scholarly journals Copper Transporter 2 Content Is Lower in Liver and Heart of Copper-Deficient Rats

2010 ◽  
Vol 11 (11) ◽  
pp. 4741-4749 ◽  
Author(s):  
Jesse Bertinato ◽  
Sébastien Duval ◽  
Mary R. L’Abbé
Metallomics ◽  
2014 ◽  
Vol 6 (3) ◽  
pp. 654 ◽  
Author(s):  
Carlos P. Huang ◽  
Mariama Fofana ◽  
Jefferson Chan ◽  
Christopher J. Chang ◽  
Stephen B. Howell

Metallomics ◽  
2015 ◽  
Vol 7 (11) ◽  
pp. 1477-1487 ◽  
Author(s):  
Cheng-Yu Tsai ◽  
Janika K. Liebig ◽  
Igor F. Tsigelny ◽  
Stephen B. Howell

We describe for the first time that the copper transporter 1 (CTR1) is important to maintain the stability of copper transporter 2 (CTR2).


2010 ◽  
Vol 79 (1) ◽  
pp. 157-166 ◽  
Author(s):  
Brian G. Blair ◽  
Christopher A. Larson ◽  
Preston L. Adams ◽  
Paolo B. Abada ◽  
Catherine E. Pesce ◽  
...  

RSC Advances ◽  
2016 ◽  
Vol 6 (6) ◽  
pp. 4335-4342 ◽  
Author(s):  
Zhe Dong ◽  
Liping Guan ◽  
Chunyu Wang ◽  
Haoran Xu ◽  
Zhengqiang Li ◽  
...  

The second transmembrane domain of human copper transporter 2 (hCtr2-TMD2) forms a trimer with a weaker intermolecular interaction and a lower affinity for Ag(I) than hCtr1-TMD2 trimer.


2010 ◽  
Vol 77 (6) ◽  
pp. 912-921 ◽  
Author(s):  
Brian G. Blair ◽  
Christopher A. Larson ◽  
Preston L. Adams ◽  
Paolo B. Abada ◽  
Roohangiz Safaei ◽  
...  

2009 ◽  
Vol 15 (13) ◽  
pp. 4312-4321 ◽  
Author(s):  
Brian G. Blair ◽  
Christopher A. Larson ◽  
Roohangiz Safaei ◽  
Stephen B. Howell

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Abigael Muchenditsi ◽  
C. Conover Talbot ◽  
Aline Gottlieb ◽  
Haojun Yang ◽  
Byunghak Kang ◽  
...  

AbstractWilson disease (WD) is caused by inactivation of the copper transporter Atp7b and copper overload in tissues. Mice with Atp7b deleted either globally (systemic inactivation) or only in hepatocyte recapitulate various aspects of human disease. However, their phenotypes vary, and neither the common response to copper overload nor factors contributing to variability are well defined. Using metabolic, histologic, and proteome analyses in three Atp7b-deficient mouse strains, we show that global inactivation of Atp7b enhances and specifically modifies the hepatocyte response to Cu overload. The loss of Atp7b only in hepatocytes dysregulates lipid and nucleic acid metabolisms and increases the abundance of respiratory chain components and redox balancing enzymes. In global knockouts, independently of their background, the metabolism of lipid, nucleic acid, and amino acids is inhibited, respiratory chain components are down-regulated, inflammatory response and regulation of chromosomal replication are enhanced. Decrease in glucokinase and lathosterol oxidase and elevation of mucin-13 and S100A10 are observed in all Atp7b mutant strains and reflect the extent of liver injury. The magnitude of proteomic changes in Atp7b−/− animals inversely correlates with the metallothioneins levels rather than liver Cu content. These findings facilitate identification of WD-specific metabolic and proteomic changes for diagnostic and treatment.


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