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shd1

S. pombe

Sla1 family protein Shd1

What the model saw

Gene: shd1
Organism: Schizosaccharomyces pombe
Known functions: Sla1 family protein Shd1. cytoskeletal protein binding. identical protein binding. protein-macromolecule adaptor activity. ubiquitin binding.
View unredacted entry
Sla1 family protein Shd1. cytoskeletal protein binding. identical protein binding. protein-macromolecule adaptor activity. ubiquitin binding.

Solver output

Predicted influence
Pro-longevity
Confidence
52%
Mechanism
Loss of proteostasis
Reasoning

Shd1 is a Sla1 family protein with ubiquitin binding and protein-macromolecule adaptor activity, suggesting it functions as an adaptor in ubiquitin-mediated protein quality control pathways. Sla1 family members in yeast are known to link ubiquitinated cargo to the endocytic and proteasomal degradation machinery, facilitating clearance of misfolded or damaged proteins. By acting as a cytoskeletal adaptor that bridges ubiquitinated substrates to degradation or sorting complexes, Shd1 would support proteostasis — a key pro-longevity function. Loss of such adaptors typically impairs protein quality control, leading to accumulation of damaged proteins, a hallmark of aging. The identical protein binding activity further suggests a role in oligomeric complex assembly relevant to proteostatic surveillance.

Key pathways
ubiquitin-mediated proteolysisendocytic protein quality controlcytoskeletal-ubiquitin cargo adaptor signaling
Longevity influence
Anti-longevity
Lifespan effect
Increase

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

Answer
Incorrect
Mechanism
Incorrect
Reasoning quality
2/5
Failure mode
Confident wrong
Notes

The model predicted pro_longevity but the ground truth is anti_longevity. The model's reasoning about Shd1 as a proteostasis-supporting adaptor is speculative and ultimately incorrect. The model assumed that ubiquitin binding and cytoskeletal adaptor activity would make shd1 pro-longevity (i.e., its loss would impair proteostasis and shorten lifespan), but the actual classification is anti_longevity, meaning shd1 deletion likely extends lifespan. The confidence was low (0.52), which is appropriate given the uncertainty, but the prediction was still wrong. The mechanistic reasoning is also incorrect since the gene is anti-longevity, suggesting shd1 may actually promote aging rather than protect against it.

Raw API responses

solver

{
  "reasoning": "Shd1 is a Sla1 family protein with ubiquitin binding and protein-macromolecule adaptor activity, suggesting it functions as an adaptor in ubiquitin-mediated protein quality control pathways. Sla1 family members in yeast are known to link ubiquitinated cargo to the endocytic and proteasomal degradation machinery, facilitating clearance of misfolded or damaged proteins. By acting as a cytoskeletal adaptor that bridges ubiquitinated substrates to degradation or sorting complexes, Shd1 would support proteostasis — a key pro-longevity function. Loss of such adaptors typically impairs protein quality control, leading to accumulation of damaged proteins, a hallmark of aging. The identical protein binding activity further suggests a role in oligomeric complex assembly relevant to proteostatic surveillance.",
  "confidence": 0.52,
  "key_pathways": [
    "ubiquitin-mediated proteolysis",
    "endocytic protein quality control",
    "cytoskeletal-ubiquitin cargo adaptor signaling"
  ],
  "mechanism_class": "loss_of_proteostasis",
  "longevity_influence": "pro_longevity"
}

advisor

{
  "notes": "The model predicted pro_longevity but the ground truth is anti_longevity. The model's reasoning about Shd1 as a proteostasis-supporting adaptor is speculative and ultimately incorrect. The model assumed that ubiquitin binding and cytoskeletal adaptor activity would make shd1 pro-longevity (i.e., its loss would impair proteostasis and shorten lifespan), but the actual classification is anti_longevity, meaning shd1 deletion likely extends lifespan. The confidence was low (0.52), which is appropriate given the uncertainty, but the prediction was still wrong. The mechanistic reasoning is also incorrect since the gene is anti-longevity, suggesting shd1 may actually promote aging rather than protect against it.",
  "failure_mode": "confident_wrong",
  "answer_correct": false,
  "mechanism_correct": false,
  "reasoning_quality": 2,
  "ground_truth_questionable": false
}