Cooperation and interplay between base and nucleotide excision repair pathways: From DNA lesions to proteins

Autor(es)

Kumar, Namrata ^{[1, 2]} ; Moreno, Natalia C. ^[3] ; Feltes, Bruno C. ^[4] ; Menck, Carlos F. M. ^[3] ; Van Houten, Bennett ^{[1, 2, 5]}

Afiliação do(s) autor(es)

^[1] Univ Pittsburgh, Sch Med, Dept Microbiol & Mol Genet, Pittsburgh, PA - USA

^[2] Univ Pittsburgh, UPMC Hillman Canc Ctr, Pittsburgh, PA - USA

^[3] Univ Sao Paulo, Inst Ciencias Biomed, Dept Microbiol, Sao Paulo, SP - Brazil

^[4] Univ Fed Rio Grande do Sul, Inst Informat, Porto Alegre, RS - Brazil

^[5] Univ Pittsburgh, Sch Med, Dept Pharmacol & Chem Biol, Pittsburgh, PA - USA

• Tipo de documento: Artigo de Revisão
• Fonte: GENETICS AND MOLECULAR BIOLOGY; v. 43, n. 1, 1 2020.
• Citações Web of Science: 0

Resumo

Base and nucleotide excision repair (BER and NER) pathways are normally associated with removal of specific types of DNA damage: small base modifications (such as those induced by DNA oxidation) and bulky DNA lesions (such as those induced by ultraviolet or chemical carcinogens), respectively. However, growing evidence indicates that this scenario is much more complex and these pathways exchange proteins and cooperate with each other in the repair of specific lesions. In this review, we highlight studies discussing the involvement of NER in the repair of DNA damage induced by oxidative stress, and BER participating in the removal of bulky adducts on DNA. Adding to this complexity, UVA light experiments revealed that oxidative stress also causes protein oxidation, directly affecting proteins involved in both NER and BER. This reduces the cell's ability to repair DNA damage with deleterious implications to the cells, such as mutagenesis and cell death, and to the organisms, such as cancer and aging. Finally, an interactome of NER and BER proteins is presented, showing the strong connection between these pathways, indicating that further investigation may reveal new functions shared by them, and their cooperation in maintaining genome stability. (AU)

• Processo FAPESP: 14/15982-6 - Consequências de deficiências de reparo de lesões no genoma
• Beneficiário: Carlos Frederico Martins Menck
• Modalidade de apoio: Auxílio à Pesquisa - Temático