NNK1
S. cerevisiae
protein kinase NNK1
What the model saw
Gene: NNK1 Organism: Saccharomyces cerevisiae Known functions: protein kinase NNK1. ATP binding. calcium-dependent protein serine/threonine kinase activity. calcium/calmodulin-dependent protein kinase activity. calmodulin binding. protein binding. protein kinase activity. protein serine kinase activity. protein serine/threonine kinase activity.
View unredacted entry
protein kinase NNK1. ATP binding. calcium-dependent protein serine/threonine kinase activity. calcium/calmodulin-dependent protein kinase activity. calmodulin binding. protein binding. protein kinase activity. protein serine kinase activity. protein serine/threonine kinase activity.
Solver output
NNK1 (also known as KIN82) encodes a calcium/calmodulin-dependent protein serine/threonine kinase in S. cerevisiae. Calcium/calmodulin-dependent kinases (CaMKs) are central mediators of calcium signaling, which intersects with nutrient-sensing pathways including TORC1 and PKA. In yeast, CaMK-type kinases can modulate stress responses and metabolic adaptation; activation of such kinases under calmodulin/calcium signaling typically promotes stress resistance and cellular homeostasis. NNK1 has been linked to the regulation of nitrogen catabolite repression and responses to nutrient limitation, processes that overlap with TOR pathway modulation — a key axis of longevity regulation. By phosphorylating downstream serine/threonine substrates in a calcium-dependent manner, NNK1 may promote adaptive responses to nutrient stress that extend replicative or chronological lifespan. The calmodulin-binding and calcium-dependent activity suggest a role in sensing environmental cues and coordinating protective cellular responses, which is generally associated with pro-longevity outcomes.
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 predicted pro_longevity but the ground truth is anti_longevity. The model's reasoning is speculative and largely incorrect - it constructs a plausible-sounding but ultimately wrong narrative about NNK1 promoting stress resistance and longevity through calcium/calmodulin signaling. The model incorrectly assumes that CaMK-type kinase activity in yeast generally promotes longevity. In reality, NNK1 is anti-longevity, meaning its deletion or loss likely extends lifespan. The model's confidence of 0.55 is relatively low, but it still committed to the wrong answer. The mechanistic reasoning about nitrogen catabolite repression and TOR pathway modulation is speculative and not well-supported. The model failed to consider that kinase activity can also be detrimental to longevity (e.g., by promoting aging-related processes), and that many kinases in yeast are anti-longevity factors.
Raw API responses
solver
{
"reasoning": "NNK1 (also known as KIN82) encodes a calcium/calmodulin-dependent protein serine/threonine kinase in S. cerevisiae. Calcium/calmodulin-dependent kinases (CaMKs) are central mediators of calcium signaling, which intersects with nutrient-sensing pathways including TORC1 and PKA. In yeast, CaMK-type kinases can modulate stress responses and metabolic adaptation; activation of such kinases under calmodulin/calcium signaling typically promotes stress resistance and cellular homeostasis. NNK1 has been linked to the regulation of nitrogen catabolite repression and responses to nutrient limitation, processes that overlap with TOR pathway modulation — a key axis of longevity regulation. By phosphorylating downstream serine/threonine substrates in a calcium-dependent manner, NNK1 may promote adaptive responses to nutrient stress that extend replicative or chronological lifespan. The calmodulin-binding and calcium-dependent activity suggest a role in sensing environmental cues and coordinating protective cellular responses, which is generally associated with pro-longevity outcomes.",
"confidence": 0.55,
"key_pathways": [
"calcium/calmodulin signaling",
"TOR/nutrient-sensing pathway",
"nitrogen catabolite repression"
],
"mechanism_class": "deregulated_nutrient_sensing",
"longevity_influence": "pro_longevity"
}advisor
{
"notes": "The model predicted pro_longevity but the ground truth is anti_longevity. The model's reasoning is speculative and largely incorrect - it constructs a plausible-sounding but ultimately wrong narrative about NNK1 promoting stress resistance and longevity through calcium/calmodulin signaling. The model incorrectly assumes that CaMK-type kinase activity in yeast generally promotes longevity. In reality, NNK1 is anti-longevity, meaning its deletion or loss likely extends lifespan. The model's confidence of 0.55 is relatively low, but it still committed to the wrong answer. The mechanistic reasoning about nitrogen catabolite repression and TOR pathway modulation is speculative and not well-supported. The model failed to consider that kinase activity can also be detrimental to longevity (e.g., by promoting aging-related processes), and that many kinases in yeast are anti-longevity factors.",
"failure_mode": "confident_wrong",
"answer_correct": false,
"mechanism_correct": false,
"reasoning_quality": 2,
"ground_truth_questionable": false
}