginner": "A widely used diabetes drug that switches on AMPK and, through that, dials down mTORC1. Exactly how much of its effect runs through AMPK versus other routes is still debated - it still works in cells that lack AMPK entirely. It's often discussed as a possible longevity drug alongside rapamycin.", "synonyms": "", "n_linked_studies": 3, "atlas_url": "https://mtor-atlas.org/drug/metformin/" }, { "name": "SAMTOR", "type": "Gene/Protein", "description": "Sensor of S-adenosylmethionine (SAM), linking methionine / one-carbon metabolism to mTORC1 via GATOR1.", "description_beginner": "A sensor for S-adenosylmethionine (SAM), a molecule that reports how much of the amino acid methionine is available. It links methionine metabolism to mTORC1 through the GATOR1 brake.", "synonyms": "", "n_linked_studies": 2, "atlas_url": "" }, { "name": "p62/SQSTM1", "type": "Gene/Protein", "description": "Autophagy cargo receptor and mTORC1-activating scaffold on lysosomes; elevated p62 accumulation indicates impaired autophagic flux.", "description_beginner": "A protein that both helps mTORC1 switch on at the lysosome and gets swept up and destroyed during cellular cleanup (autophagy). When autophagy isn't working properly, it piles up - so scientists use it as a marker of blocked cleanup.", "synonyms": "", "n_linked_studies": 3, "atlas_url": "https://mtor-atlas.org/gene/p62-sqstm1/" }, { "name": "FKBP12", "type": "Gene/Protein", "description": "Rapamycin's docking protein. Rapamycin first binds FKBP12; only the FKBP12-rapamycin pair can grab mTOR. This is why rapamycin is an 'allosteric' (indirect) inhibitor - it works through a chaperone, not by blocking the active site.", "description_beginner": "The 'docking protein' rapamycin needs to work. Rapamycin first grabs onto this protein, and only that combined pair can then latch onto and block mTOR - which is why rapamycin is called an indirect ('allosteric') inhibitor rather than one that blocks mTOR's active site directly.", "synonyms": "", "n_linked_studies": 2, "atlas_url": "" }, { "name": "Leucine", "type": "Nutrient/Metabolite", "description": "Branched-chain essential amino acid and the best-characterised nutrient input to mTORC1. Free leucine binds Sestrin2, releasing the GATOR2 brake; a competing model has leucyl-tRNA synthetase as the sensor instead.", "description_beginner": "An essential amino acid and the best-understood dietary trigger for mTORC1. Free leucine binds to the sensor Sestrin2, releasing its brake on GATOR2; a rival idea says the real sensor is actually an enzyme called leucyl-tRNA synthetase (LARS) instead.", "synonyms": "", "n_linked_studies": 5, "atlas_url": "https://mtor-atlas.org/nutrient/leucine/" }, { "name": "Rag GTPases", "type": "Gene/Protein", "description": "Family of small GTPases that let mTORC1 sense amino acids by controlling its localization near its activator Rheb inside the cell.", "description_beginner": "A family of small molecular switches that let mTORC1 sense amino acids by controlling where inside the cell it's allowed to sit - specifically, whether it can get close enough to its activator Rheb.", "synonyms": "Rag; Rag GTPase; RagA; RagB; RagC; RagD; RagA/B; RRAGA; RRAGB", "n_linked_studies": 5, "atlas_url": "https://mtor-atlas.org/gene/rag-gtpases/" }, { "name": "Alzheimer's disease", "type": "Disease", "description": "Neurodegenerative disease marked by amyloid-beta plaques and tau tangles. mTOR overactivation blocks the autophagy that would clear these toxic proteins; rapamycin restores clearance in mouse models.", "description_beginner": "A brain disease marked by sticky amyloid-beta plaques and tangled tau protein. Overactive mTOR blocks the cellular cleanup that would normally clear these toxic proteins out; rapamycin restores that clearance in mouse models.", "synonyms": "", "n_linked_studies": 3, "atlas_url": "https://mtor-atlas.org/disease/alzheimers-disease/" }, { "name": "Caloric restriction", "type": "Intervention", "description": "Reduced caloric intake without malnutrition; associated with lifespan extension across species.", "description_beginner": "Eating meaningfully fewer calories without becoming malnourished. It's linked to longer lifespan across many species and is one of the classic ways researchers dial down mTOR signaling through diet.", "synonyms": "", "n_linked_studies": 