Zobrazeno 1 - 7
of 7
pro vyhledávání: '"Ignazio Fiduccia"'
Autor:
Riccardo Perriera, Emanuele Vitale, Ivana Pibiri, Pietro Salvatore Carollo, Davide Ricci, Federica Corrao, Ignazio Fiduccia, Raffaella Melfi, Maria Grazia Zizzo, Marco Tutone, Andrea Pace, Laura Lentini
Publikováno v:
International Journal of Molecular Sciences, Vol 24, Iss 20, p 15084 (2023)
Nonsense mutations cause several genetic diseases such as cystic fibrosis, Duchenne muscular dystrophy, β-thalassemia, and Shwachman–Diamond syndrome. These mutations induce the formation of a premature termination codon (PTC) inside the mRNA sequ
Externí odkaz:
https://doaj.org/article/5663dbfb9dbc499b869eb2cb424ba1ab
Autor:
Federica Corrao, Maria Grazia Zizzo, Marco Tutone, Raffaella Melfi, Ignazio Fiduccia, Pietro Salvatore Carollo, Aldo Di Leonardo, Gaetano Caldara, Riccardo Perriera, Andrea Pace, Beatrice Belmonte, Selene Sammataro, Ivana Pibiri, Laura Lentini
Publikováno v:
Biomedicine & Pharmacotherapy, Vol 156, Iss , Pp 113886- (2022)
Stop mutations cause 11% of the genetic diseases, due to the introduction of a premature termination codon (PTC) in the mRNA, followed by the production of a truncated protein. A promising therapeutic approach is the suppression therapy by Translatio
Externí odkaz:
https://doaj.org/article/96d8fcb1f02b48969527e8b5b31f7c6a
Autor:
Pietro Salvatore Carollo, Marco Tutone, Giulia Culletta, Ignazio Fiduccia, Federica Corrao, Ivana Pibiri, Aldo Di Leonardo, Maria Grazia Zizzo, Raffaella Melfi, Andrea Pace, Anna Maria Almerico, Laura Lentini
Publikováno v:
International Journal of Molecular Sciences, Vol 24, Iss 11, p 9609 (2023)
Cystic Fibrosis (CF) is an autosomal recessive genetic disease caused by mutations in the CFTR gene, coding for the CFTR chloride channel. About 10% of the CFTR gene mutations are “stop” mutations that generate a premature termination codon (PTC)
Externí odkaz:
https://doaj.org/article/1d050d4f5ab14431b3009790e93f1566
Autor:
Carla Rizzo, Ignazio Fiduccia, Silvestre Buscemi, Antonio Palumbo Piccionello, Andrea Pace, Ivana Pibiri
Publikováno v:
Applied Sciences, Vol 13, Iss 5, p 2947 (2023)
The synthesis and thermotropic behaviour of some di-alkyloxy-phenyl-1,2,4-triazolium trifluoromethane-sulfonate salts bearing a seven-carbon atom perfluoroalkyl chain on the cation is herein described. The fluorinated salts presenting a 1,2,4-triazol
Externí odkaz:
https://doaj.org/article/59fc3313fb764233b288cc7a44a069d3
Autor:
Lentini, Pietro Salvatore Carollo, Marco Tutone, Giulia Culletta, Ignazio Fiduccia, Federica Corrao, Ivana Pibiri, Aldo Di Leonardo, Maria Grazia Zizzo, Raffaella Melfi, Andrea Pace, Anna Maria Almerico, Laura
Publikováno v:
International Journal of Molecular Sciences; Volume 24; Issue 11; Pages: 9609
Cystic Fibrosis (CF) is an autosomal recessive genetic disease caused by mutations in the CFTR gene, coding for the CFTR chloride channel. About 10% of the CFTR gene mutations are “stop” mutations that generate a premature termination codon (PTC)
Autor:
Federica Corrao, Raffaella Melfi, Marco Tutone, Ignazio Fiduccia, Riccardo Perriera, Pietro Salvatore Carollo, Emanuele Vitale, Andrea Pace, Laura Lentini, A. Colige, P. Delvenne, B. Grimbacher, M. Moutschen, I. Pibiri
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=od______3658::73d0ce54dabdc66176c3e1145b81ebc5
http://hdl.handle.net/10447/569475
http://hdl.handle.net/10447/569475
Autor:
Federica Corrao, Perriera, Riccardo, Laura Lentini, maria grazia zizzo, Melfi, Raffaella, Pietro Salvatore Carollo, Fiduccia, I., Andrea Pace, Tutone, Marco, Aldo Di Leonardo, Pibiri, Ivana
Publikováno v:
Università degli Studi di Palermo-IRIS
Objective Nonsense mutations are responsible for 15% of Cystic Fibrosis (CF) patients due to the introduction of a premature stop codon (PTC) in the mRNA and the production of a truncated CFTR (Cystic Fibrosis Transmembrane Conductance Regulator) pro
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=dedup_wf_001::39bd39ff71f7770e1389a595cbc30a7b
http://hdl.handle.net/10447/544087
http://hdl.handle.net/10447/544087