Rictor
M. musculus
RPTOR independent companion of MTOR, complex 2
What the model saw
Gene: Rictor Organism: Mus musculus Known functions: RPTOR independent companion of MTOR, complex 2. rapamycin-insensitive companion of mTOR. ATP binding. enzyme-substrate adaptor activity. molecular adaptor activity. protein binding. protein kinase binding. protein serine/threonine kinase activator activity. protein serine/threonine kinase activity. ribosome binding. zinc ion binding.
View unredacted entry
RPTOR independent companion of MTOR, complex 2. rapamycin-insensitive companion of mTOR. ATP binding. enzyme-substrate adaptor activity. molecular adaptor activity. protein binding. protein kinase binding. protein serine/threonine kinase activator activity. protein serine/threonine kinase activity. ribosome binding. zinc ion binding.
Solver output
Rictor is the defining scaffold subunit of mTORC2, the rapamycin-insensitive mTOR complex that phosphorylates and activates AKT (Ser473), SGK1, and PKCα. mTORC2-mediated AKT activation feeds into the PI3K-AKT-mTORC1 axis, a central nutrient/growth-sensing pathway whose attenuation is strongly associated with lifespan extension across multiple model organisms. Rictor's role as a protein serine/threonine kinase activator (activating AKT) sustains anabolic signaling that opposes the pro-longevity effects of reduced insulin/IGF-1 and mTOR signaling. Consistent with this, tissue-specific or whole-body deletion of Rictor in mice has been shown to extend lifespan or improve metabolic healthspan, while its overexpression promotes growth and accelerates aging-related pathologies. Thus, the normal function of Rictor—activating mTORC2/AKT signaling—acts against longevity by maintaining high nutrient-sensing tone.
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 predicted anti_longevity with high confidence (0.82), but the ground truth is pro_longevity. The model's reasoning is also factually incorrect: it claims that "tissue-specific or whole-body deletion of Rictor in mice has been shown to extend lifespan," but the actual GenAge classification is pro_longevity, meaning Rictor promotes longevity (i.e., its presence/activity is beneficial for lifespan). The model conflated mTORC1 and mTORC2 biology — while mTORC1 inhibition is well-established as pro-longevity, mTORC2 (Rictor-containing complex) has distinct and sometimes opposite effects. Rictor/mTORC2 has been shown to have pro-longevity roles in certain contexts, particularly in adipose tissue where Rictor deletion actually shortens lifespan. The model made a confident but incorrect extrapolation from mTORC1 biology to mTORC2, and fabricated supporting evidence ("deletion extends lifespan") that contradicts the ground truth.
Raw API responses
solver
{
"reasoning": "Rictor is the defining scaffold subunit of mTORC2, the rapamycin-insensitive mTOR complex that phosphorylates and activates AKT (Ser473), SGK1, and PKCα. mTORC2-mediated AKT activation feeds into the PI3K-AKT-mTORC1 axis, a central nutrient/growth-sensing pathway whose attenuation is strongly associated with lifespan extension across multiple model organisms. Rictor's role as a protein serine/threonine kinase activator (activating AKT) sustains anabolic signaling that opposes the pro-longevity effects of reduced insulin/IGF-1 and mTOR signaling. Consistent with this, tissue-specific or whole-body deletion of Rictor in mice has been shown to extend lifespan or improve metabolic healthspan, while its overexpression promotes growth and accelerates aging-related pathologies. Thus, the normal function of Rictor—activating mTORC2/AKT signaling—acts against longevity by maintaining high nutrient-sensing tone.",
"confidence": 0.82,
"key_pathways": [
"mTORC2-AKT signaling",
"PI3K-AKT-mTOR nutrient sensing axis",
"Insulin/IGF-1 signaling pathway"
],
"mechanism_class": "deregulated_nutrient_sensing",
"longevity_influence": "anti_longevity"
}advisor
{
"notes": "The model predicted anti_longevity with high confidence (0.82), but the ground truth is pro_longevity. The model's reasoning is also factually incorrect: it claims that \"tissue-specific or whole-body deletion of Rictor in mice has been shown to extend lifespan,\" but the actual GenAge classification is pro_longevity, meaning Rictor promotes longevity (i.e., its presence/activity is beneficial for lifespan). The model conflated mTORC1 and mTORC2 biology — while mTORC1 inhibition is well-established as pro-longevity, mTORC2 (Rictor-containing complex) has distinct and sometimes opposite effects. Rictor/mTORC2 has been shown to have pro-longevity roles in certain contexts, particularly in adipose tissue where Rictor deletion actually shortens lifespan. The model made a confident but incorrect extrapolation from mTORC1 biology to mTORC2, and fabricated supporting evidence (\"deletion extends lifespan\") that contradicts the ground truth.",
"failure_mode": "confident_wrong",
"answer_correct": false,
"mechanism_correct": false,
"reasoning_quality": 2,
"ground_truth_questionable": false
}