Relevant bibliographies by topics / ATP7B

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Academic literature on the topic 'ATP7B'

Author: Grafiati
Published: 4 June 2021
Last updated: 25 April 2022

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Journal articles on the topic "ATP7B"

1

Linz, Rachel, Natalie L. Barnes, Adriana M. Zimnicka, Jack H. Kaplan, Betty Eipper, and Svetlana Lutsenko. "Intracellular targeting of copper-transporting ATPase ATP7A in a normal andAtp7b−/−kidney." American Journal of Physiology-Renal Physiology 294, no. 1 (2008): F53—F61. http://dx.doi.org/10.1152/ajprenal.00314.2007.

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Kidneys regulate their copper content more effectively than many other organs in diseases of copper deficiency or excess. We demonstrate that two copper-transporting ATPases, ATP7A and ATP7B, contribute to this regulation. ATP7A is expressed, to a variable degree, throughout the kidney and shows age-dependent intracellular localization. In 2-wk-old mice, ATP7A is located in the vicinity of the basolateral membrane, whereas in 20-wk-old mice, ATP7A is predominantly in intracellular vesicles. Acute elevation of serum copper, via intraperitoneal injection, results in the in vivo redistribution of ATP7A from intracellular compartments toward the basolateral membrane, illustrating a role for ATP7A in renal response to changes in copper load. Renal copper homeostasis also requires functional ATP7B, which is coexpressed with ATP7A in renal cells of proximal and distal origin. The kidneys of Atp7b−/−mice, an animal model of Wilson disease, show metabolic alterations manifested by the appearance of highly fluorescent deposits; however, in marked contrast to the liver, renal copper is not significantly elevated. The lack of notable copper accumulation in the Atp7b−/−kidney is likely due to the compensatory export of copper by ATP7A. This interpretation is supported by the predominant localization of ATP7A at the basolateral membrane of Atp7b−/−cortical tubules. Our results suggest that both Cu-ATPases regulate renal copper, with ATP7A playing a major role in exporting copper via basolateral membranes and protecting renal tissue against copper overload.
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Braiterman, L., L. Nyasae, F. Leves, and A. L. Hubbard. "Critical roles for the COOH terminus of the Cu-ATPase ATP7B in protein stability, trans-Golgi network retention, copper sensing, and retrograde trafficking." American Journal of Physiology-Gastrointestinal and Liver Physiology 301, no. 1 (2011): G69—G81. http://dx.doi.org/10.1152/ajpgi.00038.2011.

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ATP7A and ATP7B are copper-transporting P-type ATPases that are essential to eukaryotic copper homeostasis and must traffic between intracellular compartments to carry out their functions. Previously, we identified a nine-amino acid sequence (F37–E45) in the NH2terminus of ATP7B that is required to retain the protein in the Golgi when copper levels are low and target it apically in polarized hepatic cells when copper levels rise. To understand further the mechanisms regulating the intracellular dynamics of ATP7B, using multiple functional assays, we characterized the protein phenotypes of 10 engineered and Wilson disease-associated mutations in the ATP7B COOH terminus in polarized hepatic cells and fibroblasts. We also examined the behavior of a chimera between ATP7B and ATP7A. Our results clearly demonstrate the importance of the COOH terminus of ATP7B in the protein's copper-responsive apical trafficking. L1373 at the end of transmembrane domain 8 is required for protein stability and Golgi retention in low copper, the trileucine motif (L1454–L1456) is required for retrograde trafficking, and the COOH terminus of ATP7B exhibits a higher sensitivity to copper than does ATP7A. Importantly, our results demonstrating that four Wilson disease-associated missense mutations behaved in a wild-type manner in all our assays, together with current information in the literature, raise the possibility that several may not be disease-causing mutations.
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Materia, Stephanie, Michael A. Cater, Leo W. J. Klomp, Julian F. B. Mercer, and Sharon La Fontaine. "Clusterin (Apolipoprotein J), a Molecular Chaperone That Facilitates Degradation of the Copper-ATPases ATP7A and ATP7B." Journal of Biological Chemistry 286, no. 12 (2011): 10073–83. http://dx.doi.org/10.1074/jbc.m110.190546.

