XPC deficiency is related to APE1 and OGG1 expression and functions

Publication date: Available online 16 January 2016 Source:Mutation Research/Fundamental and Molecular Mechanisms of Mutagenesis Author(s): Julliane Tamara Araújo de Melo, Ana Rafaela de Souza Timoteo, Tirzah Braz Petta Lajus, Juliana Alves Brandão, Nadja Cristhina de Souza-Pinto, Carlos Frederico Martins Menck, Anna Campalans, J.Pablo Radicella, Alexandre Teixeira Vessoni, Alysson Renato Muotri, Lucymara Fassarella Agnez-Lima Oxidative DNA damage is considered to be a major cause of neurodegeneration and internal tumors observed in syndromes that result from nucleotide excision repair (NER) deficiencies, such as Xeroderma Pigmentosum (XP) and Cockayne Syndrome (CS). Recent evidence has shown that NER aids in removing oxidized DNA damage and may interacts with base excision repair (BER) enzymes. Here, we investigated APE1 and OGG1 expression, localization and activity after oxidative stress in XPC-deficient cells. The endogenous APE1 and OGG1 mRNA levels were lower in XPC-deficient fibroblasts. However, XPC-deficient cells did not show hypersensitivity to oxidative stress compared with NER-proficient cells. To confirm the impact of an XPC deficiency in regulating APE1 and OGG1 expression and activity, we established an XPC-complemented cell line. Although the XPC complementation was only partial and transient, the transfected cells exhibited greater OGG1 expression and activity compared with XPC-deficient cells. However, the APE1 expression and acti...
Source: Mutation Research Fundamental and Molecular Mechanisms of Mutagenesis - Category: Cytology Source Type: research