4, "atlas_url": "https://mtor-atlas.org/intervention/caloric-restriction/" }, { "name": "CASTOR1", "type": "Gene/Protein", "description": "Direct cytosolic arginine sensor for the mTORC1 pathway; arginine binding releases its inhibition of GATOR2.", "description_beginner": "A sensor inside the cell that directly detects the amino acid arginine. When arginine binds it, it releases its grip on GATOR2, allowing mTORC1 signaling to proceed.", "synonyms": "", "n_linked_studies": 1, "atlas_url": "" }, { "name": "cGAS-STING pathway", "type": "Pathway/Complex", "description": "An innate immune sensing pathway triggered by cytosolic DNA; drives inflammatory senescence signaling and is activated downstream of mTOR dysfunction in aging immune cells.", "description_beginner": "An immune alarm system that detects DNA where it shouldn't be (in the cell's main fluid, not the nucleus). It drives inflammatory 'senescence' signaling and gets switched on when mTOR signaling goes wrong in aging immune cells.", "synonyms": "", "n_linked_studies": 1, "atlas_url": "" }, { "name": "Akt/PKB", "type": "Gene/Protein", "description": "Key kinase downstream of PI3K in growth signaling; activated by mTORC2.", "description_beginner": "A key signaling kinase that sits downstream of PI3K and is switched on by mTORC2. It's one of the cell's central 'growth is good, keep going' signals.", "synonyms": "Akt; AKT; AKT1; PKB; protein kinase B; Akt Ser473; phospho-Akt S473\n\nPozn.: 'Akt Ser473' je fosforylační místo, ne samostatná entita — vedeno jako synonymum, aby se studie o něm navázaly sem.", "n_linked_studies": 13, "atlas_url": "https://mtor-atlas.org/gene/akt-pkb/" }, { "name": "SLC15A3", "type": "Gene/Protein", "description": "A lysosomal dipeptide transporter that imports dipeptides to sustain mTORC1 activation and can confer antimetabolite chemotherapy resistance in lymphoma.", "description_beginner": "A transporter on the lysosome that imports small protein fragments to help keep mTORC1 switched on. In lymphoma, this can also help cancer cells resist certain chemotherapy drugs.", "synonyms": "", "n_linked_studies": 1, "atlas_url": "" }, { "name": "TNKS2 (Tankyrase-2)", "type": "Gene/Protein", "description": "Tankyrase-2, a PARP family enzyme; its loss activates AMPK and suppresses mTORC1, impairing adipocyte differentiation.", "description_beginner": "An enzyme related to the PARP family. Removing it switches on the AMPK brake and dials down mTORC1, which in mice blocks fat cells (adipocytes) from maturing properly.", "synonyms": "", "n_linked_studies": 1, "atlas_url": "" }, { "name": "Cellular senescence", "type": "Biological process", "description": "State in which a cell permanently stops dividing but stays alive, secreting inflammatory signals (the SASP). Senescent cells accumulate with age and drive age-related disease. mTOR both promotes the senescent state and powers its inflammatory secretions.", "description_beginner": "A state where a cell permanently stops dividing but stays alive and starts pumping out inflammatory signals. These 'zombie cells' build up with age and drive age-related disease; mTOR both helps push cells into this state and powers the inflammatory signals they release.", "synonyms": "", "n_linked_studies": 3, "atlas_url": "https://mtor-atlas.org/process/cellular-senescence/" }, { "name": "TBC1D7", "type": "Gene/Protein", "description": "Third constitutive subunit of the TSC complex; its loss weakens but does not abolish TSC1-TSC2 function.", "description_beginner": "A third, less essential building block of the TSC brake complex. Losing it weakens the TSC1/TSC2 brake on mTORC1 but doesn't fully knock it out.", "synonyms": "", "n_linked_studies": 1, "atlas_url": "" }, { "name": "PI3K", "type": "Gene/Protein", "description": "Phosphoinositide 3-kinase; produces signaling lipids downstream of growth-factor receptors; activates Akt and sits upstream of the entire mTOR pathway.", "description_beginner": "An enzyme that produces signaling lipids right after a growth-factor receptor is switched on. It activates Akt and sits at the very top of the whole mTOR pathway, upstream of everything else.", "synonyms": "", "n_linked_studies": 6, "atlas_url": "https://mtor-atlas.org/gene/pi3k/" }, { "name": "Sestrin2", "type": "Gene/Protein", "description": "Direct intracellular leucine sensor and a NEGATIVE regulator of mTORC1. When leucine is scarce, Sestrin2 binds and inhibits GATOR2, so GATOR1 