Cdc14b
M. musculus
CDC14 cell division cycle 14B
What the model saw
Gene: Cdc14b Organism: Mus musculus Known functions: CDC14 cell division cycle 14B. dual specificity protein phosphatase CDC14B. protein serine/threonine phosphatase activity. protein tyrosine phosphatase activity.
View unredacted entry
CDC14 cell division cycle 14B. dual specificity protein phosphatase CDC14B. protein serine/threonine phosphatase activity. protein tyrosine phosphatase activity.
Solver output
CDC14B is a dual-specificity phosphatase (serine/threonine and tyrosine) that is the mammalian ortholog of yeast Cdc14, a key regulator of mitotic exit and DNA damage response. In mice, CDC14B localizes to centrosomes and is involved in the DNA damage checkpoint, particularly in dephosphorylating and activating CDH1/FZR1 to promote APC/C-mediated degradation of mitotic regulators. Loss of CDC14B impairs the G2/M DNA damage checkpoint, leading to genomic instability and accumulation of DNA damage — a primary hallmark of aging. By maintaining proper checkpoint control and limiting mitotic errors, CDC14B's normal function suppresses genomic instability, thereby supporting cellular integrity and 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 Cdc14b in Mus musculus. The mechanistic reasoning is well-grounded: CDC14B is indeed a dual-specificity phosphatase involved in the DNA damage checkpoint (G2/M), and loss of CDC14B leads to genomic instability, which is a hallmark of aging. The model correctly identifies the APC/C-CDH1 pathway and centrosome regulation as key pathways. The reasoning is coherent and biologically accurate. Confidence of 0.62 is appropriately moderate given the specificity of the gene. Minor deduction for reasoning quality as the model could have been more specific about the actual mouse knockout phenotype (premature aging phenotype in Cdc14b-/- mice), but the overall mechanistic framework is correct.
Raw API responses
solver
{
"reasoning": "CDC14B is a dual-specificity phosphatase (serine/threonine and tyrosine) that is the mammalian ortholog of yeast Cdc14, a key regulator of mitotic exit and DNA damage response. In mice, CDC14B localizes to centrosomes and is involved in the DNA damage checkpoint, particularly in dephosphorylating and activating CDH1/FZR1 to promote APC/C-mediated degradation of mitotic regulators. Loss of CDC14B impairs the G2/M DNA damage checkpoint, leading to genomic instability and accumulation of DNA damage — a primary hallmark of aging. By maintaining proper checkpoint control and limiting mitotic errors, CDC14B's normal function suppresses genomic instability, thereby supporting cellular integrity and longevity.",
"confidence": 0.62,
"key_pathways": [
"DNA damage checkpoint (G2/M)",
"APC/C-CDH1 mitotic exit regulation",
"Centrosome duplication control"
],
"mechanism_class": "genomic_instability",
"longevity_influence": "pro_longevity"
}advisor
{
"notes": "The model correctly predicted pro_longevity for Cdc14b in Mus musculus. The mechanistic reasoning is well-grounded: CDC14B is indeed a dual-specificity phosphatase involved in the DNA damage checkpoint (G2/M), and loss of CDC14B leads to genomic instability, which is a hallmark of aging. The model correctly identifies the APC/C-CDH1 pathway and centrosome regulation as key pathways. The reasoning is coherent and biologically accurate. Confidence of 0.62 is appropriately moderate given the specificity of the gene. Minor deduction for reasoning quality as the model could have been more specific about the actual mouse knockout phenotype (premature aging phenotype in Cdc14b-/- mice), but the overall mechanistic framework is correct.",
"failure_mode": "correct",
"answer_correct": true,
"mechanism_correct": true,
"reasoning_quality": 4,
"ground_truth_questionable": false
}