ArticleMolecular cell2025
RAD23B acquires a copper metalloadaptor function in amphibian-to-reptile evolution to increase metabolism and regulate genomic integrity.
Article in Molecular cell, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Cuproptosis and the bioinorganic basis of copper-induced cell death.Journal of biological inorganic chemistry : JBIC : a publication of the Society of Biological Inorganic Chemistry · 2026Review
- Copper import via CTR1 supports the β3-Adrenergic thermogenic program.Molecular metabolism · 2026Article
- Cuproptosis inducers mediate cold lethality via SLCR-46.1 in C. elegans.Nature communications · 2026Article
- Copper Import via CTR1 Supports the β3-Adrenergic Thermogenic Program.bioRxiv : the preprint server for biology · 2026Article
- Chemoselective Histidine Bioconjugation Using Thiophosphorodichloridate Reagents.Methods in molecular biology (Clifton, N.J.) · 2026Article
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18 authors.
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Abstract
Increasing brain complexity is a major step in the evolution of species. Here, we show that, in the transition from amphibians to reptiles, the DNA repair protein RAD23B acquires a metalloadaptor function that allows it to serve as a central hub for both metabolism and protection of genomic integrity. More specifically, RAD23B gains an allosteric H274/H323 copper-binding site to enable the transfer of copper from the universal copper transporter 1 (CTR1) uptake protein to all known copper metallochaperone pathways, while simultaneously making its canonical functions in DNA repair copper dependent. This layer of nutrient regulation allows organisms to withstand elevated levels of potentially toxic copper while augmenting metabolism in cells with high energetic needs across both physiology and disease, including neurons in the locus coeruleus, a key brain structure that regulates sleep, and cancer cells.
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