Identification of p38 MAPK and JNK as new targets for correction of Wilson disease-causing ATP7B mutants

Autor: Giancarlo Chesi, 1 Ramanath N. Hegde, 2, + Simona Iacobacci, 1, + Mafalda Concilli, + Seetharaman Parashuraman, 2 Beatrice Paola Festa, 1 Elena V. Polishchuk, 1 Giuseppe Di Tullio, 1 Annamaria Carissimo, 1 Sandro Montefusco, 1 Diana Canetti, 3 Maria Monti, 3 Angela Amoresano, 3 Piero Pucci, 3 Bart van de Sluis, 4 Svetlana Lutsenko, 5 Alberto Luini, corresponding author 2, 6, Roman S. Polishchukcorresponding author 1

Publikováno v: Hepatology (Baltim. Md. : Online) (2016).
info:cnr-pdr/source/autori:Giancarlo Chesi, 1 Ramanath N. Hegde, 2, + Simona Iacobacci, 1, + Mafalda Concilli, 1, + Seetharaman Parashuraman, 2 Beatrice Paola Festa, 1 Elena V. Polishchuk, 1 Giuseppe Di Tullio, 1 Annamaria Carissimo, 1 Sandro Montefusco, 1 Diana Canetti, 3 Maria Monti, 3 Angela Amoresano, 3 Piero Pucci, 3 Bart van de Sluis, 4 Svetlana Lutsenko, 5 Alberto Luini,corresponding author 2, 6, ? and Roman S. Polishchukcorresponding author 1, ?/titolo:Identification of p38 MAPK and JNK as new targets for correction of Wilson disease-causing ATP7B mutants/doi:/rivista:Hepatology (Baltim. Md. : Online)/anno:2016/pagina_da:/pagina_a:/intervallo_pagine:/volume

Wilson disease (WD) is an autosomal recessive disorder that is caused by the toxic accumulation of copper (Cu) in the liver. The ATP7B gene, which is mutated in WD, encodes a multitransmembrane domain adenosine triphosphatase that traffics from the t

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https://publications.cnr.it/doc/365907