stays active and keeps mTORC1 switched off. Leucine binding (~20 uM affinity) releases GATOR2 - the pathway is switched on by removing a brake, not by adding a signal. Sestrin2 does not act on the Rag GTPases directly; it works two steps upstream, through GATOR2 and GATOR1.", "description_beginner": "The main sensor that directly detects leucine inside the cell, and a brake on mTORC1. When leucine is scarce, it holds down GATOR2, which keeps GATOR1 active and mTORC1 switched off. Leucine coming back releases GATOR2, so this is a brake being lifted, not a new 'go' signal being added - and it works two steps upstream of the Rag GTPases, not directly on them.", "synonyms": "", "n_linked_studies": 2, "atlas_url": "" }, { "name": "mTORC1", "type": "Pathway/Complex", "description": "mTOR Complex 1; regulates protein synthesis, autophagy, and growth in response to nutrients and growth factors.", "description_beginner": "The first of the two mTOR complexes, and the one most people mean when they just say 'mTOR.' It controls protein-building, cellular cleanup, and growth in response to nutrients and growth-factor signals.", "synonyms": "TORC1; mTOR complex 1; mTOR complex-1", "n_linked_studies": 78, "atlas_url": "https://mtor-atlas.org/complex/mtorc1/" }, { "name": "DEPTOR", "type": "Gene/Protein", "description": "Endogenous inhibitor of both mTORC1 and mTORC2; paradoxically overexpressed in a subset of multiple myelomas.", "description_beginner": "A natural brake on both mTOR complexes at once. Oddly, some multiple myeloma (bone marrow cancer) cells make extra amounts of it despite it being an inhibitor - a paradox that isn't fully explained.", "synonyms": "", "n_linked_studies": 1, "atlas_url": "" }, { "name": "Kidney transplant", "type": "Outcome", "description": "Original and still-standard clinical use of rapamycin (as sirolimus), preventing organ rejection by suppressing T cell activation.", "description_beginner": "The original medical use of rapamycin: preventing the immune system from rejecting a transplanted organ by suppressing T-cell activation.", "synonyms": "", "n_linked_studies": 1, "atlas_url": "" }, { "name": "SREBP1 / SREBP2", "type": "Gene/Protein", "description": "Sterol regulatory element-binding proteins 1 and 2; master transcription factors for de novo lipid and cholesterol biosynthesis. mTORC1 promotes SREBP nuclear entry (via Lipin-1 and S6K1), linking nutrient sensing to the lipogenic program. SREBP1/2 are thus a major downstream metabolic output of mTORC1 alongside protein synthesis and autophagy suppression.", "description_beginner": "Master genetic switches for building new fats and cholesterol from scratch. mTORC1 helps move them into the nucleus to switch these genes on, linking nutrient signals to fat-making, alongside its roles in protein building and blocking cleanup.", "synonyms": "", "n_linked_studies": 0, "atlas_url": "" }, { "name": "Energy & cellular stress", "type": "Condition", "description": "Falling ATP, glucose withdrawal and a range of other insults. They converge on mTORC1 through two routes: AMPK, and physical relocation of the TSC complex to the lysosome.", "description_beginner": "A catch-all for problems like falling energy (ATP) levels or glucose shortage. These reach mTORC1 through two separate routes: the AMPK brake, and physically moving the TSC complex to the lysosome.", "synonyms": "", "n_linked_studies": 4, "atlas_url": "https://mtor-atlas.org/condition/energy-cellular-stress/" }, { "name": "IRS-1 / IRS-2", "type": "Gene/Protein", "description": "Insulin receptor substrate proteins - the adaptors that carry the signal from the insulin/IGF-1 receptor to PI3K. S6K1 phosphorylates and represses them, which is the pathway's principal negative feedback loop: sustained mTORC1 activity deafens the cell to insulin, and blocking mTOR restores insulin signalling and raises Akt activity.", "description_beginner": "The adaptor proteins that carry the signal from the insulin/IGF-1 receptor onward to PI3K. mTORC1's partner S6K1 tags them for shutdown, which is the pathway's main feedback brake: too much mTORC1 activity 'deafens' the cell to insulin, and blocking mTOR restores that sensitivity and raises Akt activity.", "synonyms": "IRS1; IRS2; insulin receptor substrate", "n_linked_studies": 3, "atlas_url": "https://mtor-atlas.org/gene/irs-1-irs-2/" }, { "name": "Nucleotide synthesis", "type": "Biological