Rps6kb1
M. musculus
ribosomal protein S6 kinase B1
What the model saw
Gene: Rps6kb1 Organism: Mus musculus Known functions: ribosomal protein S6 kinase B1. ribosomal protein S6 kinase beta-1. ATP binding. PDZ domain binding. identical protein binding. peptide binding. protein binding. protein kinase activity. protein phosphatase 2A binding. protein serine kinase activity. protein serine/threonine kinase activity. protein serine/threonine/tyrosine kinase activity. ribosomal protein S6 kinase activity.
View unredacted entry
ribosomal protein S6 kinase B1. ribosomal protein S6 kinase beta-1. ATP binding. PDZ domain binding. identical protein binding. peptide binding. protein binding. protein kinase activity. protein phosphatase 2A binding. protein serine kinase activity. protein serine/threonine kinase activity. protein serine/threonine/tyrosine kinase activity. ribosomal protein S6 kinase activity.
Solver output
Rps6kb1 encodes S6K1 (p70-S6K1), a serine/threonine kinase that is a major downstream effector of the mTORC1 nutrient-sensing pathway. Upon activation by mTORC1, S6K1 phosphorylates ribosomal protein S6 and other translational regulators to promote protein synthesis and anabolic growth. Chronic mTORC1/S6K1 signaling is a well-established driver of accelerated aging, and genetic deletion of S6K1 in mice extends lifespan, particularly in females. S6K1 also phosphorylates and inhibits IRS-1, creating a negative feedback loop that suppresses insulin/IGF-1 signaling, further linking it to nutrient-sensing dysregulation. Its kinase activity toward ribosomal protein S6 directly couples nutrient availability to translational output, a process whose attenuation (e.g., by rapamycin) is one of the most reproducible pro-longevity interventions across model organisms.
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 identified Rps6kb1/S6K1 as anti_longevity with high confidence (0.93). The mechanistic reasoning is excellent and accurate: S6K1 is a downstream effector of mTORC1, its deletion extends lifespan in mice (especially females), it promotes protein synthesis and anabolic growth, and it creates negative feedback on insulin/IGF-1 signaling via IRS-1 phosphorylation. All key pathways identified are correct and relevant. This is a well-known longevity gene and the model's reasoning reflects the established literature accurately.
Raw API responses
solver
{
"reasoning": "Rps6kb1 encodes S6K1 (p70-S6K1), a serine/threonine kinase that is a major downstream effector of the mTORC1 nutrient-sensing pathway. Upon activation by mTORC1, S6K1 phosphorylates ribosomal protein S6 and other translational regulators to promote protein synthesis and anabolic growth. Chronic mTORC1/S6K1 signaling is a well-established driver of accelerated aging, and genetic deletion of S6K1 in mice extends lifespan, particularly in females. S6K1 also phosphorylates and inhibits IRS-1, creating a negative feedback loop that suppresses insulin/IGF-1 signaling, further linking it to nutrient-sensing dysregulation. Its kinase activity toward ribosomal protein S6 directly couples nutrient availability to translational output, a process whose attenuation (e.g., by rapamycin) is one of the most reproducible pro-longevity interventions across model organisms.",
"confidence": 0.93,
"key_pathways": [
"mTORC1-S6K1 nutrient sensing",
"insulin/IGF-1 signaling (IRS-1 negative feedback)",
"ribosomal protein S6 phosphorylation and translational control"
],
"mechanism_class": "deregulated_nutrient_sensing",
"longevity_influence": "anti_longevity"
}advisor
{
"notes": "The model correctly identified Rps6kb1/S6K1 as anti_longevity with high confidence (0.93). The mechanistic reasoning is excellent and accurate: S6K1 is a downstream effector of mTORC1, its deletion extends lifespan in mice (especially females), it promotes protein synthesis and anabolic growth, and it creates negative feedback on insulin/IGF-1 signaling via IRS-1 phosphorylation. All key pathways identified are correct and relevant. This is a well-known longevity gene and the model's reasoning reflects the established literature accurately.",
"failure_mode": "correct",
"answer_correct": true,
"mechanism_correct": true,
"reasoning_quality": 5,
"ground_truth_questionable": false
}