Ubd
M. musculus
ubiquitin D
What the model saw
Gene: Ubd Organism: Mus musculus Known functions: ubiquitin D. proteasome binding. protein binding.
View unredacted entry
ubiquitin D. proteasome binding. protein binding.
Solver output
Ubd (ubiquitin D, also known as FAT10) is a ubiquitin-like modifier that binds the proteasome and targets proteins for degradation independently of canonical ubiquitin conjugation. Unlike canonical ubiquitin, FAT10/Ubd directly tags substrates for proteasomal destruction without recycling, effectively consuming the tagged protein. Chronic or elevated FAT10 activity can dysregulate proteasomal capacity and compete with canonical ubiquitin-mediated proteostasis, impairing the cell's ability to selectively clear damaged or misfolded proteins. FAT10 expression is strongly induced by pro-inflammatory cytokines (TNF-α, IFN-γ), linking it to chronic inflammation and NF-κB signaling, both of which are hallmarks associated with accelerated aging. Overactivation of this pathway can therefore compromise proteostasis and amplify inflammatory signaling, both of which are detrimental to 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 anti_longevity for Ubd (FAT10) in Mus musculus. The mechanistic reasoning is solid and well-grounded: FAT10/Ubd is indeed a ubiquitin-like modifier that targets proteins for proteasomal degradation, is induced by pro-inflammatory cytokines, and links to NF-κB signaling and chronic inflammation. The connection between FAT10 overactivation, proteostasis disruption, and accelerated aging is reasonable and consistent with the literature. The confidence of 0.62 is appropriately moderate. The reasoning quality is good but not perfect — the model could have been more specific about the actual experimental evidence in mice (e.g., FAT10 knockout mice showing extended lifespan or reduced age-related pathology), rather than relying primarily on mechanistic inference.
Raw API responses
solver
{
"reasoning": "Ubd (ubiquitin D, also known as FAT10) is a ubiquitin-like modifier that binds the proteasome and targets proteins for degradation independently of canonical ubiquitin conjugation. Unlike canonical ubiquitin, FAT10/Ubd directly tags substrates for proteasomal destruction without recycling, effectively consuming the tagged protein. Chronic or elevated FAT10 activity can dysregulate proteasomal capacity and compete with canonical ubiquitin-mediated proteostasis, impairing the cell's ability to selectively clear damaged or misfolded proteins. FAT10 expression is strongly induced by pro-inflammatory cytokines (TNF-α, IFN-γ), linking it to chronic inflammation and NF-κB signaling, both of which are hallmarks associated with accelerated aging. Overactivation of this pathway can therefore compromise proteostasis and amplify inflammatory signaling, both of which are detrimental to longevity.",
"confidence": 0.62,
"key_pathways": [
"FAT10/ubiquitin-like proteasomal degradation",
"NF-κB-driven inflammatory signaling",
"ubiquitin-proteasome system (UPS) proteostasis"
],
"mechanism_class": "loss_of_proteostasis",
"longevity_influence": "anti_longevity"
}advisor
{
"notes": "The model correctly predicted anti_longevity for Ubd (FAT10) in Mus musculus. The mechanistic reasoning is solid and well-grounded: FAT10/Ubd is indeed a ubiquitin-like modifier that targets proteins for proteasomal degradation, is induced by pro-inflammatory cytokines, and links to NF-κB signaling and chronic inflammation. The connection between FAT10 overactivation, proteostasis disruption, and accelerated aging is reasonable and consistent with the literature. The confidence of 0.62 is appropriately moderate. The reasoning quality is good but not perfect — the model could have been more specific about the actual experimental evidence in mice (e.g., FAT10 knockout mice showing extended lifespan or reduced age-related pathology), rather than relying primarily on mechanistic inference.",
"failure_mode": "correct",
"answer_correct": true,
"mechanism_correct": true,
"reasoning_quality": 4,
"ground_truth_questionable": false
}