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The copper-transporting P1B-type ATPases (Cu-ATPases) ATP7A and ATP7B are key regulators of physiological copper levels. They function to maintain intracellular copper homeostasis by delivering copper to secretory compartments and by trafficking toward the cell periphery to export excess copper. Mutations in the genes encoding ATP7A and ATP7B lead to copper deficiency and toxicity disorders, Menkes and Wilson diseases, respectively. This report describes the interaction between the Cu-ATPases and clusterin and demonstrates a chaperone-like role for clusterin in facilitating their degradation. Clusterin interacted with both ATP7A and ATP7B in mammalian cells. This interaction increased under conditions of oxidative stress and with mutations in ATP7B that led to its misfolding and mislocalization. A Wilson disease patient mutation (G85V) led to enhanced ATP7B turnover, which was further exacerbated when cells overexpressed clusterin. We demonstrated that clusterin-facilitated degradation of mutant ATP7B is likely to involve the lysosomal pathway. The knockdown and overexpression of clusterin increased and decreased, respectively, the Cu-ATPase-mediated copper export capacity of cells. These results highlight a new role for intracellular clusterin in mediating Cu-ATPase quality control and hence in the normal maintenance of copper homeostasis, and in promoting cell survival in the context of disease. Based on our findings, it is possible that variations in clusterin expression and function could contribute to the variable clinical expression of Menkes and Wilson diseases.
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Dolgova, Nataliya V., Sergiy Nokhrin, Corey H. Yu, Graham N. George, and Oleg Y. Dmitriev. "Copper chaperone Atox1 interacts with the metal-binding domain of Wilson's disease protein in cisplatin detoxification." Biochemical Journal 454, no. 1 (2013): 147–56. http://dx.doi.org/10.1042/bj20121656.

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Human copper transporters ATP7B (Wilson's disease protein) and ATP7A (Menkes' disease protein) have been implicated in tumour resistance to cisplatin, a widely used anticancer drug. Cisplatin binds to the copper-binding sites in the N-terminal domain of ATP7B, and this binding may be an essential step of cisplatin detoxification involving copper ATPases. In the present study, we demonstrate that cisplatin and a related platinum drug carboplatin produce the same adduct following reaction with MBD2 [metal-binding domain (repeat) 2], where platinum is bound to the side chains of the cysteine residues in the CxxC copper-binding motif. This suggests the same mechanism for detoxification of both drugs by ATP7B. Platinum can also be transferred to MBD2 from copper chaperone Atox1, which was shown previously to bind cisplatin. Binding of the free cisplatin and reaction with the cisplatin-loaded Atox1 produce the same protein-bound platinum intermediate. Transfer of platinum along the copper-transport pathways in the cell may serve as a mechanism of drug delivery to its target in the cell nucleus, and explain tumour-cell resistance to cisplatin associated with the overexpression of copper transporters ATP7B and ATP7A.
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Kelleher, Shannon L., and Bo Lönnerdal. "Mammary gland copper transport is stimulated by prolactin through alterations in Ctr1 and Atp7A localization." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 291, no. 4 (2006): R1181—R1191. http://dx.doi.org/10.1152/ajpregu.00206.2005.

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Milk copper (Cu) concentration declines and directly reflects the stage of lactation. Three Cu-specific transporters (Ctr1, Atp7A, Atp7B) have been identified in the mammary gland; however, the integrated role they play in milk Cu secretion is not understood. Whereas the regulation of milk composition by the lactogenic hormone prolactin (PRL) has been documented, the specific contribution of PRL to this process is largely unknown. Using the lactating rat as a model, we determined that the normal decline in milk Cu concentration parallels declining Cu availability to the mammary gland and is associated with decreased Atp7B protein levels. Mammary gland Cu transport was highest during early lactation and was stimulated by suckling and hyperprolactinemia, which was associated with Ctr1 and Atp7A localization at the plasma membrane. Using cultured mammary epithelial cells (HC11), we demonstrated that Ctr1 stains in association with intracellular vesicles that partially colocalize with transferrin receptor (recycling endosome marker). Atp7A was primarily colocalized with mannose 6-phosphate receptor (M6PR; late endosome marker), whereas Atp7B was partially colocalized with protein disulfide isomerase (endoplasmic reticulum marker), TGN38 ( trans-Golgi network marker) and M6PR. Prolactin stimulated Cu transport as a result of increased Ctr1 and Atp7A abundance at the plasma membrane. Although the molecular mechanisms responsible for these posttranslational changes are not understood, transient changes in prolactin signaling play a role in the regulation of mammary gland Cu secretion during lactation.
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Inesi, Giuseppe, Rajendra Pilankatta, and Francesco Tadini-Buoninsegni. "Biochemical characterization of P-type copper ATPases." Biochemical Journal 463, no. 2 (2014): 167–76. http://dx.doi.org/10.1042/bj20140741.

