- The molecular basis of dysregulated metabolism in developmental disorder arising from HRAS germline mutations
- LZTR1: a novel modulator of RAS-MAPK pathway
Academic and Scientific education
11/2016 – present PhD Student Ulm University International Graduate School in Molecular Medicine(IGradU) Institute of Comparative Molecular Endocrinology Dr. rer. nat. Ion C. Cirstea
04/2015 – 11/2016 Master of Science Ulm University Molecular Medicine
09/2009 – 02/2015 Bachelor of Science Izmir Institute of Technology Molecular Biology and Genetics
3 selected publications
Engler M, Fidan M, Nandi S, Cirstea IC. Senescence in RASopathies, a possible novel
contributor to a complex pathophenoype Mech. Ageing Dev., 2021; 194:1114111.
Pfänder P, Fidan M, Burret U, Lipinski L, Vettorazzi S. Cdk5 deletion enhances the anti-inflammatory potential of GC-mediated GR activation during inflammation. Frontiers in Immunology, 2019; 10:554
Motta M*, Fidan M*, Bellacchio E, Pantaleoni F, Schneider-Heieck K, Coppola S, Borck G, Salviati L, Zenker M, Cirstea IC# and Tartaglia M#. Dominant Noonan syndrome-causing LZTR1 mutations specifically affect the Kelch domain substrate-recognition surface and enhance RAS-MAPK signaling. Hum. Mol. Genet., 2019, 28(6):1007-1022. *, Equal contribution. #, Equal contribution and joint coordination.
Fidan M, Chennappan S and Cirstea IC. Studying metabolic abnormalities in the Costello Syndrome HRAS G12V mouse model: isolation of mouse embryonic fibroblasts and their in vitro adipocyte differentiation. Methods Mol. Biol. 2262: Ras Activity and Signaling, Editors Ignacio R and Prior I, Springer.