CDC25
S. cerevisiae
Ras family guanine nucleotide exchange factor CDC25
What the model saw
Gene: CDC25 Organism: Saccharomyces cerevisiae Known functions: Ras family guanine nucleotide exchange factor CDC25. guanyl-nucleotide exchange factor activity. protein binding.
View unredacted entry
Ras family guanine nucleotide exchange factor CDC25. guanyl-nucleotide exchange factor activity. protein binding.
Solver output
CDC25 in S. cerevisiae is the guanine nucleotide exchange factor (GEF) for Ras1/Ras2, catalyzing the exchange of GDP for GTP to activate Ras proteins. Active Ras stimulates adenylyl cyclase (Cyr1), elevating cAMP levels and activating PKA (protein kinase A), which is a central pro-growth, anti-longevity signaling axis. Hyperactivation of the Ras/cAMP/PKA pathway suppresses stress resistance, inhibits autophagy, and reduces chronological and replicative lifespan in yeast. Conversely, loss-of-function mutations in RAS2 or reduction of PKA activity extend lifespan. Thus, CDC25's normal function as the activating GEF for Ras places it as a driver of the nutrient-sensing/growth signaling axis that opposes 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 correctly identified CDC25 as anti_longevity with high confidence (0.82). The mechanistic reasoning is excellent and accurate: CDC25 is indeed the GEF for Ras1/Ras2 in S. cerevisiae, activating the Ras/cAMP/PKA pathway, which is a well-established pro-growth, anti-longevity signaling axis. The model correctly notes that this pathway suppresses stress resistance and reduces lifespan, and that loss-of-function in this pathway extends lifespan. The key pathways identified are all relevant and correct.
Raw API responses
solver
{
"reasoning": "CDC25 in S. cerevisiae is the guanine nucleotide exchange factor (GEF) for Ras1/Ras2, catalyzing the exchange of GDP for GTP to activate Ras proteins. Active Ras stimulates adenylyl cyclase (Cyr1), elevating cAMP levels and activating PKA (protein kinase A), which is a central pro-growth, anti-longevity signaling axis. Hyperactivation of the Ras/cAMP/PKA pathway suppresses stress resistance, inhibits autophagy, and reduces chronological and replicative lifespan in yeast. Conversely, loss-of-function mutations in RAS2 or reduction of PKA activity extend lifespan. Thus, CDC25's normal function as the activating GEF for Ras places it as a driver of the nutrient-sensing/growth signaling axis that opposes longevity.",
"confidence": 0.82,
"key_pathways": [
"Ras/cAMP/PKA signaling",
"nutrient sensing and growth signaling",
"stress response suppression"
],
"mechanism_class": "deregulated_nutrient_sensing",
"longevity_influence": "anti_longevity"
}advisor
{
"notes": "The model correctly identified CDC25 as anti_longevity with high confidence (0.82). The mechanistic reasoning is excellent and accurate: CDC25 is indeed the GEF for Ras1/Ras2 in S. cerevisiae, activating the Ras/cAMP/PKA pathway, which is a well-established pro-growth, anti-longevity signaling axis. The model correctly notes that this pathway suppresses stress resistance and reduces lifespan, and that loss-of-function in this pathway extends lifespan. The key pathways identified are all relevant and correct.",
"failure_mode": "correct",
"answer_correct": true,
"mechanism_correct": true,
"reasoning_quality": 5,
"ground_truth_questionable": false
}