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Copper ATPases, in analogy with other members of the P-ATPase superfamily, contain a catalytic headpiece including an aspartate residue reacting with ATP to form a phosphoenzyme intermediate, and transmembrane helices containing cation-binding sites [TMBS (transmembrane metal-binding sites)] for catalytic activation and cation translocation. Following phosphoenzyme formation by utilization of ATP, bound copper undergoes displacement from the TMBS to the lumenal membrane surface, with no H+ exchange. Although PII-type ATPases sustain active transport of alkali/alkali-earth ions (i.e. Na+, Ca2+) against electrochemical gradients across defined membranes, PIB-type ATPases transfer transition metal ions (i.e. Cu+) from delivery to acceptor proteins and, prominently in mammalian cells, undergo trafficking from/to various membrane compartments. A specific component of copper ATPases is the NMBD (N-terminal metal-binding domain), containing up to six copper-binding sites in mammalian (ATP7A and ATP7B) enzymes. Copper occupancy of NMBD sites and interaction with the ATPase headpiece are required for catalytic activation. Furthermore, in the presence of copper, the NMBD allows interaction with protein kinase D, yielding phosphorylation of serine residues, ATP7B trafficking and protection from proteasome degradation. A specific feature of ATP7A is glycosylation and stabilization on plasma membranes. Cisplatin, a platinum-containing anti-cancer drug, binds to copper sites of ATP7A and ATP7B, and undergoes vectorial displacement in analogy with copper.
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Lutsenko, Svetlana, Natalie L. Barnes, Mee Y. Bartee, and Oleg Y. Dmitriev. "Function and Regulation of Human Copper-Transporting ATPases." Physiological Reviews 87, no. 3 (2007): 1011–46. http://dx.doi.org/10.1152/physrev.00004.2006.

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Copper-transporting ATPases (Cu-ATPases) ATP7A and ATP7B are evolutionarily conserved polytopic membrane proteins with essential roles in human physiology. The Cu-ATPases are expressed in most tissues, and their transport activity is crucial for central nervous system development, liver function, connective tissue formation, and many other physiological processes. The loss of ATP7A or ATP7B function is associated with severe metabolic disorders, Menkes disease, and Wilson disease. In cells, the Cu-ATPases maintain intracellular copper concentration by transporting copper from the cytosol across cellular membranes. They also contribute to protein biosynthesis by delivering copper into the lumen of the secretory pathway where metal ion is incorporated into copper-dependent enzymes. The biosynthetic and homeostatic functions of Cu-ATPases are performed in different cell compartments; targeting to these compartments and the functional activity of Cu-ATPase are both regulated by copper. In recent years, significant progress has been made in understanding the structure, function, and regulation of these essential transporters. These studies raised many new questions related to specific physiological roles of Cu-ATPases in various tissues and complex mechanisms that control the Cu-ATPase function. This review summarizes current data on the structural organization and functional properties of ATP7A and ATP7B as well as their localization and functions in various tissues, and discusses the current models of regulated trafficking of human Cu-ATPases.
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CATER, Michael A., John FORBES, Sharon La FONTAINE, Diane COX, and Julian F. B. MERCER. "Intracellular trafficking of the human Wilson protein: the role of the six N-terminal metal-binding sites." Biochemical Journal 380, no. 3 (2004): 805–13. http://dx.doi.org/10.1042/bj20031804.

