A5070581568- DNA Repair Mechanisms
- Mitochondrial Function and Pathology
- Genetics, Aging, and Longevity in Model Organisms
- Carcinogens and Genotoxicity Assessment
- DNA and Nucleic Acid Chemistry
- Acute Lymphoblastic Leukemia research
- Metabolism and Genetic Disorders
- Cancer therapeutics and mechanisms
- Genetics and Neurodevelopmental Disorders
- CRISPR and Genetic Engineering
- Telomeres, Telomerase, and Senescence
- Photosynthetic Processes and Mechanisms
- Birth, Development, and Health
- Muscle Physiology and Disorders
- Genetic Neurodegenerative Diseases
- ATP Synthase and ATPases Research
- Adipose Tissue and Metabolism
- Autophagy in Disease and Therapy
- Tryptophan and brain disorders
- FOXO transcription factor regulation
- MicroRNA in disease regulation
- Genomics and Chromatin Dynamics
- Neuroscience and Neuropharmacology Research
- PARP inhibition in cancer therapy
- Cytomegalovirus and herpesvirus research
Aarhus University
2015-2024
University of Southern Denmark
2010-2024
Danish Pain Research Center
2009-2022
Aarhus School of Architecture
2017
Universidad Complutense de Madrid
2012
University of North Carolina at Chapel Hill
2008
National Institutes of Health
1992-2007
National Institute on Aging
1995-2007
Vanderbilt University
2007
National Cancer Institute
1991-1993
Emerging findings suggest that compromised cellular bioenergetics and DNA repair contribute to the pathogenesis of Alzheimer's disease (AD), but their role in disease-defining pathology is unclear. We developed a repair-deficient 3xTgAD/Polβ
Aging is an inevitable biological process characterized by a progressive decline in physiological function and increased susceptibility to disease. The detrimental effects of aging are observed all tissues, the brain being most important one due its main role homeostasis organism. As our knowledge about underlying mechanisms increases, potential approaches preserve rise significantly. Accumulating evidence suggests that loss genomic maintenance may contribute aging, especially central...
Aging | doi:10.18632/aging.204248. Tomas Schmauck-Medina, Adrian Molière, Sofie Lautrup, Jianying Zhang, Stefan Chlopicki, Helena Borland Madsen, Shuqin Cao, Casper Soendenbroe, Els Mansell, Mark Bitsch Vestergaard, Zhiquan Li, Yosef Shiloh, Patricia L. Opresko, Jean-Marc Egly, Thomas Kirkwood, Eric Verdin, Vilhelm A. Bohr, Lynne S. Cox, Tinna Stevnsner, Lene Juel Rasmussen, Evandro F. Fang
Using methodology recently developed to assess gene-specific DNA repair, we have demonstrated that it is possible not only study mitochondrial but also directly compare and nuclear repair in the same biological sample. Complex enzymatic mechanisms recognize damage, has long been thought there was no mitochondria. Therefore, an attempt delineate more clearly which mechanisms, if any, are functioning mitochondria, investigated of several specific lesions DNA. They include cyclobutane dimers,...
Summary Genetic variation in FOXO3A has previously been associated with human longevity. Studies published so far have case–control studies and hence vulnerable to bias introduced by cohort effects. In this study we extended the previous findings cohorts of oldest old Danes (the Danish 1905 cohort, N = 1089) middle‐aged ( 736), applying a longitudinal design as well design. Fifteen SNPs were chosen order cover known common . Comparing SNP frequencies individuals, found association (after...
Cockayne syndrome (CS) is a human premature aging disorder associated with severe developmental deficiencies and neurodegeneration, phenotypically it resembles some mitochondrial DNA (mtDNA) diseases. Most patients belong to complementation group B, the CS B (CSB) protein plays role in genomic maintenance transcriptome regulation. By immunocytochemistry, fractionation, Western blotting, we demonstrate that CSB localizes mitochondria different types of cells, increased distribution following...
Telomerase is of key importance for telomere maintenance, and variants the genes encoding its major subunits, telomerase reverse transcriptase (TERT) RNA component (TERC), are candidates interindividual variation in length. Recently, two SNPs rs3772190 rs12696304 TERC locus were reported to be associated with leukocyte length (LTL) genome-wide association studies, while one haplotype TERT (rs2853669, rs2736098, rs33954691, rs2853691) has been both LTL longevity a candidate gene study. In...
Cockayne syndrome (CS) is a premature aging condition characterized by sensitivity to UV radiation. However, this phenotype does not explain the progressive neurodegeneration in CS patients. It could be due hypersensitivity of CSB-deficient cells oxidative stress. So far most studies on role CSB repair oxidatively induced DNA lesions have focused 7,8-dihydro-8-oxoguanine. This study examines formamidopyrimidines 2,6-diamino-4-hydroxy-5-formamidopyrimidine (FapyGua) and...
Summary Exogenous and endogenous damage to DNA is constantly challenging the stability of our genome. This increase frequency errors in replication, thus causing point mutations or chromosomal rearrangements has been implicated aging, cancer, neurodegenerative diseases. Therefore, efficient repair vital for maintenance genome stability. The general notion that capacity decreases with age although there are conflicting results. Here, we focused on potential age‐associated changes response...
Cockayne syndrome (CS) is a rare genetic disorder characterized as segmental premature-aging syndrome. The CS group B (CSB) protein has previously been implicated in transcription-coupled repair, transcriptional elongation, and restoration of RNA synthesis after DNA damage. Recently, evidence for role CSB base excision repair oxidative lesions accumulated. In our search to understand the molecular function this process, we identify physical functional interaction between poly(ADP-ribose)...