A glycolytic metabolite that drives BRCA2 haploinsufficiency.
editorial · Level V
Where this comes from
- Record sourced from PubMed, PMID 38670069.
- Also identified by DOI 10.1016/j.cell.2024.03.028.
- No licence information is recorded for this record.
- Because redistribution is not established, this page shows the abstract only. Follow the links below for the full text.
Abstract
Many types of tumor cells alter metabolic pathways to meet their energy and biosynthetic demands for proliferation or stress adaptation. In this issue of Cell, Kong et al. find that the glycolytic metabolite methylglyoxal causes cancer-associated mutant single-base substitution features by inducing BRCA2 proteolysis, leading to functional haploinsufficiency of BRCA2.
Medical subject headings
- Haploinsufficiency
- Glycolysis
- BRCA2 Protein