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>> Românã
 
   
 

Ion Cristian Cirstea

Leibniz Institute for Age Research, Jena, Germany

Institution web page: http://www.leibniz-fli.de/research/associated-research-groups/cirstea/
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Born: 1977

Interests: RAS oncogenes, cancer biology, developmental disorders

Details:
RAS proteins (HRAS, KRAS 4A, KRAS 4B, and NRAS) are central signal transduction molecules, which act as molecular switches through cycling between an active, GTP-bound and an inactive, GDP-bound state. Somatic mutations in the HRAS gene (codons 12, 13 and 61) lead to cancer, whereas germline mutations (codon 12 is mutated in more than 80 % of patients) lead to the Costello Syndrome (CS), a rare human disease. RAS mutations at codon 12 lead to a constitutive active RAS protein and the subsequent hyper-activation of downstream signalling pathways. Using protein biochemistry, cell biology and mouse models, we investigate the mechanistic link between aging and cancer, as well as the identification of RAS-regulated pathways triggered during organismal aging.

Selected publications:
• Ion C. Cirstea, Lothar Gremer, Radovan Dvorsky, Si-Cai Zhang, Roland P. Piekorz, Martin Denker and Mohammad Reza Ahmadian. Diverging gain-of-function mechanisms of two novel KRAS mutations associated with Noonan and cardio-facio-cutaneous syndromes. Human Molecular Genetics, 2013.
• Gremer L#, Merbitz-Zahradnik T#, Dvorsky R#, Cirstea IC#, Kratz CP, Zenker M, Wittinghofer A, Ahmadian MR. . Germline KRAS mutations cause aberrant biochemical and physical properties leading to developmental disorders. Human Mutations, 2011.
• Ion C Cirstea, Kerstin Kutsche, Radovan Dvorsky, Lothar Gremer, Claudio Carta, Denise Horn, Amy E Roberts, Francesca Lepri, Torsten Merbitz-Zahradnik, Rainer König, Christian P Kratz, Francesca Pantaleoni, Maria L Dentici, Victoria A Joshi, Raju S Kucheap. A restricted spectrum of NRAS mutations causes Noonan syndrome. Nature Genetics, 42, p. 27–29 , 2010.


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