The abstract presents a contradiction where HACE1 is inactive/protective in tumors but actively contributes to neurodegeneration pathology. The molecular mechanisms governing this context-dependent functional switch remain unexplained, limiting therapeutic targeting strategies. Gap type: contradiction Source paper: Emerging role and mechanism of HACE1 in the pathogenesis of neurodegenerative diseases: A promising target. (2024, Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie, PMID:38364733)
Landscape Summary: What determines HACE1's transition from tumor suppressor to neurodegeneration mediator? is a 0.76 priority gap in neurodegeneration. It has 0 linked hypotheses with average composite score 0.000. Status: open.
Colonna, Sevlever, et al. (TREM2 biology)
What determines HACE1's transition from tumor suppressor to neurodegeneration mediator? — INVOKE-2 (completed)
No hypotheses linked to this gap yet.
No activity recorded yet.
No discussions yet. Be the first to comment.
Create sub-tasks to investigate specific aspects of this gap: