Postdoc in DNA damage responses in Ageing

POSTDOC POSITIONS AVAILABLE
Schumacher Laboratory
Genome stability in Ageing and Disease
CECAD-Cluster of Excellence in Aging Research, University of Cologne

Institution information: CECAD Cologne Cluster of Excellence: Cellular Stress Responses in Aging-Associated Diseases, University of Cologne, Zülpicher Str. 47a, 50674 Cologne, Germany
Location: Cologne is a vibrant city with a highly international academic research environment. CECAD forms a focal point of aging research in Europe.
Website: www.schumacher-lab.cecad.uni-koeln.de
Summary: Our research aims at understanding how DNA damage accumulation causes aging. Furthering our knowledge of the mechanisms of cellular responses to accumulating DNA damage will give us a better insight into the biology of aging and might lead to the development of therapeutic strategies aimed at prevention of aging-related diseases.
Job description: We are seeking highly motivated Postdoc candidates for our ERC-funded team investigating the fundamental role of DNA damage in aging. We are using both genetic and biochemical approaches primarily in the C. elegans but also in mammalian systems to investigate the molecular basis of aging.
Qualification: Applicants should have a solid background in molecular biology and experience in cell biology, genetics, or biochemistry. Postdoc candidates should have demonstrated outstanding performance by high impact publications.
How to Apply: Please send CV, letter of intent, names and addresses of three references to bjoern.schumacher@uni-koeln.de
Selected Publications:
Ermolaeva M, Segref A, Dakhovnik A, Ou H-L, Schneider J, Utermöhlen O, Hoppe T, Schumacher B. DNA damage in germ cells induces an innate immune response that triggers systemic stress resistance. Nature 2013. doi:10.1038/nature12452. Epub 2013 Aug 25
Reinhardt HC, Schumacher B . The p53 network: Cellular and systemic DNA damage responses in aging and cancer. Trends Genet. 2012 Mar;28(3):128-36.
Garinis GA, Uittenboogaard LM, Stachelscheid H, Fousteri M, van Ijcken W, Breit TM, van Steeg H, Mullenders LHF, van der Horst GTJ, Brüning JC, Niessen CM, Hoeijmakers JHJ and Schumacher B. Persistent transcription-blocking DNA lesions trigger somatic growth attenuation associated with longevity. Nature Cell Biol. 2009 May;11(5):604-15.
Schumacher B, van der Pluijm I, Moorhouse MJ, Rasile Robinson A, Suh Y, Breit TM, van Steeg H, Niedernhofer LJ, van Ijcken W, Bartke A, Spindler SR, Hoeijmakers JHJ, van der Horst GTJ and Garinis GA. Delayed and accelerated aging share common longevity assurance mechanisms. PLoS Genet. 2008 Aug 15;4(8):e1000161.
Schumacher B, Hanazawa M, Lee M, Nayak S, Volkmann K, Hofmann R, Hengartner M, Schedl T, Gartner A. Translational Repression of C. elegans p53 by GLD-1 regulates DNA damage induced apoptosis. Cell, 11 February 2005; 120: 357-368.