Prof. Dr. Karima Djabali

Academic Career and Research Areas

The principle aim of Professor Djabali’s research on the molecular and cellular pathogenesis of premature ageing, in particular of Hutchsinson-Gildford Progeria Syndrome (HGPS), is to develop preventative strategies to slow down the ageing process and the course of age-related disease. A major focus of this research is stem cell research and its significance for tissue regeneration during the ageing process.

After completing her studies in biochemistry (Université Paris 7), Professor Djabali performed her doctoral studies in biology at the College de France (Professor Gros) and at the Rockefeller University with Professor Guenter Blobel (Nobel Prize 1999). Further positions included a postdoctoral post at EMBL Heidelberg (1992), chargé de recherche at CNRS (1994) and assistant professor at Columbia University, NY, USA (2004). Since 2009 she and her laboratory have been part of the Department of Dermatology and Allergy and the Central Institute for Medical Technology. Professor Djabali has successfully acquired funding for a significant number of projects (R03 NIH/NIAMS (2002-2005), K01 NIH/NIAMS (2003-2009) und 2x R01 NIH/NIA (2005-2010).


  • Christine Kühne Center for Allergy Research and Education (CK-CARE) (2010-2011)
  • Fellow der Alexander von Humboldt Foundation (2009-2014)         
  • Irving Clinical Research Career Award (2006-2010)
Progeria Research Foundation (2005-2007)
  • Dermatology Foundation (2002)

Key Publications

Marji J, O’Donoghue SI, McClintock D, Satagopam V, Schneider R, Ratner D, Worman HJ, Gordom LB, Djabali K: “Defective lamin A-Rb signaling in Hutchinson-Gilford progeria Syndrome and reversal by farnesyltransferase inhibition.” PLoS One. 2010; 15; 5(6): e11132.

McClintock D, Ratner D, Owens DM, Gordon LB, Collins FS, Djabali K: “The Hutchinson-Gilford Progeria mutant lamin A is a biomarker of cellular aging in human skin”.  PLoS One. 2007; Dec 5,2(12): e1269.

McClintock D, Gordon LB, Djabali K: “Hutchinson-Gilford Progeria mutant lamin A primarily targets human vascular cells as detected by an anti-lamin A G608G antibody”. Proc. Natl. Acad. Sci. USA. 2006; 103, 2154-2159.

Paradisi M, McClintock D, Boguslavsky RL, Pedicelli C, Worman HJ, Djabali K: “Dermal fibroblasts in Hutchinson Gilford Progeria Syndrome with lamin A G608G mutation have dysmorphic nuclei and are hypersensitive to heat stress.” BMC. Cell. Biol. 2005; 27 (6): 27.