Fxn
M. musculus
frataxin
What the model saw
Gene: Fxn Organism: Mus musculus Known functions: frataxin. frataxin, mitochondrial. 2 iron, 2 sulfur cluster binding. enzyme activator activity. enzyme binding. ferric iron binding. ferrous iron binding. ferroxidase activity. iron chaperone activity.
View unredacted entry
frataxin. frataxin, mitochondrial. 2 iron, 2 sulfur cluster binding. enzyme activator activity. enzyme binding. ferric iron binding. ferrous iron binding. ferroxidase activity. iron chaperone activity.
Solver output
Frataxin (FXN) is a mitochondrial iron chaperone that facilitates iron-sulfur (Fe-S) cluster biogenesis and regulates mitochondrial iron homeostasis. By binding ferric and ferrous iron and acting as a ferroxidase, FXN prevents the accumulation of free labile iron in the mitochondrial matrix, thereby suppressing Fenton chemistry and reactive oxygen species (ROS) production. FXN also activates key Fe-S cluster assembly enzymes (e.g., the ISC machinery including NFS1/ISCU), which are essential for the function of mitochondrial respiratory chain complexes I, II, and III. Loss of FXN leads to mitochondrial iron overload, oxidative damage, impaired OXPHOS, and bioenergetic failure — the hallmarks of Friedreich's ataxia. By maintaining mitochondrial integrity and limiting iron-driven oxidative stress, normal FXN function is strongly pro-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 predicted pro_longevity for Fxn (frataxin) in Mus musculus with high confidence (0.88). The mechanistic reasoning is excellent and accurate: frataxin is a mitochondrial iron chaperone involved in Fe-S cluster biogenesis, iron homeostasis, and ROS suppression. Loss of frataxin leads to mitochondrial iron overload, oxidative damage, and bioenergetic failure (Friedreich's ataxia). The model correctly identifies that normal FXN function is pro-longevity by maintaining mitochondrial integrity. The key pathways identified are all relevant and accurate.
Raw API responses
solver
{
"reasoning": "Frataxin (FXN) is a mitochondrial iron chaperone that facilitates iron-sulfur (Fe-S) cluster biogenesis and regulates mitochondrial iron homeostasis. By binding ferric and ferrous iron and acting as a ferroxidase, FXN prevents the accumulation of free labile iron in the mitochondrial matrix, thereby suppressing Fenton chemistry and reactive oxygen species (ROS) production. FXN also activates key Fe-S cluster assembly enzymes (e.g., the ISC machinery including NFS1/ISCU), which are essential for the function of mitochondrial respiratory chain complexes I, II, and III. Loss of FXN leads to mitochondrial iron overload, oxidative damage, impaired OXPHOS, and bioenergetic failure — the hallmarks of Friedreich's ataxia. By maintaining mitochondrial integrity and limiting iron-driven oxidative stress, normal FXN function is strongly pro-longevity.",
"confidence": 0.88,
"key_pathways": [
"mitochondrial iron-sulfur cluster biogenesis",
"mitochondrial iron homeostasis and ROS suppression",
"oxidative phosphorylation (respiratory chain complex assembly)"
],
"mechanism_class": "mitochondrial_dysfunction",
"longevity_influence": "pro_longevity"
}advisor
{
"notes": "The model correctly predicted pro_longevity for Fxn (frataxin) in Mus musculus with high confidence (0.88). The mechanistic reasoning is excellent and accurate: frataxin is a mitochondrial iron chaperone involved in Fe-S cluster biogenesis, iron homeostasis, and ROS suppression. Loss of frataxin leads to mitochondrial iron overload, oxidative damage, and bioenergetic failure (Friedreich's ataxia). The model correctly identifies that normal FXN function is pro-longevity by maintaining mitochondrial integrity. The key pathways identified are all relevant and accurate.",
"failure_mode": "correct",
"answer_correct": true,
"mechanism_correct": true,
"reasoning_quality": 5,
"ground_truth_questionable": false
}