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The Wilson protein (ATP7B) is a copper-transporting CPx-type ATPase defective in the copper toxicity disorder Wilson disease. In hepatocytes, ATP7B delivers copper to apo-ceruloplasmin and mediates the excretion of excess copper into bile. These distinct functions require the protein to localize at two different subcellular compartments. At the trans-Golgi network, ATP7B transports copper for incorporation into apo-ceruloplasmin. When intracellular copper levels are increased, ATP7B traffics to post-Golgi vesicles in close proximity to the canalicular membrane to facilitate biliary copper excretion. In the present study, we investigated the role of the six N-terminal MBSs (metal-binding sites) in the trafficking process. Using site-directed mutagenesis, we mutated or deleted various combinations of the MBSs and assessed the effect of these changes on the localization and trafficking of ATP7B. Results show that the MBSs required for trafficking are the same as those previously found essential for the copper transport function. Either MBS 5 or MBS 6 alone was sufficient to support the redistribution of ATP7B to vesicular compartments. The first three N-terminal motifs were not required for copper-dependent intracellular trafficking and could not functionally replace sites 4–6 when placed in the same sequence position. Furthermore, the N-terminal region encompassing MBSs 1–5 (amino acids 64–540) was not essential for trafficking, with only one MBS close to the membrane channel, necessary and sufficient to support trafficking. Our findings were similar to those obtained for the closely related ATP7A protein, suggesting similar mechanisms for trafficking between copper-transporting CPx-type ATPases.
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Guo, Y., L. Nyasae, L. T. Braiterman, and A. L. Hubbard. "NH2-terminal signals in ATP7B Cu-ATPase mediate its Cu-dependent anterograde traffic in polarized hepatic cells." American Journal of Physiology-Gastrointestinal and Liver Physiology 289, no. 5 (2005): G904—G916. http://dx.doi.org/10.1152/ajpgi.00262.2005.

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Cu is an essential cofactor of cellular proteins but is toxic in its free state. The hepatic Cu-ATPase ATP7B has two functions in Cu homeostasis: it loads Cu+onto newly synthesized apoceruloplasmin in the secretory pathway, thereby activating the plasma protein; and it participates in the excretion of excess Cu+into the bile. To carry out these two functions, the membrane protein responds to changes in intracellular Cu levels by cycling between the Golgi and apical region. We used polarized hepatic WIF-B cells and high-resolution confocal microscopy to map the itinerary of endogenous and exogenous ATP7B under different Cu conditions. In Cu-depleted cells, ATP7B resided in a post- trans-Golgi network compartment that also contained syntaxin 6, whereas in Cu-loaded cells, the protein relocated to unique vesicles very near to the apical plasma membrane as well as the membrane itself. To determine the role of ATP7B's cytoplasmic NH2terminus in regulating its intracellular movements, we generated seven mutations/deletions in this large [∼650 amino acid (AA)] domain and analyzed the Cu-dependent behavior of the mutant ATP7B proteins in WIF-B cells. Truncation of the ATP7B NH2terminus up to the fifth copper-binding domain (CBD5) yielded an active ATPase that was insensitive to cellular Cu levels and constitutively trafficked to the opposite (basolateral) plasma membrane domain. Fusion of the NH2-terminal 63 AA of ATP7B to the truncated protein restored both its Cu responsiveness and correct intracellular targeting. These results indicate that important targeting information is contained in this relatively short sequence, which is absent from the related CuATPase, ATP7A.
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Petruzzelli, Raffaella, and Roman S. Polishchuk. "Activity and Trafficking of Copper-Transporting ATPases in Tumor Development and Defense against Platinum-Based Drugs." Cells 8, no. 9 (2019): 1080. http://dx.doi.org/10.3390/cells8091080.

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Membrane trafficking pathways emanating from the Golgi regulate a wide range of cellular processes. One of these is the maintenance of copper (Cu) homeostasis operated by the Golgi-localized Cu-transporting ATPases ATP7A and ATP7B. At the Golgi, these proteins supply Cu to newly synthesized enzymes which use this metal as a cofactor to catalyze a number of vitally important biochemical reactions. However, in response to elevated Cu, the Golgi exports ATP7A/B to post-Golgi sites where they promote sequestration and efflux of excess Cu to limit its potential toxicity. Growing tumors actively consume Cu and employ ATP7A/B to regulate the availability of this metal for oncogenic enzymes such as LOX and LOX-like proteins, which confer higher invasiveness to malignant cells. Furthermore, ATP7A/B activity and trafficking allow tumor cells to detoxify platinum (Pt)-based drugs (like cisplatin), which are used for the chemotherapy of different solid tumors. Despite these noted activities of ATP7A/B that favor oncogenic processes, the mechanisms that regulate the expression and trafficking of Cu ATPases in malignant cells are far from being completely understood. This review summarizes current data on the role of ATP7A/B in the regulation of Cu and Pt metabolism in malignant cells and outlines questions and challenges that should be addressed to understand how ATP7A and ATP7B trafficking mechanisms might be targeted to counteract tumor development.
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Dissertations / Theses on the topic "ATP7B"

