Ctf1
M. musculus
cardiotrophin 1
What the model saw
Gene: Ctf1 Organism: Mus musculus Known functions: cardiotrophin 1. cardiotrophin-1. cytokine activity. leukemia inhibitory factor receptor binding.
View unredacted entry
cardiotrophin 1. cardiotrophin-1. cytokine activity. leukemia inhibitory factor receptor binding.
Solver output
Cardiotrophin-1 (CT-1) is an IL-6 family cytokine that signals through the leukemia inhibitory factor receptor (LIFR)/gp130 complex, activating JAK-STAT3, MAPK, and PI3K pathways. Chronic activation of IL-6/gp130/STAT3 signaling is a well-established driver of inflammaging and age-related pathology. CT-1 promotes cardiac hypertrophy and fibrosis, and elevated circulating CT-1 is associated with heart failure and metabolic dysfunction — conditions that shorten lifespan. As a pro-inflammatory cytokine with sustained gp130-mediated signaling, its normal function contributes to the chronic low-grade inflammation and tissue remodeling that characterize aging rather than opposing it. While CT-1 has acute cardioprotective roles, its chronic overactivation of STAT3 and inflammatory cascades aligns it with anti-longevity mechanisms.
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 Ctf1 (Cardiotrophin-1) in mice. The mechanistic reasoning is sound: CT-1 is an IL-6 family cytokine signaling through LIFR/gp130, activating JAK-STAT3 pathways associated with inflammaging, cardiac hypertrophy, fibrosis, and metabolic dysfunction. The model appropriately notes the distinction between acute cardioprotective roles and chronic pro-inflammatory/anti-longevity effects. The confidence of 0.62 is reasonable given the complexity. The reasoning is well-grounded in known biology, though the specific GenAge evidence (e.g., knockout studies showing extended lifespan) is not cited, the mechanistic logic is coherent and correct.
Raw API responses
solver
{
"reasoning": "Cardiotrophin-1 (CT-1) is an IL-6 family cytokine that signals through the leukemia inhibitory factor receptor (LIFR)/gp130 complex, activating JAK-STAT3, MAPK, and PI3K pathways. Chronic activation of IL-6/gp130/STAT3 signaling is a well-established driver of inflammaging and age-related pathology. CT-1 promotes cardiac hypertrophy and fibrosis, and elevated circulating CT-1 is associated with heart failure and metabolic dysfunction — conditions that shorten lifespan. As a pro-inflammatory cytokine with sustained gp130-mediated signaling, its normal function contributes to the chronic low-grade inflammation and tissue remodeling that characterize aging rather than opposing it. While CT-1 has acute cardioprotective roles, its chronic overactivation of STAT3 and inflammatory cascades aligns it with anti-longevity mechanisms.",
"confidence": 0.62,
"key_pathways": [
"IL-6/gp130/STAT3 signaling",
"JAK-STAT inflammatory cascade",
"cardiac hypertrophy and fibrosis"
],
"mechanism_class": "chronic_inflammation",
"longevity_influence": "anti_longevity"
}advisor
{
"notes": "The model correctly predicted anti_longevity for Ctf1 (Cardiotrophin-1) in mice. The mechanistic reasoning is sound: CT-1 is an IL-6 family cytokine signaling through LIFR/gp130, activating JAK-STAT3 pathways associated with inflammaging, cardiac hypertrophy, fibrosis, and metabolic dysfunction. The model appropriately notes the distinction between acute cardioprotective roles and chronic pro-inflammatory/anti-longevity effects. The confidence of 0.62 is reasonable given the complexity. The reasoning is well-grounded in known biology, though the specific GenAge evidence (e.g., knockout studies showing extended lifespan) is not cited, the mechanistic logic is coherent and correct.",
"failure_mode": "correct",
"answer_correct": true,
"mechanism_correct": true,
"reasoning_quality": 4,
"ground_truth_questionable": false
}