9VFE

Solution structure of XPC binding domain of hHR23B (apo form)

9VFE の概要

• エントリーDOI: 10.2210/pdb9vfe/pdb
• 分子名称: UV excision repair protein RAD23 homolog B (1 entity in total)
• 機能のキーワード: metal-free form, metal binding protein
• 由来する生物種: Homo sapiens (human)
• タンパク質・核酸の鎖数: 1
• 化学式量合計: 8071.01

構造登録者

Xiao, T.,He, D.,Kelly, M.J.S.,Chang, C.J. (登録日: 2025-06-11, 公開日: 2025-10-01)

主引用文献

Xiao, T.,He, D.,Liu, D.,Jia, S.,Chen, Q.,Silverman, D.,Maitra, N.,Huang, A.Y.,Pezacki, A.,Nguyen, T.T.,Rao, G.,Tillage, R.,Deng, K.,Weinshenker, D.,Britt, R.D.,Kelly, M.J.S.,Dan, Y.,Chang, C.J.
RAD23B acquires a copper metalloadaptor function in amphibian-to-reptile evolution to increase metabolism and regulate genomic integrity.
Mol.Cell, 85:3443-3459.e11, 2025

PubMed 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.

PubMed: 40972527
DOI: 10.1016/j.molcel.2025.08.024

実験手法

SOLUTION NMR