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ubc-13

C. elegans

Ubiquitin-conjugating enzyme E2 13

What the model saw

Gene: ubc-13
Organism: Caenorhabditis elegans
Known functions: Ubiquitin-conjugating enzyme E2 13. protein binding. ubiquitin conjugating enzyme activity. ubiquitin-protein transferase activity.
View unredacted entry
Ubiquitin-conjugating enzyme E2 13. protein binding. ubiquitin conjugating enzyme activity. ubiquitin-protein transferase activity.

Solver output

Predicted influence
Pro-longevity
Confidence
62%
Mechanism
Loss of proteostasis
Reasoning

UBC-13 is the C. elegans ortholog of the E2 ubiquitin-conjugating enzyme UBC13 (UBE2N in mammals), which specifically catalyzes K63-linked polyubiquitin chain synthesis in partnership with UEV proteins. K63-linked ubiquitination is a non-degradative signal primarily involved in DNA damage response (DDR), NF-κB signaling, and selective autophagy receptor activation. By facilitating K63-linked ubiquitination, UBC-13 supports proteostasis through autophagy cargo recognition and also contributes to genomic stability via DDR signaling. Loss of UBC-13 function in C. elegans impairs these pathways, leading to accumulation of damaged proteins and DNA lesions, which are hallmarks of accelerated aging. Its role in maintaining proteostasis and genome integrity places it as a pro-longevity factor.

Key pathways
K63-linked ubiquitin chain synthesisDNA damage response signalingselective autophagy cargo recognition
Longevity influence
Pro-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 pro_longevity for ubc-13 in C. elegans. The mechanistic reasoning is sound and well-grounded: UBC-13 is indeed the E2 ubiquitin-conjugating enzyme responsible for K63-linked polyubiquitin chains, and its roles in DNA damage response, proteostasis, and selective autophagy are well-established. The reasoning that loss of UBC-13 impairs these pathways and leads to accelerated aging is plausible and consistent with the literature. The confidence of 0.62 is appropriately moderate. The mechanism class of "loss_of_proteostasis" is a reasonable categorization, though the DDR and ubiquitin signaling aspects are arguably more central than proteostasis per se. Overall, a solid prediction with good mechanistic reasoning.

Raw API responses

solver

{
  "reasoning": "UBC-13 is the C. elegans ortholog of the E2 ubiquitin-conjugating enzyme UBC13 (UBE2N in mammals), which specifically catalyzes K63-linked polyubiquitin chain synthesis in partnership with UEV proteins. K63-linked ubiquitination is a non-degradative signal primarily involved in DNA damage response (DDR), NF-κB signaling, and selective autophagy receptor activation. By facilitating K63-linked ubiquitination, UBC-13 supports proteostasis through autophagy cargo recognition and also contributes to genomic stability via DDR signaling. Loss of UBC-13 function in C. elegans impairs these pathways, leading to accumulation of damaged proteins and DNA lesions, which are hallmarks of accelerated aging. Its role in maintaining proteostasis and genome integrity places it as a pro-longevity factor.",
  "confidence": 0.62,
  "key_pathways": [
    "K63-linked ubiquitin chain synthesis",
    "DNA damage response signaling",
    "selective autophagy cargo recognition"
  ],
  "mechanism_class": "loss_of_proteostasis",
  "longevity_influence": "pro_longevity"
}

advisor

{
  "notes": "The model correctly predicted pro_longevity for ubc-13 in C. elegans. The mechanistic reasoning is sound and well-grounded: UBC-13 is indeed the E2 ubiquitin-conjugating enzyme responsible for K63-linked polyubiquitin chains, and its roles in DNA damage response, proteostasis, and selective autophagy are well-established. The reasoning that loss of UBC-13 impairs these pathways and leads to accelerated aging is plausible and consistent with the literature. The confidence of 0.62 is appropriately moderate. The mechanism class of \"loss_of_proteostasis\" is a reasonable categorization, though the DDR and ubiquitin signaling aspects are arguably more central than proteostasis per se. Overall, a solid prediction with good mechanistic reasoning.",
  "failure_mode": "correct",
  "answer_correct": true,
  "mechanism_correct": true,
  "reasoning_quality": 4,
  "ground_truth_questionable": false
}