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Minghetti, Matteo. "Characterisation and expression of copper homeostasis genes in sea bream (Sparus aurata)." Thesis, University of Stirling, 2009. http://hdl.handle.net/1893/1113.

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The redox properties of Copper (Cu) make it both an ideal cofactor for many enzymes, and, in its free form, a highly toxic molecule capable of stimulating production of reactive oxygen species or binding to protein thiol groups. Therefore, living organisms have evolved homeostatic systems to “handle” Cu avoiding dangerous and wasteful aspecific interactions. These systems comprise uptake, carrier, storage and excretion proteins. The importance of Cu-homeostatic systems was initially discovered in humans where alterations of Cu-excretory proteins were shown to be responsible for two lethal genetic disorders; the Wilson and Menkes diseases. The levels of bioavailable Cu in the aquatic environment is important because concentrations in oceanic waters tend to be minute, whilst in some fresh and coastal waters, particularly around areas of mineral extraction, viniculture and farming operations, concentrations can be excessive. In contrast to terrestrial vertebrates, fish are not only exposed to dietary sources of copper but are also exposed to dissolved ionic copper that may enter via the skin and gills. Indeed, the latter route is important in fish and it has been demonstrated in physiological studies that under conditions of dietary deficiency, fish can satisfy their own body requirements by uptake from water. Therefore, fish must have systems relating to both gill and gut to enable maintenance of body homeostasis of this essential, yet toxic, metal. In an attempt to understand the mechanisms of Cu homeostasis in fish, whether under conditions of deficiency, adequacy or excess, it is essential to consider the expression of known Cu-homeostasis proteins. Thus, cDNAs for sea bream (Sparus aurata) homologues of copper transporter 1 (Ctr1), antioxidant protein 1 (Atox1), Menkes protein (ATP7A), Wilson protein (ATP7B), and metallothionein (MT), which are responsible for the uptake, delivery to the secretory pathway and scavenging of intracellular Cu, were cloned and their mRNA tissue expression levels measured. To investigate the molecular basis of the different homeostatic and toxic responses to waterborne or dietary Cu, sea bream were exposed to sub-toxic levels of Cu in the diet (130 mg/Kg of dry diet) or water (0.3 mg/L) and tissue mRNA and Cu levels were measured. Moreover, to discriminate between the effect of different metals on the transcriptional regulation of Cu homeostasis genes in fish, Sparus aurata fibroblast (SAF1) cells were exposed to sub-toxic levels of Cu (25 μM), Zn (100 μM) and Cd (10 μM). In addition, a microarray was used to gain a broader overview of the transcriptional response of SAF1 cells to Cu (25 μM). Waterborne or dietary Cu resulted in distinct expression profiles of Cu-homeostasis genes and markers of oxidative stress. After dietary exposure, Cu increased in intestine and liver, whilst after waterborne exposure Cu increased in gill and liver. Exposure to dietary Cu resulted in decreases in Ctr1 and ATP7A mRNA in both liver and intestine. Renal Ctr1 levels remained unchanged, whilst ATP7A mRNA decreased. In contrast, waterborne Cu exposure increased intestinal Ctr1 and ATP7A mRNA, and increased renal Ctr1 and decreased renal ATP7A mRNA. Both dietary and waterborne Cu increased ATP7B mRNA in liver. Metallothionein (MT) mRNA increased in liver and gill after waterborne Cu. Glutathione reductase (GR), a marker of oxidative stress, increased expression in liver and gill after waterborne Cu exposure, but decreased in intestine. Thus, exposure to Cu via water or diet has different, often opposite effects on Cu-homeostasis genes. The decrease in expression of both Cu-transport genes in intestine after dietary exposure may indicate a defensive mechanism to limit uptake of Cu. The opposite effects in intestine after waterborne exposure are more difficult to explain, but again may reflect a defence mechanism against excess bloodborne Cu coming from the gill. Since both dietary and waterborne Cu increased Cu levels in liver and increased hepatic ATP7B it is likely that well-characterised mammalian route of Cu excretion to bile is active in sea bream. However, only hepatic Cu derived from gill increased the expression of the stress markers MT and GR. This suggests that Cu is delivered to liver in a different form from gill as that from intestine, the intestinally derived pool being less toxic. Thus the increase in copper transport gene expression in intestine after gill exposure might be a mechanism to enable incorporation of excess bloodborne Cu into the intestinal pathway of Cu delivery to liver, thus minimizing toxicity. The in vitro exposure of SAF1 cells to Cu showed a similar response to liver of fish exposed to waterborne Cu indicating similar Cu availability and complexation. ATP7A mRNA levels were induced by Cu but not by Zn or Cd suggesting Cu-specific regulation. Conversely, MT and GR were induced by all metals tested. The transcriptomic analysis highlighted that the biological processes most significantly affected by Cu were secretion, protein trafficking and stress. Overall, these results show that in fish copper has distinct effects on tissue Cu transporter genes and oxidative stress depending on whether it is taken up via the gill or gut and that intestinal absorption may be required for normal uptake and metabolism of Cu, regardless of the route of uptake. Moreover, changes in mRNA levels indicate that Cu homeostasis genes, at least in fish, may be regulated at the transcriptional level. Although more work needs to be done to identify genes that are robust predictors of Cu toxicity, the microarray results presented here show a clear transcriptional fingerprint which may characterize Cu toxicity in fish.
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Concilli, Mafalda. "HSP70 as a target for correction of Wilson disease causing ATP7B mutants." Thesis, Open University, 2017. http://oro.open.ac.uk/50813/.

