The UGHS Scientific Journal, Vol. 1
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Anónimo. (2000). Lección 1:Introducción a la eExpression of the Base
Excision Repair Protein APE1 in a Huntington’s Disease In Vitro Model Melody Rivera-Hernández¹, Sulay Rivera-Sánchez², and Sylvette Ayala-Peña³ University Gardens High School¹; University of Puerto Rico, Medical Sciences Campus, Department of Biochemistry²; University of Puerto Rico, Medical Sciences Campus, Department of Pharmacology and Toxicology³. Synopsis: Huntington’s disease (HD) is a fatal, neurodegenerative disease caused by a mutation in the huntingtin gene. The mechanisms leading to HD remain unclear, however, studies support the role of oxidative stress and mitochondrial dysfunction in HD. The base excision repair (BER) pathway plays an important role in the repair of oxidative mitochondrial DNA (mtDNA) lesions. Deficiency in APE1, the main endonuclease in BER, has been linked to increased oxidative stress. It was recently shown that silencing of APE1 leads to mitochondrial dysfunction and to impaired localization of APE1 into the mitochondria of mutant huntingtin-expressing mouse cells after an oxidative insult [4]. It is not known if protein expression levels of APE1 are associated to the accumulation of
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