{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Jun YW"],"funding":["National Institute of Neurological Disorders and Stroke","Howard Hughes Medical Institute","NCI NIH HHS","NINDS NIH HHS"],"pagination":["e202111829"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC8792287"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["61(6)"],"pubmed_abstract":["Mitochondrial function in cells declines with aging and with neurodegeneration, due in large part to accumulated mutations in mitochondrial DNA (mtDNA) that arise from deficient DNA repair. However, measuring this repair activity is challenging. We employ a molecular approach for visualizing mitochondrial base excision repair (BER) activity in situ by use of a fluorescent probe (UBER) that reacts rapidly with AP sites resulting from BER activity. Administering the probe to cultured cells revealed signals that were localized to mitochondria, enabling selective observation of mtDNA BER intermediates. The probe showed elevated DNA repair activity under oxidative stress, and responded to suppression of glycosylase activity. Furthermore, the probe illuminated the time lag between the initiation of oxidative stress and the initial step of BER. Absence of MTH1 in cells resulted in elevated demand for BER activity upon extended oxidative stress, while the absence of OGG1 activity limited glycosylation capacity."],"journal":["Angewandte Chemie (International ed. in English)"],"pubmed_title":["Fluorescence Imaging of Mitochondrial DNA Base Excision Repair Reveals Dynamics of Oxidative Stress Responses."],"pmcid":["PMC8792287"],"funding_grant_id":["NS075136","R01 CA217809","K99 NS075136","R00 NS075136"],"pubmed_authors":["Jun YW","Kool ET","Wilson DL","Albarran E","Ding J"],"additional_accession":[]},"is_claimable":false,"name":"Fluorescence Imaging of Mitochondrial DNA Base Excision Repair Reveals Dynamics of Oxidative Stress Responses.","description":"Mitochondrial function in cells declines with aging and with neurodegeneration, due in large part to accumulated mutations in mitochondrial DNA (mtDNA) that arise from deficient DNA repair. However, measuring this repair activity is challenging. We employ a molecular approach for visualizing mitochondrial base excision repair (BER) activity in situ by use of a fluorescent probe (UBER) that reacts rapidly with AP sites resulting from BER activity. Administering the probe to cultured cells revealed signals that were localized to mitochondria, enabling selective observation of mtDNA BER intermediates. The probe showed elevated DNA repair activity under oxidative stress, and responded to suppression of glycosylase activity. Furthermore, the probe illuminated the time lag between the initiation of oxidative stress and the initial step of BER. Absence of MTH1 in cells resulted in elevated demand for BER activity upon extended oxidative stress, while the absence of OGG1 activity limited glycosylation capacity.","dates":{"release":"2022-01-01T00:00:00Z","publication":"2022 Feb","modification":"2025-04-19T17:55:43.642Z","creation":"2025-04-19T17:55:43.642Z"},"accession":"S-EPMC8792287","cross_references":{"pubmed":["34851014"],"doi":["10.1002/anie.202111829"]}}