Recognition of DNA damage by the Rad4 nucleotide excision repair protein

摘要: Mutations in the nucleotide excision repair (NER) pathway can cause xeroderma pigmentosum skin cancer predisposition syndrome. NER lesions are limited to one DNA strand, but otherwise they chemically and structurally diverse, being caused by a wide variety of genotoxic chemicals ultraviolet radiation. The C (XPC) protein has central role initiating global-genome recognizing lesion recruiting downstream factors. Here we present crystal structure yeast XPC orthologue Rad4 bound containing cyclobutane pyrimidine dimer (CPD) lesion. shows that inserts β-hairpin through duplex, causing two damaged base pairs flip out double helix. expelled nucleotides undamaged strand recognized Rad4, whereas CPD-linked become disordered. These findings indicate Rad4/XPC thermodynamically destabilize Watson–Crick helix manner facilitates flipping-out pairs. A lasing effect with single artificial atom (a Josephson-junction charge qubit) is embedded superconducting resonator demonstrated, making use property such atoms strongly controllably coupled modes. device essentially different from existing lasers masers; same excited current injection produces many photons.