Publications
  • The crystal structure of a low molecular weight phosphotyrosine protein phosphatase (X.D. Su, N. Taddei, M. Stefani, G. Ramponi, and P. Nordlund) Nature (1994) 6490: 575-578. [LINK]
  • Mutational analysis of acylphosphatase suggests the importance of topology and contact order in protein folding (F. Chiti, N. Taddei, P.M. White, M. Bucciantini, F. Magherini, M. Stefani e C.M. Dobson) Nat. Struct. Biol. (1999) 6:1005-1009. [LINK]
  • Designing conditions for in vitro formation of amyloid protofilaments and fibrils (F. Chiti, P. Webster, N. Taddei, A. Clark, M. Stefani, G. Ramponi e C.M. Dobson) Proc. Natl. Acad. Sci. USA (1999) 96:3590-94. [LINK]
  • Kinetic partitioning of protein folding and aggregation (F. Chiti, N. Taddei, F. Baroni, C. Capanni, M. Stefani, G. Ramponi & C.M. Dobson) Nat. Struct. Biol. (2002) 9: 137-143. [LINK]
  • Studies on the aggregation of mutant proteins in vitro provide insights into the genetics of amyloid diseases (F. Chiti, M. Calamai, N. Taddei, M. Stefani, G. Ramponi & C.M. Dobson) Proc. Natl. Acad Sci. USA (2002) 4: 16419-26. [LINK]
  • Inherent toxicity of aggregates implies a common mechanism for protein misfolding diseases (M. Bucciantini, E. Giannoni, F. Chiti, F. Baroni, L. Formigli, J. Zurdo, N. Taddei, G. Ramponi, C.M. Dobson & M. Stefani) Nature (2002) 416: 507-511. [LINK]
  • Rationalization of the effects of mutations on peptide and protein aggregation rates (F. Chiti, M. Stefani, N. Taddei, G. Ramponi & C.M. Dobson) Nature (2003) 424: 805-808. [LINK]
  • Pre-fibrillar amyloid protein aggregates share common features of cytotoxicity. (M. Bucciantini, G. Calloni, F. Chiti, L. Formigli, D. Nosi, C.M. Dobson & M. Stefani) J. Biol. Chem. (2004) 279:31374-31382. [LINK]
  • Patterns of cell death triggered in two different cell lines by HypF-N pre-fibrillar aggregates (M. Bucciantini, S. Rigacci, A. Berti, L. Pieri, C. Cecchi, D. Nosi, L. Formigli, F. Chiti & M. Stefani) FASEB J. (2005) 19:437-439. [LINK]
  • Insights into the molecular basis of the differing susceptibility of varying cell types to the toxicity of amyloid aggregates (C. Cecchi,, S. Baglioni, C. Fiorillo, A. Pensalfini, G. Liguri, D. Nosi, S. Rigacci, M. Bucciantini & M. Stefani,) J. Cell Sci. (2005) 118: 3459-3470. [LINK]
  • Prefibrillar amyloid aggregates could be generic toxins in higher organisms (S. Baglioni, F. Casamenti, M. Bucciantini, L.M. Luheshi, N. Taddei, F. Chiti, C.M. Dobson & M. Stefani) J. Neurosci.(2006) 26:8160-8167. [LINK]
  • Seladin-1/dhcr24 protects neuroblastoma cells against a? toxicity by increasing membrane cholesterol content (C. Cecchi, F. Rosati, A. Pensalfini, L. Formigli, D. Nosi, G. Liguri, F. Dichiara, M. Morello, G. Danza, G. Pieraccini, A. Peri, M. Serio & M. Stefani) J. Cell. Mol. Med. (2008) 12: 1990-2002. [LINK]
  • Biological function in a non-native partially folded state of a protein (Bemporad F, Gsponer J, Hopearuoho HI, Plakoutsi G, Stati G, Stefani M, Taddei N, Vendruscolo M, Chiti F.) EMBO J. (2008) 27:1525-35. [LINK]
  • Aberrant protein oligomer structures are causatively linked to cellular dysfunction (Campioni S, Mannini B, Pensalfini A, Zampagni M, Parrini C, Evangelisti E, Relini A, Stefani M, Dobson CM, Cecchi C, Chiti F) Nat. Chem. Biol. (2010) 6:140-147. [LINK]
  • Toxic effects of amyloid fibrils on cell membranes: the importance of ganglioside GM1 (M. Bucciantini, D. Nosi, M. Forzan, E. Russo, M. Calamai, L. Pieri, L. Formigli, F. Quercioli, S. Soria, F. Pavone,J. Savistchenko, R. Melki & M. Stefani) FASEB J. (2012) 26:818-830. [LINK]
  • Growth, structural features and cytotoxicity of amyloid oligomers (M. Stefani) Progr. Neurobiol. (2012) EPub March 13, 2012. [LINK]

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