process", "description": "De novo purine and pyrimidine production. mTORC1 matches supply to demand here, which is why proliferating cells are so dependent on it.", "description_beginner": "Building the raw materials (DNA/RNA letters) from scratch. mTORC1 ramps this up to match how fast a cell is dividing, which is a big part of why rapidly growing cells depend on mTOR so heavily.", "synonyms": "", "n_linked_studies": 4, "atlas_url": "https://mtor-atlas.org/process/nucleotide-synthesis/" }, { "name": "Green tea extract", "type": "Drug", "description": "Polyphenol-rich supplement tested by the ITP for lifespan effects; no significant effect found overall.", "description_beginner": "A polyphenol-rich supplement tested for anti-aging effects in a formal mouse study. Overall, it showed no significant lifespan benefit.", "synonyms": "", "n_linked_studies": 1, "atlas_url": "" }, { "name": "LKB1 (STK11)", "type": "Gene/Protein", "description": "A serine/threonine kinase that activates AMPK and acts upstream of mTOR to regulate cellular energy sensing, autophagy, and metabolism.", "description_beginner": "An enzyme that switches on AMPK and, through it, helps regulate the cell's energy sensing, cleanup (autophagy), and metabolism - sitting upstream of the mTOR pathway.", "synonyms": "", "n_linked_studies": 1, "atlas_url": "" }, { "name": "Protein synthesis", "type": "Biological process", "description": "Cap-dependent translation - the main output mTORC1 exists to control, and the step where a signalling decision becomes physical growth.", "description_beginner": "Building proteins from mRNA - the main job mTORC1 exists to control, and the step where a signaling decision (mTOR is on) turns into an actual physical outcome (the cell grows).", "synonyms": "", "n_linked_studies": 6, "atlas_url": "https://mtor-atlas.org/process/protein-synthesis/" }, { "name": "SLC38A9", "type": "Gene/Protein", "description": "Lysosomal amino-acid transporter and signaling component; acts as an arginine sensor on the lysosomal membrane. Works together with v-ATPase and Ragulator to relay luminal arginine availability to the Rag GTPases and thereby recruit mTORC1. Loss of SLC38A9 impairs arginine-dependent mTORC1 activation.", "description_beginner": "A transporter on the lysosome membrane that acts as an arginine sensor. Working together with v-ATPase and Ragulator, it relays how much arginine is stored inside the lysosome so the Rag GTPases can recruit and switch on mTORC1. Without it, arginine can't properly activate mTORC1.", "synonyms": "", "n_linked_studies": 5, "atlas_url": "https://mtor-atlas.org/gene/slc38a9/" }, { "name": "Tuberous sclerosis complex", "type": "Disease", "description": "Genetic disorder from TSC1/TSC2 loss causing constitutive mTOR activation and benign tumors in brain, kidney, and elsewhere. Everolimus shrinks these tumors (EXIST trials) - the clearest randomised human evidence that blocking mTOR helps a human disease driven by mTOR overactivation.", "description_beginner": "A genetic disease caused by loss of the TSC1 or TSC2 brake, leaving mTOR stuck in the 'on' position and causing benign tumors in the brain, kidneys, and elsewhere. Everolimus shrinks these tumors - the clearest, most direct evidence in humans that blocking mTOR helps a disease actually caused by too much mTOR activity.", "synonyms": "", "n_linked_studies": 5, "atlas_url": "https://mtor-atlas.org/disease/tuberous-sclerosis-complex/" }, { "name": "S-adenosylmethionine (SAM)", "type": "Nutrient/Metabolite", "description": "Universal methyl donor whose level reports methionine availability. SAM binds SAMTOR, which otherwise inhibits mTORC1 through the GATOR1-KICSTOR complex.", "description_beginner": "A universal 'methyl donor' molecule whose level reflects how much of the amino acid methionine is available. It binds the sensor SAMTOR, which would otherwise keep mTORC1 suppressed.", "synonyms": "", "n_linked_studies": 1, "atlas_url": "" }, { "name": "Autophagy", "type": "Biological process", "description": "Cellular recycling process suppressed by mTORC1 and activated upon its inhibition; linked to longevity.", "description_beginner": "The cell's built-in recycling system. mTORC1 normally keeps it switched off; when mTORC1 is blocked, it switches on, clearing out damaged proteins and organelles - and it's linked to longer lifespan.", "synonyms": "", "n_linked_studies": 