aakb-1
C. elegans
5'-AMP-activated protein kinase subunit beta-1
What the model saw
Gene: aakb-1 Organism: Caenorhabditis elegans Known functions: 5'-AMP-activated protein kinase subunit beta-1. protein kinase binding.
View unredacted entry
5'-AMP-activated protein kinase subunit beta-1. protein kinase binding.
Solver output
aakb-1 encodes the beta-1 regulatory subunit of AMP-activated protein kinase (AMPK) in C. elegans. AMPK is a master energy sensor that is activated under low-energy (high AMP/ATP ratio) conditions. The beta subunit serves as a scaffold that bridges the catalytic alpha subunit (aak-1/aak-2) and the regulatory gamma subunit, and contains a carbohydrate-binding module that regulates kinase activity and localization. Active AMPK promotes longevity by inhibiting mTORC1 (let-363 in C. elegans), activating autophagy, and phosphorylating transcription factors such as DAF-16/FOXO, thereby coordinating metabolic adaptation to nutrient stress. In C. elegans, loss of AMPK subunits shortens lifespan, while enhanced AMPK activity extends it, placing aakb-1 firmly in the pro-longevity nutrient-sensing axis.
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
The model correctly predicted pro_longevity for aakb-1 with high confidence (0.82). The mechanistic reasoning is excellent: it accurately describes aakb-1 as the beta-1 regulatory subunit of AMPK, explains the scaffold role of the beta subunit, correctly identifies the carbohydrate-binding module, and accurately describes AMPK's role in longevity through mTORC1 inhibition, autophagy activation, and DAF-16/FOXO regulation. The model also correctly notes that loss of AMPK subunits shortens lifespan in C. elegans while enhanced activity extends it. The mechanism class (deregulated_nutrient_sensing) is appropriate. Overall, this is a high-quality, well-reasoned prediction.
Raw API responses
solver
{
"reasoning": "aakb-1 encodes the beta-1 regulatory subunit of AMP-activated protein kinase (AMPK) in C. elegans. AMPK is a master energy sensor that is activated under low-energy (high AMP/ATP ratio) conditions. The beta subunit serves as a scaffold that bridges the catalytic alpha subunit (aak-1/aak-2) and the regulatory gamma subunit, and contains a carbohydrate-binding module that regulates kinase activity and localization. Active AMPK promotes longevity by inhibiting mTORC1 (let-363 in C. elegans), activating autophagy, and phosphorylating transcription factors such as DAF-16/FOXO, thereby coordinating metabolic adaptation to nutrient stress. In C. elegans, loss of AMPK subunits shortens lifespan, while enhanced AMPK activity extends it, placing aakb-1 firmly in the pro-longevity nutrient-sensing axis.",
"confidence": 0.82,
"key_pathways": [
"AMPK/mTORC1 nutrient sensing",
"DAF-16/FOXO transcription factor regulation",
"autophagy induction"
],
"mechanism_class": "deregulated_nutrient_sensing",
"longevity_influence": "pro_longevity"
}advisor
{
"notes": "The model correctly predicted pro_longevity for aakb-1 with high confidence (0.82). The mechanistic reasoning is excellent: it accurately describes aakb-1 as the beta-1 regulatory subunit of AMPK, explains the scaffold role of the beta subunit, correctly identifies the carbohydrate-binding module, and accurately describes AMPK's role in longevity through mTORC1 inhibition, autophagy activation, and DAF-16/FOXO regulation. The model also correctly notes that loss of AMPK subunits shortens lifespan in C. elegans while enhanced activity extends it. The mechanism class (deregulated_nutrient_sensing) is appropriate. Overall, this is a high-quality, well-reasoned prediction.",
"failure_mode": "correct",
"answer_correct": true,
"mechanism_correct": true,
"reasoning_quality": 5,
"ground_truth_questionable": false
}