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Dr. Miriam Bibel

 
 

Dr. Miriam Bibel
Senior Research Investigator
Autoimmunity/Transplantation /Inflammation
CHBS, WSJ-386.8.08.20
Novartis Institutes for Biomedical Research
Novartis Campus
CH-4056 Basel

 
E-mail miriam.bibel@novartis.com
Phone +41 79 863 45 33
 
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Miriam Bibel is Senior Research Investigator at The Novartis Institutes for BioMedical Research. In her current position she is Project Head in Autoimmunity/Transplantation/Inflammation with a focus on cell fate and cell plasticity in the immune system.
Previously her postdoctoral work at the Friedrich Miescher Institute on establishing a novel system to differentiate mouse embryonic stem (ES) cells into neurons (for which a collaboration with the lab of Austin Smith was key) led her to establish this system for drug discovery within Novartis. Its novel aspect of generating a defined and especially uniform population of CNS neurons opened new opportunities to study mechanisms of neurodegeneration and neuroregeneration in vitro, identify and validate targets of neurodegenerative diseases and also use neuronal populations for screening assays in drug discovery.


Selected recent publications

  • Wollscheid B, Bausch-Fluck D, Henderson C, O`Brien R, Bibel M, Schiess R, Aebersold R. and Watts JD. (2009). Mass-spectrometric identification and relative quantification of N-linked cell surface glycoproteins. Nature Biotechnology 27:378-386.
  • Krol J, Busskamp V, Markiewicz I, Stadler MB, Ribi S, Richter J, Duebel J, Bicker S, Fehling HJ, Schübeler D, Oertner TG, Schratt G, Bibel M, Roska B. and Filipowicz W. (2010). Characterizing light-regulated retinal microRNAs reveals rapid turnover as a common property of neuronal microRNAs. Cell 141:618-631.
  • Nikoletopoulou V, Lickert H, Frade JM, Rencurel C, Giallonardo P, Zhang L, Bibel M. and Barde YA. (2010). Neurotrophin receptors TrkA and TrkC cause neuronal death whereas TrkB does not. Nature 467:59-63.
  • Baldo B, Weiss A, Parker CN, Bibel M, Paganetti P. and Kaupmann K. (2012). A screen for enhancers of clearance identifies huntingtin as a heat shock protein 90 (Hsp90) client protein. J Biol Chem. 287:1406-14.
  • Marcellin D, Abramowski D, Young D, Richter J, Weiss A, Marcel A, Maassen J, Kauffmann M, Bibel M, Shimshek DR, Faull RL, Bates GP, Kuhn RR, Van der Putten PH, Schmid P, Lotz GP. (2012). Fragments of HdhQ150 mutant huntingtin form a soluble oligomer pool that declines with aggregate deposition upon aging. PLoS One 7:e44457. doi: 10.1371/journal.pone.0044457.