Adra1b
M. musculus
adrenergic receptor, alpha 1b
What the model saw
Gene: Adra1b Organism: Mus musculus Known functions: adrenergic receptor, alpha 1b. alpha-1B adrenergic receptor. G protein-coupled receptor activity. adrenergic receptor activity. alpha1-adrenergic receptor activity. protein heterodimerization activity.
View unredacted entry
adrenergic receptor, alpha 1b. alpha-1B adrenergic receptor. G protein-coupled receptor activity. adrenergic receptor activity. alpha1-adrenergic receptor activity. protein heterodimerization activity.
Solver output
Adra1b encodes the alpha-1B adrenergic receptor, a GPCR that mediates sympathetic nervous system signaling via catecholamines (norepinephrine/epinephrine). Chronic activation of alpha-1 adrenergic signaling promotes vasoconstriction, cardiac hypertrophy, and sustained sympathoadrenal tone — all hallmarks of age-associated cardiovascular deterioration. Elevated sympathetic nervous system activity is a well-documented driver of aging-related pathology, including hypertension, cardiac fibrosis, and metabolic dysregulation. Alpha-1B adrenergic receptor overexpression in mice has been shown to cause dilated cardiomyopathy and premature death, while loss-of-function models show improved cardiac outcomes. The receptor's role in protein heterodimerization further amplifies adrenergic signaling networks, reinforcing pro-aging intercellular communication via neuroendocrine stress axes.
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 anti_longevity for Adra1b. The mechanistic reasoning is solid and well-grounded: alpha-1B adrenergic receptor overexpression causing dilated cardiomyopathy and premature death in mice is a real finding, and the connection between chronic sympathoadrenal signaling and aging-related cardiovascular pathology is well-established. The mechanism class of "altered_intercellular_communication" is reasonable, though one could argue "cellular stress" or "cardiovascular dysfunction" might be more precise. The confidence of 0.65 is appropriately calibrated. Minor deduction for reasoning quality: the claim about "loss-of-function models show improved cardiac outcomes" could be more precisely cited, and the mechanism class choice is slightly imprecise.
Raw API responses
solver
{
"reasoning": "Adra1b encodes the alpha-1B adrenergic receptor, a GPCR that mediates sympathetic nervous system signaling via catecholamines (norepinephrine/epinephrine). Chronic activation of alpha-1 adrenergic signaling promotes vasoconstriction, cardiac hypertrophy, and sustained sympathoadrenal tone — all hallmarks of age-associated cardiovascular deterioration. Elevated sympathetic nervous system activity is a well-documented driver of aging-related pathology, including hypertension, cardiac fibrosis, and metabolic dysregulation. Alpha-1B adrenergic receptor overexpression in mice has been shown to cause dilated cardiomyopathy and premature death, while loss-of-function models show improved cardiac outcomes. The receptor's role in protein heterodimerization further amplifies adrenergic signaling networks, reinforcing pro-aging intercellular communication via neuroendocrine stress axes.",
"confidence": 0.65,
"key_pathways": [
"sympathoadrenal/catecholamine signaling",
"Gq/11-PLC-PKC cascade",
"cardiac hypertrophy signaling"
],
"mechanism_class": "altered_intercellular_communication",
"longevity_influence": "anti_longevity"
}advisor
{
"notes": "The model correctly predicted anti_longevity for Adra1b. The mechanistic reasoning is solid and well-grounded: alpha-1B adrenergic receptor overexpression causing dilated cardiomyopathy and premature death in mice is a real finding, and the connection between chronic sympathoadrenal signaling and aging-related cardiovascular pathology is well-established. The mechanism class of \"altered_intercellular_communication\" is reasonable, though one could argue \"cellular stress\" or \"cardiovascular dysfunction\" might be more precise. The confidence of 0.65 is appropriately calibrated. Minor deduction for reasoning quality: the claim about \"loss-of-function models show improved cardiac outcomes\" could be more precisely cited, and the mechanism class choice is slightly imprecise.",
"failure_mode": "correct",
"answer_correct": true,
"mechanism_correct": true,
"reasoning_quality": 4,
"ground_truth_questionable": false
}