scholarly journals Cisplatin Stabilizes a Multimeric Complex of the Human Ctr1 Copper Transporter

2004 ◽  
Vol 279 (45) ◽  
pp. 46393-46399 ◽  
Author(s):  
Yan Guo ◽  
Kathryn Smith ◽  
Michael J. Petris
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.


2021 ◽  
Vol 228 ◽  
pp. 60-73
Author(s):  
Kirsten E. Schoonover ◽  
Charlene B. Farmer ◽  
Charity J. Morgan ◽  
Vidushi Sinha ◽  
Laura Odom ◽  
...  
Keyword(s):  

2021 ◽  
pp. 2004303
Author(s):  
Jianping Guo ◽  
Ji Cheng ◽  
Nana Zheng ◽  
Xiaomei Zhang ◽  
Xiaoming Dai ◽  
...  

Nutrients ◽  
2020 ◽  
Vol 13 (1) ◽  
pp. 104
Author(s):  
Aneta Jończy ◽  
Rafał Mazgaj ◽  
Rafał Radosław Starzyński ◽  
Piotr Poznański ◽  
Mateusz Szudzik ◽  
...  

In mammals, 2 × 1012 red blood cells (RBCs) are produced every day in the bone marrow to ensure a constant supply of iron to maintain effective erythropoiesis. Impaired iron absorption in the duodenum and inefficient iron reutilization from senescent RBCs by macrophages contribute to the development of anemia. Ferroportin (Fpn), the only known cellular iron exporter, as well as hephaestin (Heph) and ceruloplasmin, two copper-dependent ferroxidases involved in the above-mentioned processes, are key elements of the interaction between copper and iron metabolisms. Crosslinks between these metals have been known for many years, but metabolic effects of one on the other have not been elucidated to date. Neonatal iron deficiency anemia in piglets provides an interesting model for studying this interplay. In duodenal enterocytes of young anemic piglets, we identified iron deposits and demonstrated increased expression of ferritin with a concomitant decline in both Fpn and Heph expression. We postulated that the underlying mechanism involves changes in copper distribution within enterocytes as a result of decreased expression of the copper transporter—Atp7b. Obtained results strongly suggest that regulation of iron absorption within enterocytes is based on the interaction between proteins of copper and iron metabolisms and outcompetes systemic regulation.


2010 ◽  
Vol 107 (6) ◽  
pp. 787-799 ◽  
Author(s):  
Takashi Ashino ◽  
Varadarajan Sudhahar ◽  
Norifumi Urao ◽  
Jin Oshikawa ◽  
Gin-Fu Chen ◽  
...  

2010 ◽  
Vol 30 (28) ◽  
pp. 9500-9509 ◽  
Author(s):  
S. S. More ◽  
O. Akil ◽  
A. G. Ianculescu ◽  
E. G. Geier ◽  
L. R. Lustig ◽  
...  
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