18, "atlas_url": "https://mtor-atlas.org/process/autophagy/" }, { "name": "AMPK", "type": "Gene/Protein", "description": "AMP-activated protein kinase; cellular energy sensor; inhibits mTORC1 under low-energy conditions.", "description_beginner": "The cell's energy-shortage alarm. When energy is running low, it switches on and puts the brakes on mTORC1.", "synonyms": "", "n_linked_studies": 9, "atlas_url": "https://mtor-atlas.org/gene/ampk/" }, { "name": "Beclin-1 (BECN1)", "type": "Gene/Protein", "description": "Core autophagy protein required for autophagosome nucleation; regulated by mTOR and inhibited by Bcl-2 family members.", "description_beginner": "A core protein required to start building autophagosomes, the sacs that carry out cellular cleanup. It's controlled by mTOR and held back by the Bcl-2 family of proteins.", "synonyms": "", "n_linked_studies": 1, "atlas_url": "" }, { "name": "Temsirolimus", "type": "Drug", "description": "Intravenous rapamycin ester (CCI-779); mTOR inhibitor approved for advanced renal cell carcinoma.", "description_beginner": "An injectable, water-soluble version of rapamycin. It's an approved mTOR-blocking treatment for advanced kidney cancer.", "synonyms": "", "n_linked_studies": 1, "atlas_url": "" }, { "name": "Actin cytoskeleton", "type": "Biological process", "description": "Cell shape and motility machinery. The first function ever attributed to mTORC2 - and noticed precisely because rapamycin failed to block it.", "description_beginner": "The scaffolding that gives a cell its shape and lets it move. This was the very first job ever pinned on mTORC2 - and it was discovered precisely because rapamycin failed to block it, which is how scientists first realized there had to be a second mTOR complex.", "synonyms": "", "n_linked_studies": 3, "atlas_url": "https://mtor-atlas.org/process/actin-cytoskeleton/" }, { "name": "Hypoxia", "type": "Condition", "description": "Low oxygen. Acts on mTORC1 transcriptionally through REDD1 rather than through AMPK, so it is slower to engage and slower to release.", "description_beginner": "Low oxygen levels. It reaches mTORC1 through a gene called REDD1 rather than through the AMPK energy-sensing route, so it's slower to switch the brake on and slower to release it again.", "synonyms": "", "n_linked_studies": 1, "atlas_url": "" }, { "name": "ERK / RSK (MAPK)", "type": "Gene/Protein", "description": "The Ras-MAPK growth-signalling arm. ERK and its effector RSK phosphorylate TSC2 and inactivate the TSC complex, so MAPK signalling converges on the same brake that Akt releases (MA2005). This is the third major upstream input to mTORC1 alongside PI3K/Akt and AMPK, and it is a route to mTORC1 activation that PI3K inhibitors do not close. mTORC1 inhibition also feeds back to activate MAPK (CAR2008).", "description_beginner": "A separate growth-signaling chain that reaches mTORC1 through its own route. Two of its members disable the TSC brake, the same brake that Akt also releases - so this is a third major way to switch mTORC1 on, one that drugs blocking PI3K don't touch. mTORC1 can also feed back and switch this chain on.", "synonyms": "ERK; ERK1/2; MAPK; RSK; p90RSK; Ras-MAPK", "n_linked_studies": 2, "atlas_url": "" }, { "name": "RTB101", "type": "Drug", "description": "An oral ATP-competitive mTOR inhibitor (formerly BEZ235) tested for boosting immune function in the elderly; improved antiviral gene expression but failed its phase 3 clinical endpoint.", "description_beginner": "An oral mTOR-blocking drug tested for boosting immune function in older adults. It improved antiviral gene activity in early trials but ultimately failed to meet its goal in a larger, phase 3 clinical trial.", "synonyms": "", "n_linked_studies": 2, "atlas_url": "" }, { "name": "RUBCN (Rubicon)", "type": "Gene/Protein", "description": "Run domain Beclin-1-interacting and cysteine-rich domain-containing protein; a negative regulator of autophagy whose suppression activates autophagic flux.", "description_beginner": "A protein that normally acts as a brake on autophagy (the cell's self-cleaning process). Suppressing it releases that brake and ramps up autophagy - a strategy some cancer cells exploit to resist chemotherapy.", "synonyms": "", "n_linked_studies": 1, "atlas_url": "" }, { "name": "PFKFB3", "type": "Gene/Protein", "description": "6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase 3, a rate-limiting glycolytic regulator controlled downstream of mTORC2.", "description_beginner": "A control enzyme for glycolysis, the fast way cells burn sugar. It sets the pace of that pathway, and mTORC2 sits upstream of it deciding how much of it the cell makes.", "synonyms": "", "n_linked_studies": 0, "atlas_url": "" }, { "name": "PIP4K2A", "type": "Gene/Protein", "description": "Phosphatidylinositol-5-phosphate 4-kinase type II alpha; regulates autophagy and AKT/mTOR signaling and is neuroprotective in cerebral ischemia/reperfusion models.", "description_beginner": "An enzyme that helps regulate both cellular cleanup (autophagy) and Akt/mTOR signaling; in animal models it also appears to protect brain cells after a stroke-like injury.", "synonyms": "", "n_linked_studies": 1, "atlas_url": "" }, { "name": "TET1", "type": "Gene/Protein", "description": "Ten-eleven translocation methylcytosine dioxygenase 1, an epigenetic eraser that drives DNA demethylation of target promoters.", "description_beginner": "An enzyme that erases chemical 'off' tags (methyl groups) from DNA. Stripping those tags lets genes that had been silenced be read again, so it helps decide which parts of the genome a cell actually uses.", "synonyms": "", "n_linked_studies": 0, "atlas_url": "" }, { "name": "mTORC2", "type": "Pathway/Complex", "description": "mTOR Complex 2; phosphorylates Akt/PKB, affects cell survival and glucose metabolism.", "description_beginner": "The second, less-studied of the two mTOR complexes. It switches on Akt and affects cell survival and how cells handle sugar.", "synonyms": "TORC2; mTOR complex 2; mTOR complex-2", "n_linked_studies": 14, "atlas_url": "https://mtor-atlas.org/complex/mtorc2/" }, { "name": "REDD1 (DDIT4)", "type": "Gene/Protein", "description": "Hypoxia-induced protein that suppresses mTORC1 through the TSC complex - the mechanism by which low oxygen and low growth factors share a single brake.", "description_beginner": "A protein switched on by low oxygen that suppresses mTORC1 by acting through the TSC brake complex - the shared mechanism by which both low oxygen and weak growth-factor signals apply the same brake.", "synonyms": "", "n_linked_studies": 1, "atlas_url": "" }, { "name": "S6K1", "type": "Gene/Protein", "description": "Direct downstream effector of mTORC1 controlling protein synthesis, and the source of the pathway's main negative feedback: S6K1 phosphorylates and represses IRS-1, uncoupling the insulin receptor from PI3K (HAR2004, SHA2004). Its deletion extends lifespan in FEMALE mice (+19% median, not significant in males; SEL2009) and protects against diet-induced obesity.", "description_beginner": "A direct downstream partner of mTORC1 that helps control protein building, and the source of the pathway's main feedback brake: it tags the insulin-signaling adaptor IRS-1 for shutdown, disconnecting the insulin receptor from the rest of the pathway. Removing it extends lifespan in female mice (not clearly in males) and protects against diet-driven weight gain.", "synonyms": "p70 S6K; p70 S6 kinase; S6 kinase 1; RPS6KB1; p70S6K", "n_linked_studies": 9, "atlas_url": "https://mtor-atlas.org/gene/s6k1/" }, { "name": "Rheb", "type": "Gene/Protein", "description": "Small GTPase that directly activates mTORC1 when in its GTP-bound state; held inactive by TSC1/TSC2.", "description_beginner": "A small molecular switch that directly turns mTORC1 on when it's in its 'active' state. The TSC1/TSC2 brake keeps it held inactive until nutrient and growth signals say otherwise.", "synonyms": "", "n_linked_studies": 8, "atlas_url": "https://mtor-atlas.org/gene/rheb/" }, { "name": "GADD45alpha", "type": "Gene/Protein", "description": "Stress-inducible DNA repair protein regulated downstream of the mTOR-TFEB axis; restoration of its expression by TFEB activation confers protection against nephrotoxicity.", "description_beginner": "A stress-response, DNA-repair protein controlled downstream of the mTOR-TFEB signaling chain. Restoring its levels - by activating TFEB - has helped protect against drug-induced kidney damage in animal studies.", "synonyms": "", "n_linked_studies": 1, "atlas_url": "" }, { "name": "Insulin resistance", "type": "Outcome", "description": "Metabolic side effect of chronic mTOR inhibition. In mice, mTORC2 disruption is a major contributor (LAM2012). In humans the relative contributions are not resolved: mTORC2 loss, S6K1-IRS-1 feedback relief (HAR2004, SHA2004) and direct beta-cell effects are all plausible, and no study has apportioned them.", "description_beginner": "A metabolic side effect sometimes seen with long-term mTOR blocking. In mice this is mostly traced to disrupting mTORC2; in humans it's less clear-cut, since mTORC2 loss, a feedback loop involving S6K1/IRS-1, and direct effects on insulin-making cells could all be contributing, and no study has yet worked out how much each one matters.", "synonyms": "", "n_linked_studies": 4, "atlas_url": "https://mtor-atlas.org/outcome/insulin-resistance/" }, { "name": "Osteoarthritis", "type": "Disease", "description": "Age-related degenerative joint disease characterised by cartilage matrix loss, inflammation and impaired chondrocyte autophagy.", "description_beginner": "The 'wear and tear' joint disease of ageing, in which the cartilage cushioning a joint breaks down. The cartilage cells lose their ability to clear out damaged parts by autophagy, and inflammation speeds the loss along.", "synonyms": "", "n_linked_studies": 0, "atlas_url": "" }, { "name": "Resveratrol", "type": "Drug", "description": "Plant polyphenol popularized as a sirtuin activator and 'calorie-restriction mimetic'; failed to extend lifespan in ITP mouse studies and showed no metabolic benefit in a human RCT.", "description_beginner": "A plant compound found in red wine, popularized as an activator of 'sirtuin' longevity genes and a calorie-restriction mimic. It failed to extend lifespan in a rigorous mouse study and showed no metabolic benefit in a human clinical trial.", "synonyms": "", "n_linked_studies": 3, "atlas_url": "https://mtor-atlas.org/drug/resveratrol/" }, { "name": "Urolithin A", "type": "Drug", "description": "Gut microbiome-derived polyphenol metabolite that activates mitophagy via the AMPK-mTOR axis, with cardioprotective effects in heart failure models.", "description_beginner": "A compound made by gut bacteria from certain plant polyphenols. It switches on mitophagy (cleanup of damaged mitochondria) through the AMPK-mTOR pathway, and has shown heart-protective effects in animal models of heart failure.", "synonyms": "", "n_linked_studies": 1, "atlas_url": "" }, { "name": "FLCN / FNIP1/2", "type": "Gene/Protein", "description": "Folliculin and its binding partners FNIP1/2; act as a GTPase-activating protein (GAP) for RagC/D, switching the Rag heterodimer into the configuration that recruits mTORC1 to the lysosome. FLCN-FNIP complements the GATOR1/GATOR2 arm by regulating the RagC/D half of the cycle. Loss of FLCN causes Birt-Hogg-Dube syndrome through a SUBSTRATE-SPECIFIC defect rather than blanket mTORC1 hyperactivation: canonical outputs (S6K1, 4E-BP1) are largely preserved, while TFEB and TFE3 escape phosphorylation and accumulate in the nucleus (NAP2020).", "description_beginner": "A protein complex that helps switch the Rag GTPases into the right configuration to bring mTORC1 to the lysosome - working alongside, but through a different route than, the GATOR1/GATOR2 system. Losing it causes a genetic disease (Birt-Hogg-Dube syndrome) not because mTORC1 goes generally haywire, but because a couple of its specific outputs (TFEB and TFE3) stop being properly turned off.", "synonyms": "FLCN; folliculin; FNIP1; FNIP2; FNIP1/2", "n_linked_studies": 3, "atlas_url": "https://mtor-atlas.org/gene/flcn-fnip1-2/" }, { "name": "NF-κB", "type": "Pathway/Complex", "description": "Master pro-inflammatory transcription factor complex that cross-talks extensively with PI3K/AKT/mTOR signalling.", "description_beginner": "The cell's main inflammation switch: a protein complex that, once released, moves into the nucleus and turns on hundreds of immune genes. It talks back and forth constantly with the PI3K/AKT/mTOR growth pathway.", "synonyms": "", "n_linked_studies": 0, "atlas_url": "" }, { "name": "4E-BP1", "type": "Gene/Protein", "description": "Translational repressor; the master effector through which mTORC1 controls protein synthesis. mTORC1 phosphorylates 4E-BP1 to release eIF4E and switch translation ON.", "description_beginner": "A protein that holds the translation-starter eIF4E hostage - until mTORC1 phosphorylates it, releasing eIF4E and switching protein production on. It's the main effector through which mTORC1 controls how much protein a cell makes.", "synonyms": "4E-BP; 