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Copper (Cu) is an essential micronutrient, which operates as a cofactor of enzymes regulating a wide range of critical physiological processes. However, Cu overload compromises the redox balance in cells and tissues causing serious toxicity. Removal of excess Cu from the body is driven be Cu-transporting ATPase ATP7B, which sequesters the potentially toxic metal and mediates its excretion into the bile. Mutations in the ATP7B result in Wilson disease (WD) that is caused by the toxic accumulation of Cu in the liver due to the loss of ATP7B function. The most frequent ATP7B mutant, H1069Q, still preserves a significant Cu-transporting activity, but undergoes retention and degradation in the endoplasmic reticulum (ER). Thus, rescue of ATP7B-H1069Q from the ER is expected to recover mutant function and, hence, would be beneficial for a large group of WD patients. Unfortunately, specific targets as well as safe drugs for correction of ATP7B-H1069Q mutant remain to be uncovered. Comparing interactomes of WT and H1069Q variants of ATP7B, I found HSP70 as a specific mutant interactor that regulates ER retention and degradation of ATP7B-H1069Q. HSP70 suppression (with either RNAi or allosteric inhibitor) improved stability of the mutant and facilitated its export from the ER to the Golgi and post-Golgi copper excretion sites. These findings prompted me to look for a safe way to inhibit HSP70 and rescue the ATP7B mutant. To this end several bioinformatics tools were employed to search for FDA-approved drugs that modulate HSP70 expression or exhibit structural similarity to HSP70 inhibitors. As a result, Domperidone and glucocorticoid receptor agonists were identified and validated as effective correctors of ATP7B mutant. In summary, my findings suggest a key role for HSP70 in proteostasis of ATP7B-H1069Q and revealed FDA-approved compounds as safe drugs for ATP7B mutant correction and, thus, for the normalization of Cu homeostasis in Wilson disease patients.
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Tsay, Mike J. "Expression, purification and characterization of the LEC-rat N-terminal metal binding domain from Atp7b, an orthologue to ATP7B, a copper transporting P-type ATPase implicated in Wilson disease." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2001. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp04/MQ62903.pdf.

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Kühne, Angelika. "Funktionelle Untersuchungen der Auswirkung von Mutationen auf das humane Kupfertransportprotein ATP7B (Wilson ATPase)." Doctoral thesis, Universitätsbibliothek Leipzig, 2013. http://nbn-resolving.de/urn:nbn:de:bsz:15-qucosa-102080.

