ArticleNature communications2025
C1q drives neural stem cell quiescence by regulating cell cycle and metabolism through BAI1.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
2 citing papers in PubMed.
- Unveiling the mysteries of C1QBP in gynecological tumors (Review).Molecular and clinical oncology · 2026Review
- BAI adhesion-GPCRs perform distinct functions in neural development differentially controlled by RTN4R and C1ql ligands.Nature communications · 2025Article
Corrections and comments
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Authors and funding
17 authors.
Funding
Abstract
C1q levels in the CNS are elevated by inflammation and neurovascular trauma, yet the consequence of this increase for neural stem cell (NSC) regeneration response remain unknown. We have recently identified C1q receptor candidates that regulate NSC behavior. One of these is Brain Angiogenesis Inhibitor 1 (BAI1, ADGRB1), which has no previously discovered role in NSC. Here, we show that C1q acts in a BAI1-dependent manner to modulate NSC quiescence via two parallel mechanisms. First, negative regulation of MDM2, driving cell cycle suppression through p53. Second, endocytic internalization of C1q-BAI1-complex, driving regulation of p32 (C1qBP) and metabolic reprogramming towards aerobic glycolysis. We validated the biological significance of BAI1 in a male hNSC line in vivo using a female mouse model of acute spinal cord injury (SCI). These findings are relevant for a multiplicity of CNS disorders, and illuminate complex connections between C1q, cell cycle, and metabolism. Together, these data provide valuable insight into C1q-mediated regulation of NSC transition between activation and quiescence, processes fundamental for tissue development and repair.
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Registered trials
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