4EBP1; EIF4EBP1; PHAS-I", "n_linked_studies": 7, "atlas_url": "https://mtor-atlas.org/gene/4e-bp1/" }, { "name": "Salvianolic acid B", "type": "Drug", "description": "Polyphenol from Salvia miltiorrhiza that engages AKT1 and the AKT/mTOR/HIF-1α axis to promote angiogenesis and repair.", "description_beginner": "A polyphenol from red sage (Salvia miltiorrhiza), used in Chinese medicine for circulation. In lab studies it binds AKT1 and drives the AKT/mTOR/HIF-1α chain that tells damaged tissue to build new blood vessels and repair itself.", "synonyms": "", "n_linked_studies": 0, "atlas_url": "" }, { "name": "Skin aging", "type": "Outcome", "description": "Visible and molecular aging of skin (photodamage, dermal thinning, senescence markers like p16). Topical rapamycin reduced these markers in a human trial.", "description_beginner": "Visible and molecular changes in aging skin - sun damage, thinning, and buildup of 'senescent' cells. In a human trial, a topical rapamycin cream reduced some of these markers.", "synonyms": "", "n_linked_studies": 1, "atlas_url": "" }, { "name": "Dihydromyricetin", "type": "Drug", "description": "Flavonoid from Ampelopsis grossedentata reported to reduce fibrosis with accompanying suppression of PI3K/AKT/mTOR signalling.", "description_beginner": "A flavonoid from vine tea. In animal studies it reduces fibrosis - the stiff scarring that replaces healthy tissue - and this comes together with a quieting of PI3K/AKT/mTOR signalling.", "synonyms": "", "n_linked_studies": 0, "atlas_url": "" }, { "name": "Tumor growth", "type": "Biological process", "description": "The shared endpoint of the pathway's oncogenic lesions, and the outcome every mTOR inhibitor trial in this Atlas was actually measuring.", "description_beginner": "How much a tumor grows and spreads - the outcome that every mTOR-inhibitor cancer trial in this Atlas was ultimately trying to measure.", "synonyms": "", "n_linked_studies": 5, "atlas_url": "https://mtor-atlas.org/process/tumor-growth/" }, { "name": "GATOR1", "type": "Pathway/Complex", "description": "Negative regulator of the Rag GTPases (a GAP); switches mTORC1 OFF when amino acids are scarce. Tumor suppressor - mutated in some cancers.", "description_beginner": "The main 'off switch' for mTORC1 in the amino-acid sensing system - it acts on the Rag GTPases to shut mTORC1 down when nutrients run low. It's a tumor suppressor, and it's found mutated in some cancers.", "synonyms": "", "n_linked_studies": 2, "atlas_url": "" }, { "name": "Ragulator", "type": "Pathway/Complex", "description": "Lysosome-anchored scaffold that recruits the Rag GTPases and positions mTORC1 on the lysosomal surface for activation.", "description_beginner": "A scaffold anchored to the lysosome that recruits the Rag GTPases and holds mTORC1 in position on the lysosome's surface so it can be switched on there.", "synonyms": "", "n_linked_studies": 3, "atlas_url": "https://mtor-atlas.org/complex/ragulator/" }, { "name": "ASCL1", "type": "Gene/Protein", "description": "Achaete-scute homolog 1, a bHLH transcription factor that acts upstream of a CCNB1/mTOR axis in renal injury.", "description_beginner": "A transcription factor - a protein that switches genes on - best known for steering cells toward a nerve-cell identity. In kidney injury it sits at the top of a chain that runs through CCNB1 to mTOR.", "synonyms": "", "n_linked_studies": 0, "atlas_url": "" }, { "name": "Spalt-related (Salr)", "type": "Gene/Protein", "description": "Transcription factor in Drosophila identified as a novel inhibitor of mTORC1-mediated growth, activated by the integrated stress response to restrict anabolic processes during nutrient stress.", "description_beginner": "A gene switch found in fruit flies that blocks mTORC1-driven growth. It's turned on by the cell's stress-alarm system to slow down growth-related processes when nutrients are scarce.", "synonyms": "", "n_linked_studies": 1, "atlas_url": "" }, { "name": "Macronutrient ratio", "type": "Intervention", "description": "Ratio of protein:carbohydrate:fat in the diet; affects mTOR activation independently of total caloric intake.", "description_beginner": "The balance of protein, carbohydrate, and fat in the diet. Changing this ratio can switch mTOR activity up or down independently of how many total calories are eaten.", "synonyms": "", "n_linked_studies": 1, "atlas_url": "" } ]