Cirstea Lab

From left: Dr. Ion Cirstea, Dr. Miray Fidan, Moses Ireri, Melanie Engler

Funding Agencies




Name First name   Title  Fon Fax Email Lab Building Function
Cirstea Ion Cristian Dr. 36214 36202 ion.cirstea(at) 3.30 N26 Group leader
Engler Melanie M.Sc. 36214 36202 melanie.engler(at) 3.30 N26 PhD student
Ireri Moses Munene M.Sc. 36214 36202 moses.ireri(at) 3.30 N26 PhD student

Welcome to Cirstea Research Group

Cirstea Research Group focuses on the identification of novel RAS-controlled biological processes and -signaling pathways that are implicated in cancer, RASopathies and neuronal development, energy metabolism, and premature aging and aging-related diseases. For our research, we use cellular and mouse models and a wide variety of cell-based and biochemical techniques.


Most Important Research Directions

  • Novel treatment strategies in neurodevelopmental RASopathies




Dr. Ion Cristian Cirstea

Institute of Applied Physiology

89081 Ulm, Germany

Email: ion.cirstea(at)

Fon: +49 731 50-32630
Fax: +49 731 50-36202

Selected Publications

Engler M, Albers D, Von Maltitz P, Groß R, Münch J, Cirstea IC. ACE2-EGFR-MAPK signaling contributes to SARS-CoV-2 infection. Life Sci. Alliance 2023, 6(9):e202201880.

Cirstea IC*#, Moll HP*#, Tuckermann J*#. Glucocorticoid receptor-RAS - an unexpected couple in cancer. Trends in Cell Biology. 2023, S0962-8924(22)00253-7. *#, Equal contribution and correspondence

Nandi S, Chennappan S, Andrasch Y, Fidan M, Engler M, Ahmad M, Tuckermann JP, Zenker M, Cirstea IC. Increased osteoclastogenesis contributes to bone loss in the Costello syndrome Hras G12V mouse model. Front. Cell Dev. Biol. 2022, 10:1000575.

Caratti B, Fidan M, Caratti G, Breitenecker K, Engler M, Kazemitash N, Traut R, Wittig R, Casanova E, Ahmadian MR, Tuckermann JP, Moll HP, Cirstea IC. The glucocorticoid receptor associates with RAS protein complex to inhibit cell proliferation and tumor growth. Science Signaling 2022, 22;15(726):eabm4452. , equal contribution and joint coordination

Motta M*, Fidan M*, Bellacchio E, Pantaleoni F, Schneider-Heieck K, Coppola S, Borck G, Salviati L, Zenker M, Cirstea IC**, 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

Cirstea IC, Gremer L, Dvorsky R, Zenker M, Ahmadian MR. Diverging gain-of-function mechanisms of two novel KRAS mutations associated with Noonan and Cardio-Facio-Cutaneous syndromes. Hum. Mol. Genet. 2013, 22(2):262-70.

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. Hum. Mutat. 2011, 32(1):33-43. #, equal contribution.

Cirstea IC, Kutsche K, Dvorsky R, Gremer L, Carta C, Horn D, Roberts AE, Lepri F, Merbitz-Zahradnik T, König R, Kratz CP, Pantaleoni F, Dentici ML, Joshi VA, Kucherlapati RS, Mazzanti L, Mundlos S, Patton MA, Silengo MC, Rossi C, Zampino G, Digilio C, Stuppia L, Seemanova E, Pennacchio LA, Gelb BD, Dallapiccola B, Wittinghofer A, Ahmadian MR, Tartaglia M, Zenker M. A restricted spectrum of NRAS mutations causes Noonan syndrome. Nat. Genet. 2010, 42(1):27-9.