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Das Schwermetall Kupfer ist von essentieller Bedeutung für zahlreiche zelluläre Funktionen. Aufgrund seines Redoxpotentials muss die Kupferhomöostase im Organismus eng reguliert werden. Die Schlüsselrolle spielt dabei das Kupfertransportprotein ATP7B (Wilson ATPase) in der Leber. Ein Funktionsverlust dieses Proteins wird in der autosomal-rezessiv vererbten Erkrankung Morbus Wilson deutlich. Der Kupfertransportdefekt der Hepatozyten führt zu einer Kupferüberladung in der Leber mit nachfolgender Schädigung. Ferner kommt es zu einer Kupferakkumulation im Zentralnervensystem mit neurologischen Störungen. Das bei der Erkrankung betroffene Gen ATP7B wurde 1993 kloniert. Bis heute sind über 500 krankheitsverursachende Genmutationen entdeckt worden. Eine Schlüsselfunktion dieser Enzymgruppe ist die katalytische Phosphorylierung. Die Auswirkungen von Mutationen auf die Funktion des Proteins sind jedoch nur unzureichend verstanden. ATP7B kann mit Hilfe des Baculovirusexpressionssystems hergestellt und anschließend proteinbiochemischen Untersuchungen unterzogen werden. In dieser experimentellen Arbeit wurde untersucht, ob Punktmutationen diesen Phosphorylierungsmechanismus von ATP7B beeinflussen. Dafür wurden, neben dem Wildtyp-Protein, 25 patientenspezifische und eine noch nicht beim Menschen beobachtete Mutation der Phosphorylierungsstelle D1027A als Negativkontrolle generiert und die katalytische Aktivität in einem Phosphorylierungsassay untersucht. In der vorliegenden Arbeit wurde gezeigt, dass bestimmte Punktmutationen zum Funktionsverlust von ATP7B führen. Als weiterer Mechanismus der Mutationswirkung wurde, neben der Inaktivierung von ATP7B, die Hyperphosphorylierung entdeckt. Die biochemische Charakterisierung dieser Mutationen führt zu einem tieferen Verständnis in der Pathophysiologie des Morbus Wilson und ebnet den Weg für detaillierte Untersuchungen der Genotyp-Phänotyp-Korrelation sowie für innovative Diagnostik- und Therapiestrategien.
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Forbes, John Richard. "Functional analysis of the copper-transporting P-type ATPase, ATP7B, defective in Wilson disease." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2000. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape2/PQDD_0008/NQ59959.pdf.

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Schirrmeister, Wiebke [Verfasser]. "Kupfertoxizität, Regeneration und Lipidmetabolismus in der Atp7b-/- - Maus, einem Tiermodell des Morbus Wilson / Wiebke Schirrmeister." Magdeburg : Universitätsbibliothek, 2013. http://d-nb.info/1054421234/34.

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Araújo, Thiago Ferreira de. "Importância da detecção de mutações do gene ATP7B para o diagnóstico da doença de Wilson." Universidade de São Paulo, 2014. http://www.teses.usp.br/teses/disponiveis/5/5168/tde-14082014-091501/.

