Cardiac copper deficiency activates a systemic signaling mechanism that communicates with the copper acquisition and storage organs.

[1]  K. Fritsche,et al.  A Role for the ATP7A Copper-transporting ATPase in Macrophage Bactericidal Activity* , 2009, The Journal of Biological Chemistry.

[2]  D. Harrison,et al.  Role of Menkes ATPase in Angiotensin II–Induced Hypertension: A Key Modulator for Extracellular Superoxide Dismutase Function , 2008, Hypertension.

[3]  S. Lutsenko,et al.  Cellular multitasking: the dual role of human Cu-ATPases in cofactor delivery and intracellular copper balance. , 2008, Archives of biochemistry and biophysics.

[4]  M. Muckenthaler.  Fine tuning of hepcidin expression by positive and negative regulators. , 2008, Cell metabolism.

[5]  J. Camakaris,et al.  ATP7B Expression in Human Breast Epithelial Cells Is Mediated by Lactational Hormones , 2008, The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society.

[6]  J. Prohaska,et al.  Copper deficient rats and mice both develop anemia but only rats have lower plasma and brain iron levels. , 2008, Comparative biochemistry and physiology. Toxicology & pharmacology : CBP.

[7]  D. Thiele,et al.  Mechanisms for copper acquisition, distribution and regulation. , 2008, Nature chemical biology.

[8]  S. Lutsenko,et al.  Copper-transporting ATPases ATP7A and ATP7B: cousins, not twins , 2007, Journal of bioenergetics and biomembranes.

[9]  D. Thiele,et al.  Drosophila Ctr1A Functions as a Copper Transporter Essential for Development* , 2007, Journal of Biological Chemistry.

[10]  U. Shinde,et al.  Biochemical basis of regulation of human copper-transporting ATPases. , 2007, Archives of biochemistry and biophysics.

[11]  J. Gitlin,et al.  Copper and iron disorders of the brain. , 2007, Annual review of neuroscience.

[12]  N. Andrews,et al.  Hepcidin antimicrobial peptide transgenic mice exhibit features of the anemia of inflammation. , 2007, Blood.

[13]  Corey L. Reynolds,et al.  Dietary copper supplementation reverses hypertrophic cardiomyopathy induced by chronic pressure overload in mice , 2007, The Journal of experimental medicine.

[14]  J. Prohaska,et al.  Rodent brain and heart catecholamine levels are altered by different models of copper deficiency. , 2007, Comparative biochemistry and physiology. Toxicology & pharmacology : CBP.

[15]  J. Camakaris,et al.  Hormonal regulation of the Menkes and Wilson copper-transporting ATPases in human placental Jeg-3 cells. , 2007, The Biochemical journal.

[16]  N. Dalton,et al.  Inducible Cardiac-Restricted Expression of Enteroviral Protease 2A Is Sufficient to Induce Dilated Cardiomyopathy , 2006, Circulation.

[17]  D. Thiele,et al.  Structure of the Ctr1 copper trans'PORE'ter reveals novel architecture. , 2006, Trends in biochemical sciences.

[18]  K. Allen,et al.  Chronological changes in tissue copper, zinc and iron in the toxic milk mouse and effects of copper loading , 2006, Biometals.

[19]  D. Thiele,et al.  Ctr1 drives intestinal copper absorption and is essential for growth, iron metabolism, and neonatal cardiac function. , 2006, Cell metabolism.

[20]  D. Winge,et al.  Copper trafficking to the mitochondrion and assembly of copper metalloenzymes. , 2006, Biochimica et biophysica acta.

[21]  T. O’Halloran,et al.  Activation of superoxide dismutases: putting the metal to the pedal. , 2006, Biochimica et biophysica acta.

[22]  J. Gitlin,et al.  Mechanisms of the Copper-dependent Turnover of the Copper Chaperone for Superoxide Dismutase* , 2006, Journal of Biological Chemistry.

[23]  J. Prohaska,et al.  Variable response of selected cuproproteins in rat choroid plexus and cerebellum following perinatal copper deficiency , 2006, Genes & Nutrition.

[24]  Joseph A Izatt,et al.  Drosophila as a model for the identification of genes causing adult human heart disease , 2006, Proceedings of the National Academy of Sciences of the United States of America.

[25]  C. Epstein,et al.  CuZnSOD deficiency leads to persistent and widespread oxidative damage and hepatocarcinogenesis later in life , 2005, Oncogene.

[26]  Jerry Kaplan,et al.  Hepcidin Regulates Cellular Iron Efflux by Binding to Ferroportin and Inducing Its Internalization , 2004, Science.

[27]  J. Prohaska,et al.  Cu, Zn-Superoxide Dismutase is Lower and Copper Chaperone CCS is Higher in Erythrocytes of Copper-Deficient Rats and Mice , 2004, Experimental biology and medicine.

[28]  E. Olson,et al.  Cardiac hypertrophy: the good, the bad, and the ugly. , 2003, Annual review of physiology.

[29]  M. L’Abbé,et al.  Copper Modulates the Degradation of Copper Chaperone for Cu,Zn Superoxide Dismutase by the 26 S Proteosome* , 2003, Journal of Biological Chemistry.

[30]  R. Carthew,et al.  Making a better RNAi vector for Drosophila: use of intron spacers. , 2003, Methods.

[31]  E. Kranias,et al.  Calcium: Phospholamban: a crucial regulator of cardiac contractility , 2003, Nature Reviews Molecular Cell Biology.

