Detalhe da pesquisa
1.
Pharmacoproteomics pinpoints HSP70 interaction for correction of the most frequent Wilson disease-causing mutant of ATP7B.
Proc Natl Acad Sci U S A
; 117(51): 32453-32463, 2020 12 22.
Artigo
em Inglês
| MEDLINE | ID: mdl-33288711
2.
Golgi-Dependent Copper Homeostasis Sustains Synaptic Development and Mitochondrial Content.
J Neurosci
; 41(2): 215-233, 2021 01 13.
Artigo
em Inglês
| MEDLINE | ID: mdl-33208468
3.
Activation of Autophagy, Observed in Liver Tissues From Patients With Wilson Disease and From ATP7B-Deficient Animals, Protects Hepatocytes From Copper-Induced Apoptosis.
Gastroenterology
; 156(4): 1173-1189.e5, 2019 03.
Artigo
em Inglês
| MEDLINE | ID: mdl-30452922
4.
Identification of p38 MAPK and JNK as new targets for correction of Wilson disease-causing ATP7B mutants.
Hepatology
; 63(6): 1842-59, 2016 06.
Artigo
em Inglês
| MEDLINE | ID: mdl-26660341
5.
A systems biology approach reveals new endoplasmic reticulum-associated targets for the correction of the ATP7B mutant causing Wilson disease.
Metallomics
; 8(9): 920-930, 2016 09 01.
Artigo
em Inglês
| MEDLINE | ID: mdl-27714068
6.
The Menkes and Wilson disease genes counteract in copper toxicosis in Labrador retrievers: a new canine model for copper-metabolism disorders.
Dis Model Mech
; 9(1): 25-38, 2016 Jan.
Artigo
em Inglês
| MEDLINE | ID: mdl-26747866
7.
Wilson disease protein ATP7B utilizes lysosomal exocytosis to maintain copper homeostasis.
Dev Cell
; 29(6): 686-700, 2014 Jun 23.
Artigo
em Inglês
| MEDLINE | ID: mdl-24909901