Marco Chiaravalli
  • Division of Genetics and Cell Biology, San Raffaele Scientific Institute, Italy
Research fields
  • Cell biology
Personal information

Education

B.S. in Tecniche di Laboratorio Biomedico, achieved at the Università degli Studi dell’Insubria of Varese, 2005

Current position

Successive fellowships at Division of Genetics and Cell Biology, San Raffaele Hospital, DIBIT; as laboratory technician (reserch assistant) in the group of Dr. Alessandra Bolette (Dulbecco Telethon Institute, Molecular Basis of Polycistyc Kidney Disease)

Publications

  1. Rowe I, Chiaravalli M, Piontek KB, Germino GG, Boletta A. “Polycystin-1 is essential to a proper kidney development ex vivo”. In preparation
  2. Franco I, Costa C, Gulluni F, Margaria J, Monteyne D, Ranghino A, Chiaravalli M, Maffucci T, Campa CC, De Luca E, Domin J, Falasca M, Perez-Morga D, Boletta A, Merlo G and Hirsch E.“Impaired gatekeeping at the basal body of the primary cilium, ciliopathy and renal cyst susceptibility in mice lacking the class II PI3K-C2a.” Submitted.
  3. Castelli, M., Boca, M., Chiaravalli, M., Ramalingam, H., Rowe, I., Distefano, G., Carroll, T. and Boletta, A. (2013). Polycystin-1 binds Par3/aPKC and controls convergent extension during renal tubular morphogenesis. Nat Commun 4: 2658.
  4. Isaline Rowe, Marco Chiaravalli, Alessandra BolettaDifetti nel metabolismo del glucosio nel rene policistico: primi studi e prospettive future; Defects of glucose metabolism in polycystic kidney disease: first studies and future perspectivespublished online 6/12/2013 1:26:58 PM DOI:10.5301/GTND.2013.11218
  5. Rowe, I., Chiaravalli, M., Mannella, V., Ulisse, V., Quilici, G., Pema, M., Song, X. W., Xu, H., Mari, S., Qian, F., Pei, Y., Musco, G. and Boletta, A. (2013). Defective glucose metabolism in polycystic kidney disease identifies a new therapeutic strategy. Nat Med 19(4): 488-493.
  6. Wodarczyk, C., Rowe, I., Chiaravalli, M., Pema, M., Qian, F. and Boletta, A. (2009). A novel mouse model reveals that polycystin-1 deficiency in ependyma and choroid plexus results in dysfunctional cilia and hydrocephalus. PLoS One 4(9): e7137.
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