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Ion Cristian Cirstea

Leibniz Institute for Age Research, Jena, Germany

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Born: 1977

Interests: RAS oncogenes, cancer biology, developmental disorders

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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