Her primary areas of study are Cell biology, Telomere, Senescence, DNA damage and Genetics. Her Cell biology study focuses on Mitochondrion in particular. Her biological study deals with issues like Mitochondrial DNA, which deal with fields such as Mitochondrial ROS and Telomerase.
The Senescence study combines topics in areas such as NFKB1, Molecular biology, Ageing and Liver regeneration. The various areas that Gabriele Saretzki examines in her Molecular biology study include Fibroblast, Cell cycle checkpoint, Checkpoint Kinase 2 and Gene product. Her DNA damage study which covers DNA repair that intersects with Stem cell, Cellular differentiation, MDC1, CHEK1 and G2-M DNA damage checkpoint.
The scientist’s investigation covers issues in Telomere, Cell biology, Telomerase, Senescence and Telomerase reverse transcriptase. In her study, Cancer is inextricably linked to Apoptosis, which falls within the broad field of Telomere. Her Cell biology research integrates issues from Oxidative stress, Embryonic stem cell, DNA damage and Genetics.
Her DNA damage research is multidisciplinary, relying on both Stem cell and DNA repair. Gabriele Saretzki combines subjects such as Cell culture, Cancer research, Immunology, Molecular biology and Endometrium with her study of Telomerase. A large part of her Senescence studies is devoted to Cell aging.
Gabriele Saretzki spends much of her time researching Telomerase, Telomere, Cell biology, Cancer research and Telomerase reverse transcriptase. Her Telomerase research incorporates themes from Endometrium, Cancer cell and Endometrial cancer. Her Telomere study combines topics in areas such as Autophagy, Oxidative stress, Ex vivo, In vitro and Cell cycle checkpoint.
Her Cell biology study incorporates themes from Cellular differentiation, DNA damage and Induced pluripotent stem cell. She interconnects Argan oil, Pharmacology and DNA repair in the investigation of issues within DNA damage. Her Telomerase reverse transcriptase research is multidisciplinary, incorporating perspectives in Stem cell, Neural stem cell, Immunology and Human brain.
The scientist’s investigation covers issues in Cell biology, Telomerase, Immunology, Telomere and Induced pluripotent stem cell. Her Cell biology research is multidisciplinary, incorporating elements of Sarcopenia and Skeletal muscle. Telomerase reverse transcriptase is the focus of her Telomerase research.
Her research integrates issues of Cellular differentiation, Gene expression profiling, Reprogramming and Transforming growth factor beta, Signal transduction in her study of Immunology. Her Telomere study frequently draws connections to other fields, such as DNA damage. Her work deals with themes such as Phenotype, mTORC1, In vivo and Mitochondrial biogenesis, which intersect with Senescence.
This overview was generated by a machine learning system which analysed the scientist’s body of work. If you have any feedback, you can contact us here.
A DNA damage checkpoint response in telomere-initiated senescence
Fabrizio d'Adda di Fagagna;Philip M. Reaper;Lorena Clay-Farrace;Heike Fiegler.
Nature (2003)
Mild Hyperoxia Shortens Telomeres and Inhibits Proliferation of Fibroblasts: A Model for Senescence?
T von Zglinicki;G Saretzki;W Döcke;C Lotze.
Experimental Cell Research (1995)
Feedback between p21 and reactive oxygen production is necessary for cell senescence
João F Passos;Glyn Nelson;Chunfang Wang;Torsten Richter.
Molecular Systems Biology (2010)
Mitochondrial dysfunction accounts for the stochastic heterogeneity in telomere-dependent senescence.
João F Passos;Gabriele Saretzki;Gabriele Saretzki;Shaheda Ahmed;Shaheda Ahmed;Glyn Nelson.
PLOS Biology (2007)
Chronic inflammation induces telomere dysfunction and accelerates ageing in mice
Diana Jurk;Caroline Wilson;Joao F. Passos;Fiona Oakley.
Nature Communications (2014)
Preferential Accumulation of Single-Stranded Regions in Telomeres of Human Fibroblasts
Simone Petersen;Gabriele Saretzki;Thomas von Zglinicki.
Experimental Cell Research (1998)
Human cell senescence as a DNA damage response
T. von Zglinicki;G. Saretzki;J. Ladhoff;F. d’Adda di Fagagna.
Mechanisms of Ageing and Development (2005)
Mitochondria are required for pro‐ageing features of the senescent phenotype
Clara Correia-Melo;Clara Correia-Melo;Francisco D.M. Marques;Rhys Anderson;Graeme Hewitt.
The EMBO Journal (2016)
Telomerase does not counteract telomere shortening but protects mitochondrial function under oxidative stress.
Shaheda Ahmed;João F. Passos;Matthew J. Birket;Tina Beckmann.
Journal of Cell Science (2008)
Short Telomeres in Patients with Vascular Dementia: An Indicator of Low Antioxidative Capacity and a Possible Risk Factor?
T von Zglinicki;V Serra;M Lorenz;G Saretzki.
Laboratory Investigation (2000)
If you think any of the details on this page are incorrect, let us know.
We appreciate your kind effort to assist us to improve this page, it would be helpful providing us with as much detail as possible in the text box below:
Newcastle University
Newcastle University
Mayo Clinic
Newcastle University
Durham University
Newcastle University
Newcastle University
University of Kragujevac
University of Cambridge
Newcastle University
Feng Chia University
Sandia National Laboratories
Forschungszentrum Jülich
Shanghai University
Indiana University
Stony Brook University
Oregon State University
University of Melbourne
Tohoku University
Utrecht University
Purdue University West Lafayette
Microsoft (United States)
University of Leon
University of Colorado Boulder
National Institutes of Health
Harvard University