Cbr-daf-2
Caenorhabditis briggsae
What the model saw
Gene: Cbr-daf-2 Organism: Caenorhabditis briggsae Known functions: Protein CBR-DAF-2. ATP binding. insulin receptor activity. insulin receptor substrate binding.
View unredacted entry
Protein CBR-DAF-2. ATP binding. insulin receptor activity. insulin receptor substrate binding.
Solver output
CBR-DAF-2 is the C. briggsae ortholog of the canonical insulin/IGF-1 receptor DAF-2 in C. elegans. Its molecular functions—insulin receptor activity, ATP binding (kinase domain), and insulin receptor substrate binding—place it as the primary receptor tyrosine kinase of the insulin/IGF-1 signaling (IIS) pathway. Active DAF-2 phosphorylates downstream substrates (e.g., AGE-1/PI3K), leading to phosphorylation and cytoplasmic retention of the FOXO transcription factor DAF-16, thereby suppressing expression of stress-resistance, detoxification, and longevity-promoting genes. Loss-of-function mutations in daf-2 dramatically extend lifespan in C. elegans (and by extension C. briggsae) by derepressing DAF-16/FOXO target genes. Thus, the normal (wild-type) function of CBR-DAF-2 actively suppresses longevity by driving IIS-mediated inhibition of DAF-16/FOXO.
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 CBR-DAF-2 as anti_longevity with high confidence (0.95). The mechanistic reasoning is thorough and accurate: CBR-DAF-2 is the C. briggsae ortholog of the C. elegans insulin/IGF-1 receptor DAF-2, which suppresses longevity by activating the IIS pathway and inhibiting DAF-16/FOXO transcription factor. Loss-of-function mutations extend lifespan. The mechanism class (deregulated_nutrient_sensing), key pathways, and molecular details are all correct and well-explained.
Raw API responses
solver
{
"reasoning": "CBR-DAF-2 is the C. briggsae ortholog of the canonical insulin/IGF-1 receptor DAF-2 in C. elegans. Its molecular functions—insulin receptor activity, ATP binding (kinase domain), and insulin receptor substrate binding—place it as the primary receptor tyrosine kinase of the insulin/IGF-1 signaling (IIS) pathway. Active DAF-2 phosphorylates downstream substrates (e.g., AGE-1/PI3K), leading to phosphorylation and cytoplasmic retention of the FOXO transcription factor DAF-16, thereby suppressing expression of stress-resistance, detoxification, and longevity-promoting genes. Loss-of-function mutations in daf-2 dramatically extend lifespan in C. elegans (and by extension C. briggsae) by derepressing DAF-16/FOXO target genes. Thus, the normal (wild-type) function of CBR-DAF-2 actively suppresses longevity by driving IIS-mediated inhibition of DAF-16/FOXO.",
"confidence": 0.95,
"key_pathways": [
"Insulin/IGF-1 signaling (IIS) pathway",
"DAF-2/DAF-16 FOXO signaling axis",
"PI3K-AKT nutrient sensing cascade"
],
"mechanism_class": "deregulated_nutrient_sensing",
"longevity_influence": "anti_longevity"
}advisor
{
"notes": "The model correctly identified CBR-DAF-2 as anti_longevity with high confidence (0.95). The mechanistic reasoning is thorough and accurate: CBR-DAF-2 is the C. briggsae ortholog of the C. elegans insulin/IGF-1 receptor DAF-2, which suppresses longevity by activating the IIS pathway and inhibiting DAF-16/FOXO transcription factor. Loss-of-function mutations extend lifespan. The mechanism class (deregulated_nutrient_sensing), key pathways, and molecular details are all correct and well-explained.",
"failure_mode": "correct",
"answer_correct": true,
"mechanism_correct": true,
"reasoning_quality": 5,
"ground_truth_questionable": false
}