mTOR Academy · Practice
Eight games built on the Atlas's own pathway model and its own studies. Points reward calibration, not speed — and nothing here rewards simply showing up.
The pathway is the board you are playing on. Every question you answer colours in a piece of it — and two of its questions are ones the field itself has not closed, so they never fill in.
Your pathway and badges →Two you have seen, two new, one a level up. Three minutes.
Sixty seconds of arrows: does this one activate or inhibit?
Rebuild a route from loose parts — and get the direct steps right.
Set the controls, predict the readout before it is revealed.
One result, four readings. Which one the evidence will not carry?
One real result, four readings. Which one the paper cannot carry?
A claim from the map. Which study in the Atlas is it standing on?
Established, emerging, contested or open? Say where the field actually is.
Progress lives in this browser only. No account, nothing sent anywhere. Export it if you want to move it.
Points are called XP. Every number you see with a plus sign — +8 XP, +30 XP — is XP added to the total in the bar above; the ranks are XP thresholds. Every question asks how sure you are before the answer appears. Being right while sure is worth the most; being right while unsure is worth less; being wrong while sure is worth nothing at all. There are no points for opening a page, no daily-login bonus and no streak to lose — the only thing that earns anything here is a judgement that could have been wrong.
Open questions never reach full mastery. That is not a bug in the game — the field has not closed them.
This page needs JavaScript for scoring and for saving progress in this browser. The practice questions themselves are below in full, with answers — the page is readable and usable without it.
Answer: B. mTOR is an enzyme. It changes what other proteins do by phosphorylating them, and everything downstream in this course follows from that one activity.
Answer: C. RAPTOR is the mTORC1-defining partner and RICTOR and SIN1 belong to mTORC2. mLST8 is the distractor worth remembering, because it sits in both complexes.
Answer: B. Rheb is a switch protein whose two nucleotide states behave differently, and it is the GTP-bound state that activates the kinase. Everything the TSC complex does is about how much Rheb-GTP there is.
Answer: B. A GTPase-activating protein speeds up a reaction the GTPase already performs. That is why the TSC complex sets a rate rather than flipping a switch, and why the amount of Rheb-GTP is a balance.
Answer: B. The Rags are not membrane-anchored on their own. Ragulator tethers them to the lysosome and acts on their nucleotide state, which is what makes the surface a platform rather than a passive membrane.
Answer: B. Sestrin2 is the leucine-binding protein of this set; CASTOR1 handles arginine and SAMTOR reads S-adenosylmethionine, the metabolite downstream of methionine.
Answer: C. Almost everything in this lesson was worked out in cultured cells and in laboratory animals, and the summary sentence compresses a network with many parallel inputs and outputs into one verb. The compression is useful for learning and it is not a finding; when you meet a claim about mTOR and human health later in the Atlas, the evidence tier attached to it is doing real work.
Answer: C. Every study cited in this lesson sits at tier D or C: biochemistry, cell work and mouse genetics. That is the honest state of complex-level evidence. Selectivity in particular is a claim about an experiment, and the experiment has a duration — which is exactly the thing summaries drop.
Answer: D. Several of the foundational experiments in this lesson raised the amount of a protein far above its normal level in order to see its effect. That design is informative about what a protein can do and much weaker evidence about what it normally does — and the studies below sit at tier D and C, which marks the design, not the quality.
mTOR regulates memory CD8 T-cell differentiation (2009, Mouse)
mTOR is a key regulator of memory CD8 T-cell differentiation; rapamycin enhances memory responses.
Sample: not stated
Answer: A. Its own limitation, as recorded in the Atlas: mTOR knockdown does not completely mimic rapamycin treatment.
Alternative rapamycin treatment regimens mitigate the impact of rapamycin on glucose homeostasis and the immune system (2015, Mouse)
Intermittent rapamycin regimens (weekly, or every 5 days) largely spared glucose tolerance, pyruvate tolerance, fasting glucose and insulin, beta-cell function and the immune system, while still inhibiting mTORC1 -- unlike daily dosing, which impaired all of…
Sample: 9-11 male C57BL/6J mice per treatment group for glucose tolerance tests; 3-6 mice per group for blood rapamycin concentration; 4-9 mice per group for…
Answer: D. Its own limitation, as recorded in the Atlas: No lifespan or healthspan endpoint. Side-effect endpoints only; benefit retention is inferred, not tested.
Unphosphorylated 4E-BP1 clamps onto eIF4E and stops it assembling the cap-binding complex. mTORC1 phosphorylates 4E-BP1 to release that grip - so the brake on translation is released, not the accelerator pressed.
Answer: A. Curated in the Atlas as consensus established, mechanistic evidence high, human relevance plausible.
Keeping 4E-BP active extends lifespan under dietary restriction in flies, by preserving mitochondrial activity. One of the few places where a single downstream node, not the whole pathway, carries the lifespan effect.
Answer: B. Curated in the Atlas as consensus emerging, mechanistic evidence medium, human relevance untested. Scope: Fly only, and only under dietary restriction - the effect was not seen on a full diet.
Unphosphorylated 4E-BP1 clamps onto eIF4E and stops it assembling the cap-binding complex. mTORC1 phosphorylates 4E-BP1 to release that grip - so the brake on translation is released, not the accelerator pressed.
Answer: C. The Atlas records MAX2009, THO2012, SCH2003 as evidence for this step.
Answer: B. Unphosphorylated 4E-BP1 clamps onto eIF4E and stops it assembling the cap-binding complex. mTORC1 phosphorylates 4E-BP1 to release that grip - so the brake on translation is released, not the accelerator pressed.
Answer: A. Keeping 4E-BP active extends lifespan under dietary restriction in flies, by preserving mitochondrial activity. One of the few places where a single downstream node, not the whole pathway, carries the lifespan effect.
Answer: B. Akt phosphorylates TSC2, disabling the complex. Growth-factor signalling works by removing a brake, not by pressing an accelerator.
Answer: A. The LKB1-AMPK axis keeps damaged mitochondria being cleared; lose it and mitochondrial DNA leaks into the cytosol and inflames the cell.
In the game these arrive as loose parts to be put back in order. Here they are written out, with the answer.
Leucine ⊣ Sestrin2 ⊣ GATOR2 ⊣ GATOR1 ⊣ Rag GTPases
Growth hormone / IGF-1 axis → PI3K → Akt/PKB ⊣ TSC1/TSC2 ⊣ Rheb → mTORC1 → S6K1 ⊣ IRS-1 / IRS-2 — 2 of these steps is indirect: it runs through a step this route does not draw.