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jnk-1

C. elegans

Stress-activated protein kinase jnk-1

What the model saw

Gene: jnk-1
Organism: Caenorhabditis elegans
Known functions: Stress-activated protein kinase jnk-1. ATP binding. JUN kinase activity. MAP kinase activity. RNA polymerase II-specific DNA-binding transcription factor binding. protein binding. protein kinase activity. protein serine kinase activity.
View unredacted entry
Stress-activated protein kinase jnk-1. ATP binding. JUN kinase activity. MAP kinase activity. RNA polymerase II-specific DNA-binding transcription factor binding. protein binding. protein kinase activity. protein serine kinase activity.

Solver output

Predicted influence
Pro-longevity
Confidence
72%
Mechanism
Cellular senescence
Reasoning

JNK-1 is the C. elegans ortholog of mammalian JNK (c-Jun N-terminal kinase), a stress-activated MAP kinase. In C. elegans, jnk-1 has been shown to phosphorylate and activate the DAF-16/FOXO transcription factor by promoting its nuclear localization, thereby enhancing expression of stress-resistance and longevity genes downstream of the insulin/IGF-1 signaling pathway. JNK-1 acts in parallel to the canonical DAF-2/AGE-1/PDK-1 axis, providing an alternative route to DAF-16 activation under stress conditions. Its JUN kinase and MAP kinase activities also mediate phosphorylation of transcription factors that regulate oxidative stress responses and proteostasis. Overexpression of jnk-1 extends lifespan in C. elegans, consistent with a pro-longevity role through stress-response pathway activation.

Key pathways
DAF-16/FOXO transcription factor activationInsulin/IGF-1 signaling (DAF-2 pathway)Stress-activated MAPK signaling
Longevity influence
Pro-longevity
Lifespan effect
Increase and 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
5/5
Failure mode
Correct
Notes

The model correctly predicted pro_longevity for jnk-1 in C. elegans. The mechanistic reasoning is accurate and detailed: JNK-1 phosphorylates DAF-16/FOXO to promote nuclear localization, acts in parallel to the DAF-2/AGE-1/PDK-1 axis, and overexpression extends lifespan. The only minor issue is the mechanism_class being labeled "cellular_senescence," which is not the most precise classification for a stress-activated MAPK pathway in C. elegans (which doesn't undergo cellular senescence in the same way mammals do). However, the textual reasoning is mechanistically sound and well-supported by the literature. The confidence level of 0.72 is appropriate.

Raw API responses

solver

{
  "reasoning": "JNK-1 is the C. elegans ortholog of mammalian JNK (c-Jun N-terminal kinase), a stress-activated MAP kinase. In C. elegans, jnk-1 has been shown to phosphorylate and activate the DAF-16/FOXO transcription factor by promoting its nuclear localization, thereby enhancing expression of stress-resistance and longevity genes downstream of the insulin/IGF-1 signaling pathway. JNK-1 acts in parallel to the canonical DAF-2/AGE-1/PDK-1 axis, providing an alternative route to DAF-16 activation under stress conditions. Its JUN kinase and MAP kinase activities also mediate phosphorylation of transcription factors that regulate oxidative stress responses and proteostasis. Overexpression of jnk-1 extends lifespan in C. elegans, consistent with a pro-longevity role through stress-response pathway activation.",
  "confidence": 0.72,
  "key_pathways": [
    "DAF-16/FOXO transcription factor activation",
    "Insulin/IGF-1 signaling (DAF-2 pathway)",
    "Stress-activated MAPK signaling"
  ],
  "mechanism_class": "cellular_senescence",
  "longevity_influence": "pro_longevity"
}

advisor

{
  "notes": "The model correctly predicted pro_longevity for jnk-1 in C. elegans. The mechanistic reasoning is accurate and detailed: JNK-1 phosphorylates DAF-16/FOXO to promote nuclear localization, acts in parallel to the DAF-2/AGE-1/PDK-1 axis, and overexpression extends lifespan. The only minor issue is the mechanism_class being labeled \"cellular_senescence,\" which is not the most precise classification for a stress-activated MAPK pathway in C. elegans (which doesn't undergo cellular senescence in the same way mammals do). However, the textual reasoning is mechanistically sound and well-supported by the literature. The confidence level of 0.72 is appropriate.",
  "failure_mode": "correct",
  "answer_correct": true,
  "mechanism_correct": true,
  "reasoning_quality": 5,
  "ground_truth_questionable": false
}