[32]  G. Dorn,et al.  Phenotyping hypertrophy: eschew obfuscation. , 2003, Circulation research.

[33]  R. Soldi,et al.  Copper chelation represses the vascular response to injury , 2003, Proceedings of the National Academy of Sciences of the United States of America.

[34]  R. Mains,et al.  Supplying Copper to the Cuproenzyme Peptidylglycine α-Amidating Monooxygenase* , 2003, The Journal of Biological Chemistry.

[35]  J. Gitlin,et al.  Essential role for Atox1 in the copper-mediated intracellular trafficking of the Menkes ATPase , 2003, Proceedings of the National Academy of Sciences of the United States of America.

[36]  B. Carabello.  Concentric versus eccentric remodeling. , 2002, Journal of cardiac failure.

[37]  G. Mancini,et al.  Mechanisms of Copper Incorporation into Human Ceruloplasmin* , 2002, The Journal of Biological Chemistry.

[38]  B. Strauer,et al.  Left ventricular diastolic function in physiologic and pathologic hypertrophy. , 2002, American journal of hypertension.

[39]  B. Strauer,et al.  Left Ventricular Hypertrophy and Diastolic Dysfunction in Healthy Pregnant Women , 2002, Cardiology.

[40]  J. Mercer,et al.  The molecular basis of copper homeostasis copper-related disorders. , 2002, DNA and cell biology.

[41]  M. Crackower,et al.  Temporally Regulated and Tissue-Specific Gene Manipulations in the Adult and Embryonic Heart Using a Tamoxifen-Inducible Cre Protein , 2001, Circulation research.

[42]  M. Frasch,et al.  A role for the COUP-TF-related gene seven-up in the diversification of cardioblast identities in the dorsal vessel of Drosophila , 2001, Mechanisms of Development.

[43]  L. Klevay.  Iron overload can induce mild copper deficiency. , 2001, Journal of trace elements in medicine and biology : organ of the Society for Minerals and Trace Elements.

[44]  W. Lederer,et al.  Cellular and functional defects in a mouse model of heart failure. , 2000, American journal of physiology. Heart and circulatory physiology.

[45]  J. Mercer,et al.  The Menkes copper transporter is required for the activation of tyrosinase. , 2000, Human molecular genetics.

[46]  J. Prohaska.  Long-term functional consequences of malnutrition during brain development: copper. , 2000, Nutrition.

[47]  E. Shoubridge,et al.  Mutations in SCO2 are associated with a distinct form of hypertrophic cardiomyopathy and cytochrome c oxidase deficiency. , 2000, Human molecular genetics.

[48]  Y. Ho,et al.  Targeted disruption of the mouse Sod I gene makes the hearts vulnerable to ischemic reperfusion injury. , 2000, Circulation research.

[49]  P. Anikijenko,et al.  Expression of Menkes Copper-transporting ATPase, MNK, in the Lactating Human Breast: Possible Role in Copper Transport into Milk , 1999, The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society.

[50]  P Chambon,et al.  Temporally-controlled site-specific mutagenesis in the basal layer of the epidermis: comparison of the recombinase activity of the tamoxifen-inducible Cre-ER(T) and Cre-ER(T2) recombinases. , 1999, Nucleic acids research.

[51]  J. Turnlund.  Human whole-body copper metabolism. , 1998, The American journal of clinical nutrition.

[52]  B. A. French,et al.  Gene recombination in postmitotic cells. Targeted expression of Cre recombinase provokes cardiac-restricted, site-specific rearrangement in adult ventricular muscle in vivo. , 1997, The Journal of clinical investigation.

[53]  C. Klee,et al.  Superoxide dismutase protects calcineurin from inactivation , 1996, Nature.

[54]  P. Lockhart,et al.  Expression of the Menkes gene homologue in mouse tissues lack of effect of copper on the mRNA levels , 1994, FEBS letters.

[55]  D. Medeiros,et al.  A Unified Perspective on Copper Deficiency and Cardiomyopathy , 1993, Proceedings of the Society for Experimental Biology and Medicine. Society for Experimental Biology and Medicine.

[56]  J. Robbins,et al.  Tissue-specific regulation of the alpha-myosin heavy chain gene promoter in transgenic mice. , 1991, The Journal of biological chemistry.

[57]  A. Spradling,et al.  Constructing deletions with defined endpoints in Drosophila. , 1990, Proceedings of the National Academy of Sciences of the United States of America.

[58]  J. Prohaska.  Changes in tissue growth, concentrations of copper, iron, cytochrome oxidase and superoxide dismutase subsequent to dietary or genetic copper deficiency in mice. , 1983, The Journal of nutrition.

[59]  J. Prohaska,et al.  Mechanical properties of the copper-deficient rat heart. , 1982, The Journal of nutrition.

[60]  W. A. Kelly,et al.  Myocardial lesions in the offspring of female rats fed a copper deficient diet. , 1974, Experimental and molecular pathology.

[61]  W. Schaffner,et al.  Human copper transporter Ctr1 is functional in Drosophila, revealing a high degree of conservation between mammals and insects , 2009, JBIC Journal of Biological Inorganic Chemistry.

[62]  Jerry Kaplan,et al.  Regulation of iron acquisition and storage: consequences for iron-linked disorders , 2008, Nature Reviews Molecular Cell Biology.

[63]  Y. Kuo,et al.  Copper transport protein (Ctr1) levels in mice are tissue specific and dependent on copper status. , 2006, The Journal of nutrition.