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AMPKalpha

D. melanogaster

AMP-activated protein kinase alpha subunit

What the model saw

Gene: AMPKalpha
Organism: Drosophila melanogaster
Known functions: AMP-activated protein kinase alpha subunit. AMP-activated protein kinase activity. ATP binding. nucleotide binding. protein kinase activity. protein serine/threonine kinase activity.
View unredacted entry
AMP-activated protein kinase alpha subunit. AMP-activated protein kinase activity. ATP binding. nucleotide binding. protein kinase activity. protein serine/threonine kinase activity.

Solver output

Predicted influence
Pro-longevity
Confidence
93%
Mechanism
Deregulated nutrient sensing
Reasoning

AMPKα is the catalytic subunit of AMP-activated protein kinase, a master energy sensor that is activated when cellular AMP:ATP ratios rise (low energy states). In Drosophila, AMPK phosphorylates and inhibits anabolic targets such as TOR complex 1 (via TSC2 and Raptor phosphorylation) and activates catabolic processes including autophagy (via ULK1/Atg1 phosphorylation), fatty acid oxidation, and mitochondrial biogenesis. This activity directly opposes the pro-aging effects of hyperactive TOR/insulin-IGF signaling, a well-established longevity axis. Genetic activation of AMPK in Drosophila has been shown to extend lifespan, while loss of AMPKα shortens it, consistent with its role as a nutrient-sensing longevity effector. Additionally, AMPK promotes mitochondrial quality control and suppresses cellular senescence-associated metabolic dysfunction, further reinforcing its pro-longevity role.

Key pathways
AMPK-TOR nutrient sensing axisAutophagy induction via ULK1/Atg1 phosphorylationInsulin-IGF signaling antagonism
Longevity influence
Pro-longevity
Lifespan effect
Increase

GenAge curators classify each gene's normal function as promoting (Pro-Longevity) or opposing (Anti-Longevity) longevity, based on synthesis across studies. Loss-of-function effects can vary from this depending on the manipulation.

Advisor judgment

Answer
Correct
Mechanism
Correct
Reasoning quality
5/5
Failure mode
Correct
Notes

The model correctly predicted pro_longevity for AMPKalpha in Drosophila with high confidence (0.93). The mechanistic reasoning is thorough and accurate: AMPK as an energy sensor, its inhibition of TOR via TSC2/Raptor phosphorylation, activation of autophagy via ULK1/Atg1, and antagonism of insulin-IGF signaling are all well-established mechanisms. The model correctly notes that genetic activation extends lifespan while loss shortens it in Drosophila. The mechanism class of "deregulated_nutrient_sensing" is appropriate. Overall, this is an excellent prediction with solid mechanistic reasoning.

Raw API responses

solver

{
  "reasoning": "AMPKα is the catalytic subunit of AMP-activated protein kinase, a master energy sensor that is activated when cellular AMP:ATP ratios rise (low energy states). In Drosophila, AMPK phosphorylates and inhibits anabolic targets such as TOR complex 1 (via TSC2 and Raptor phosphorylation) and activates catabolic processes including autophagy (via ULK1/Atg1 phosphorylation), fatty acid oxidation, and mitochondrial biogenesis. This activity directly opposes the pro-aging effects of hyperactive TOR/insulin-IGF signaling, a well-established longevity axis. Genetic activation of AMPK in Drosophila has been shown to extend lifespan, while loss of AMPKα shortens it, consistent with its role as a nutrient-sensing longevity effector. Additionally, AMPK promotes mitochondrial quality control and suppresses cellular senescence-associated metabolic dysfunction, further reinforcing its pro-longevity role.",
  "confidence": 0.93,
  "key_pathways": [
    "AMPK-TOR nutrient sensing axis",
    "Autophagy induction via ULK1/Atg1 phosphorylation",
    "Insulin-IGF signaling antagonism"
  ],
  "mechanism_class": "deregulated_nutrient_sensing",
  "longevity_influence": "pro_longevity"
}

advisor

{
  "notes": "The model correctly predicted pro_longevity for AMPKalpha in Drosophila with high confidence (0.93). The mechanistic reasoning is thorough and accurate: AMPK as an energy sensor, its inhibition of TOR via TSC2/Raptor phosphorylation, activation of autophagy via ULK1/Atg1, and antagonism of insulin-IGF signaling are all well-established mechanisms. The model correctly notes that genetic activation extends lifespan while loss shortens it in Drosophila. The mechanism class of \"deregulated_nutrient_sensing\" is appropriate. Overall, this is an excellent prediction with solid mechanistic reasoning.",
  "failure_mode": "correct",
  "answer_correct": true,
  "mechanism_correct": true,
  "reasoning_quality": 5,
  "ground_truth_questionable": false
}
AMPKalpha · Drosophila melanogaster | Aging biology eval