Trpv1
M. musculus
transient receptor potential cation channel, subfamily V, member 1
What the model saw
Gene: Trpv1 Organism: Mus musculus Known functions: transient receptor potential cation channel, subfamily V, member 1. transient receptor potential cation channel subfamily V member 1. ATP binding. calcium channel activity. calmodulin binding. excitatory extracellular ligand-gated monoatomic ion channel activity. extracellular ligand-gated monoatomic ion channel activity. identical protein binding. intracellularly gated calcium channel activity. ligand-gated monoatomic ion channel activity. monoatomic cation channel activity. monoatomic cation transmembrane transporter activity. monoatomic ion channel activity. phosphatidylinositol binding. phosphoprotein binding. protein binding. temperature-gated ion channel activity. transmembrane signaling receptor activity.
View unredacted entry
transient receptor potential cation channel, subfamily V, member 1. transient receptor potential cation channel subfamily V member 1. ATP binding. calcium channel activity. calmodulin binding. excitatory extracellular ligand-gated monoatomic ion channel activity. extracellular ligand-gated monoatomic ion channel activity. identical protein binding. intracellularly gated calcium channel activity. ligand-gated monoatomic ion channel activity. monoatomic cation channel activity. monoatomic cation transmembrane transporter activity. monoatomic ion channel activity. phosphatidylinositol binding. phosphoprotein binding. protein binding. temperature-gated ion channel activity. transmembrane signaling receptor activity.
Solver output
TRPV1 is a thermosensitive, ligand-gated calcium channel expressed prominently in sensory neurons that mediates nociception and thermoregulation. In mice, genetic ablation or pharmacological desensitization of TRPV1-expressing sensory neurons has been shown to extend lifespan and improve metabolic health, suggesting that chronic TRPV1 signaling is detrimental to longevity. TRPV1 activation drives calcium influx and downstream release of neuropeptides (e.g., substance P, CGRP), promoting neurogenic inflammation and altered intercellular communication between sensory neurons and peripheral tissues including adipose and pancreatic islets. Sustained TRPV1-mediated signaling contributes to chronic low-grade inflammation and impaired metabolic regulation, both hallmarks associated with accelerated aging. Because loss of TRPV1 function (not its presence) is associated with longevity benefits in mice, the normal function of TRPV1 is anti-longevity.
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's mechanistic reasoning is actually correct - it correctly identifies that TRPV1 ablation extends lifespan, that chronic TRPV1 signaling is detrimental, and that TRPV1 is therefore anti-longevity. However, the model then contradicts itself by outputting "pro_longevity" as the final prediction, which is the wrong answer. The ground truth is "anti_longevity." The model's reasoning explicitly states "the normal function of TRPV1 is anti-longevity" but then labels it as "pro_longevity" in the structured output field. This is a clear internal contradiction where the reasoning arrives at the correct conclusion but the final answer field is wrong. This is a notable failure mode where the model's reasoning is correct but the final answer is incorrect.
Raw API responses
solver
{
"reasoning": "TRPV1 is a thermosensitive, ligand-gated calcium channel expressed prominently in sensory neurons that mediates nociception and thermoregulation. In mice, genetic ablation or pharmacological desensitization of TRPV1-expressing sensory neurons has been shown to extend lifespan and improve metabolic health, suggesting that chronic TRPV1 signaling is detrimental to longevity. TRPV1 activation drives calcium influx and downstream release of neuropeptides (e.g., substance P, CGRP), promoting neurogenic inflammation and altered intercellular communication between sensory neurons and peripheral tissues including adipose and pancreatic islets. Sustained TRPV1-mediated signaling contributes to chronic low-grade inflammation and impaired metabolic regulation, both hallmarks associated with accelerated aging. Because loss of TRPV1 function (not its presence) is associated with longevity benefits in mice, the normal function of TRPV1 is anti-longevity.",
"confidence": 0.62,
"key_pathways": [
"neurogenic inflammation via neuropeptide release (substance P/CGRP)",
"calcium-dependent sensory neuron signaling",
"thermoregulation and metabolic homeostasis"
],
"mechanism_class": "altered_intercellular_communication",
"longevity_influence": "pro_longevity"
}advisor
{
"notes": "The model's mechanistic reasoning is actually correct - it correctly identifies that TRPV1 ablation extends lifespan, that chronic TRPV1 signaling is detrimental, and that TRPV1 is therefore anti-longevity. However, the model then contradicts itself by outputting \"pro_longevity\" as the final prediction, which is the wrong answer. The ground truth is \"anti_longevity.\" The model's reasoning explicitly states \"the normal function of TRPV1 is anti-longevity\" but then labels it as \"pro_longevity\" in the structured output field. This is a clear internal contradiction where the reasoning arrives at the correct conclusion but the final answer field is wrong. This is a notable failure mode where the model's reasoning is correct but the final answer is incorrect.",
"failure_mode": "right_answer_wrong_reasoning",
"answer_correct": false,
"mechanism_correct": true,
"reasoning_quality": 3,
"ground_truth_questionable": false
}