Myc
M. musculus
Myc proto-oncogene, bHLH transcription factor
What the model saw
Gene: Myc Organism: Mus musculus Known functions: Myc proto-oncogene, bHLH transcription factor. myc proto-oncogene protein. DNA binding. DNA-binding transcription activator activity, RNA polymerase II-specific. DNA-binding transcription factor activity. DNA-binding transcription factor activity, RNA polymerase II-specific. DNA-binding transcription factor binding. DNA-binding transcription repressor activity, RNA polymerase II-specific. E-box binding. RNA polymerase II cis-regulatory region sequence-specific DNA binding. SCF ubiquitin ligase complex binding. cis-regulatory region sequence-specific DNA binding. core promoter sequence-specific DNA binding. double-stranded DNA binding. identical protein binding. protein binding. protein dimerization activity. protein-containing complex binding. sequence-specific DNA binding. transcription coregulator binding. ubiquitin protein ligase binding.
View unredacted entry
Myc proto-oncogene, bHLH transcription factor. myc proto-oncogene protein. DNA binding. DNA-binding transcription activator activity, RNA polymerase II-specific. DNA-binding transcription factor activity. DNA-binding transcription factor activity, RNA polymerase II-specific. DNA-binding transcription factor binding. DNA-binding transcription repressor activity, RNA polymerase II-specific. E-box binding. RNA polymerase II cis-regulatory region sequence-specific DNA binding. SCF ubiquitin ligase complex binding. cis-regulatory region sequence-specific DNA binding. core promoter sequence-specific DNA binding. double-stranded DNA binding. identical protein binding. protein binding. protein dimerization activity. protein-containing complex binding. sequence-specific DNA binding. transcription coregulator binding. ubiquitin protein ligase binding.
Solver output
Myc is a bHLH transcription factor that binds E-box elements and acts as a potent transcriptional activator driving cell proliferation, growth, and biosynthetic programs. Chronic or elevated Myc activity promotes oncogenesis, accelerates cellular aging through replication stress and DNA damage, and drives pro-growth signaling that antagonizes longevity-associated pathways such as FOXO and autophagy. Notably, Myc hypomorphic mice (with reduced Myc expression) show extended lifespan in mice, directly demonstrating that normal/high Myc activity is anti-longevity. Myc also suppresses autophagy and activates mTORC1-related anabolic programs, further opposing longevity. Its interaction with SCF ubiquitin ligase complexes and protein dimerization (with Max) amplifies transcriptional programs that favor rapid growth over somatic maintenance, a classical trade-off associated with shortened lifespan.
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 Myc in Mus musculus with high confidence (0.85). The mechanistic reasoning is excellent and well-supported: it correctly identifies Myc hypomorphic mice showing extended lifespan, Myc's role in driving proliferation/growth programs, suppression of autophagy, mTORC1 activation, and the trade-off between rapid growth and somatic maintenance. The mention of Myc-Max dimerization via E-box binding and SCF ubiquitin ligase interactions is accurate. The mechanism class of "cellular_senescence" is somewhat secondary to the primary mechanism (pro-growth/oncogenic signaling), but the overall reasoning is comprehensive and correct.
Raw API responses
solver
{
"reasoning": "Myc is a bHLH transcription factor that binds E-box elements and acts as a potent transcriptional activator driving cell proliferation, growth, and biosynthetic programs. Chronic or elevated Myc activity promotes oncogenesis, accelerates cellular aging through replication stress and DNA damage, and drives pro-growth signaling that antagonizes longevity-associated pathways such as FOXO and autophagy. Notably, Myc hypomorphic mice (with reduced Myc expression) show extended lifespan in mice, directly demonstrating that normal/high Myc activity is anti-longevity. Myc also suppresses autophagy and activates mTORC1-related anabolic programs, further opposing longevity. Its interaction with SCF ubiquitin ligase complexes and protein dimerization (with Max) amplifies transcriptional programs that favor rapid growth over somatic maintenance, a classical trade-off associated with shortened lifespan.",
"confidence": 0.85,
"key_pathways": [
"Myc-Max E-box transcriptional activation driving proliferation and growth",
"mTORC1/anabolic signaling and suppression of autophagy",
"Replication stress and DNA damage response leading to accelerated cellular senescence"
],
"mechanism_class": "cellular_senescence",
"longevity_influence": "anti_longevity"
}advisor
{
"notes": "The model correctly predicted anti_longevity for Myc in Mus musculus with high confidence (0.85). The mechanistic reasoning is excellent and well-supported: it correctly identifies Myc hypomorphic mice showing extended lifespan, Myc's role in driving proliferation/growth programs, suppression of autophagy, mTORC1 activation, and the trade-off between rapid growth and somatic maintenance. The mention of Myc-Max dimerization via E-box binding and SCF ubiquitin ligase interactions is accurate. The mechanism class of \"cellular_senescence\" is somewhat secondary to the primary mechanism (pro-growth/oncogenic signaling), but the overall reasoning is comprehensive and correct.",
"failure_mode": "correct",
"answer_correct": true,
"mechanism_correct": true,
"reasoning_quality": 5,
"ground_truth_questionable": false
}