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npf

D. melanogaster

neuropeptide F

What the model saw

Gene: NPF
Organism: Drosophila melanogaster
Known functions: neuropeptide F. G protein-coupled receptor binding. neuropeptide F receptor binding. neuropeptide hormone activity.
View unredacted entry
neuropeptide F. G protein-coupled receptor binding. neuropeptide F receptor binding. neuropeptide hormone activity.

Solver output

Predicted influence
Anti-longevity
Confidence
72%
Mechanism
Deregulated nutrient sensing
Reasoning

Neuropeptide F (NPF) is the Drosophila homolog of mammalian neuropeptide Y (NPY), a key neuroendocrine regulator of feeding behavior, energy balance, and nutrient sensing. NPF signals through G protein-coupled receptors (NPF receptors) to promote food-seeking behavior and increase food intake, thereby activating downstream nutrient-sensing pathways including insulin/IGF-1 signaling (IIS). Elevated IIS activity is well-established as anti-longevity in Drosophila, as it suppresses FOXO transcription factor activity and reduces stress resistance. NPF signaling also modulates reward and satiety circuits that, when overactive, drive overconsumption and metabolic dysregulation. Because NPF promotes nutrient-sensing pathway activation rather than restraining it, its normal function is expected to shorten lifespan rather than extend it.

Key pathways
insulin/IGF-1 signaling (IIS)neuropeptide Y-like neuroendocrine signalingFOXO transcription factor regulation
Longevity influence
Anti-longevity
Lifespan effect
Decrease

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
Correct
Mechanism
Correct
Reasoning quality
4/5
Failure mode
Correct
Notes

The model correctly predicted NPF as anti_longevity. The mechanistic reasoning is sound and well-grounded: NPF is indeed the Drosophila homolog of mammalian NPY, it signals through GPCRs to promote feeding and nutrient sensing, and its activation of IIS/suppression of FOXO is a well-established anti-longevity mechanism in Drosophila. The reasoning is coherent and biologically plausible. Confidence of 0.72 is appropriate given the indirect nature of some of the mechanistic links. Minor caveat: the model's reasoning is somewhat inferential (connecting NPF → IIS → anti-longevity) rather than citing direct experimental evidence of NPF overexpression/knockout lifespan studies, but the logic is solid.

Raw API responses

solver

{
  "reasoning": "Neuropeptide F (NPF) is the Drosophila homolog of mammalian neuropeptide Y (NPY), a key neuroendocrine regulator of feeding behavior, energy balance, and nutrient sensing. NPF signals through G protein-coupled receptors (NPF receptors) to promote food-seeking behavior and increase food intake, thereby activating downstream nutrient-sensing pathways including insulin/IGF-1 signaling (IIS). Elevated IIS activity is well-established as anti-longevity in Drosophila, as it suppresses FOXO transcription factor activity and reduces stress resistance. NPF signaling also modulates reward and satiety circuits that, when overactive, drive overconsumption and metabolic dysregulation. Because NPF promotes nutrient-sensing pathway activation rather than restraining it, its normal function is expected to shorten lifespan rather than extend it.",
  "confidence": 0.72,
  "key_pathways": [
    "insulin/IGF-1 signaling (IIS)",
    "neuropeptide Y-like neuroendocrine signaling",
    "FOXO transcription factor regulation"
  ],
  "mechanism_class": "deregulated_nutrient_sensing",
  "longevity_influence": "anti_longevity"
}

advisor

{
  "notes": "The model correctly predicted NPF as anti_longevity. The mechanistic reasoning is sound and well-grounded: NPF is indeed the Drosophila homolog of mammalian NPY, it signals through GPCRs to promote feeding and nutrient sensing, and its activation of IIS/suppression of FOXO is a well-established anti-longevity mechanism in Drosophila. The reasoning is coherent and biologically plausible. Confidence of 0.72 is appropriate given the indirect nature of some of the mechanistic links. Minor caveat: the model's reasoning is somewhat inferential (connecting NPF → IIS → anti-longevity) rather than citing direct experimental evidence of NPF overexpression/knockout lifespan studies, but the logic is solid.",
  "failure_mode": "correct",
  "answer_correct": true,
  "mechanism_correct": true,
  "reasoning_quality": 4,
  "ground_truth_questionable": false
}