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O diagnóstico da doença de Wilson (DW) é realizado por exames clínicos, laboratoriais, anatomopatológicos e de imagem. Mais de 500 mutações no gene ATP7B foram descritas como causadoras da DW. Para avaliar a importância da detecção de mutações no diagnóstico da DW em nosso meio, analisamos 35 pacientes com DW, 20 familiares de wilsonianos a partir de rastreamento familiar, 18 com hepatite crônica criptogênica e sete com insuficiência hepática aguda grave. Para o diagnóstico da DW foi utilizado o sistema de escore sugerido pela Sociedade Europeia para o Estudo do Fígado de 2012. Os dados demográficos, clínicos, laboratoriais e histológicos foram obtidos retrospectivamente. Obteve-se o DNA genômico de cada paciente a partir de sangue periférico e realizou-se o sequenciamento direto dos 21 éxons e suas bordas intrônicas do gene ATP7B. Todos os pacientes com DW apresentavam no mínimo quatro pontos. No grupo de rastreamento familiar o sequenciamento foi importante para o diagnóstico de DW em 14 familiares; no grupo de hepatite crônica criptogênica em oito pacientes e no grupo de insuficiência hepática aguda grave em três pacientes. Foi caracterizada uma família com cinco genótipos diferentes (dois homozigotos p.A1135Qfs/p.A1135Qfs e p.M645R/p.M645R), um heterozigoto composto (p.A1135Qfs/p.M645R) e dois heterozigotos simples (p.A1135Qfs/0 e p.M645R/0) com fenótipos variados. Foram detectadas duas mutações em heterozigose simples em pacientes com insuficiência hepática aguda grave. A mutação p.A1135Qfs e p.L708P foram as mais frequentes em todos os grupos. Foi identificada pela primeira vez a mutação p.M645R em homozigose. Concluímos que os resultados confirmaram que o sequenciamento do gene ATP7B foi útil: 1) para confirmar que as mutações p.A1135Qfs e p.L708P são as mais importantes na população brasileira; 2) para demonstrar que a mutação tida como a mais frequente na Europa, a p.H1069Q, tem bem menor importância em nosso meio, embora mais frequentemente do que o observado anteriormente; 3) para confirmar (ou excluir) precocemente o diagnóstico e evitar a realização de exames desnecessários e invasivos e iniciar (ou não realizar) o tratamento, com base mais sólida, em pacientes com hepatopatia crônica idiopática e em familiares de portadores de DW; 4) para definir o diagnóstico de DW em casos de insuficiência hepática aguda grave, diagnóstico ainda que tardio, mas de suma importância para realização de estudo familiar subsequente, 5) para identificação não esperada de heterozigotos simples e polimorfismos de significado ainda não esclarecido em pacientes com insuficiência hepática aguda grave; 6) para identificação de casos inusitados de três genótipos diferentes causadores da doença na mesma família (homozigose de duas mutações diferentes e heterozigose composta); 7) para melhor definir que a mutação p.M645R em homozigose tem potencial para desenvolver a DW, embora resultados de estudos em in vitro sugiram função normal da proteína defeituosa sintetizada; 8) para definir que há casos de doentes com a mutação p.M645R em heterozigose composta de evolução extremamente benigna, com diagnóstico após a quinta década de vida, com discretas alterações hepáticas. Porém há casos com evolução mais grave tanto do ponto de vista hepático quanto neurológico, possivelmente influenciados pelas mutações que a acompanham<br>Wilson\'s disease (WD) is an autosomal recessive disorder secondary to mutations in the ATP7B gene resulting in toxic accumulation of copper in various tissues. The diagnosis of WD is made by the analysis of clinical, laboratory, histological findings and imaging tests. More than 500 mutations have been described in the ATP7B gene as the cause of WD. In order to expand the knowledge of the importance of mutation detection in the diagnosis of WD, we analyzed 36 patients with WD, 20 individuals from family screening, 18 with cryptogenic chronic hepatitis and seven with severe acute liver failure. For the diagnosis of WD the International Scoring System suggested by the European Association for the Study of the Liver (EASL) in 2012 was used. Demographic, clinical, laboratory and histological data were obtained retrospectively. Direct sequencing of 21 exons and intron boundaries of ATP7B gene was performed in genomic DNA extracted from peripheral blood leucocytes of all subjects. All patients with WD have at least four points of the scoring system without considering the DPA challenge test. In the family screening group, sequencing was important for the diagnosis of DW in fourteen patients; eight patients in the group of cryptogenic chronic hepatitis, and three patients in the group of severe acute liver failure. Five different genotypes were identified in one family (two homozygous, p.A1135Qfs/p.A1135Qfs and p.M645R/p.M645R, one compound heterozygous p.A1135Qfs/p.M645R, and two simple heterozygous p.A1135Qfs/0 and p.M645R/0). Two patients with acute liver failure were detected as simple heterozygous. The p.A1135Qfs and p.L708P were the most frequent mutations in all groups. It is the first time p.M645R mutation was detected in homozygosity. The ATP7B gene sequencing was useful: 1) to confirm that p.A1135Qfs and p.L708P mutations are the most frequent in the Brazilian population; 2) to confirm that the most common mutation in Europe, p.H1069Q has lower frequency in our area; 3) to confirm (or exclude) an early diagnosis and to avoid unnecessary and invasive tests and to initiate (or not) the specific treatment with a stronger basis in patients with chronic liver disease and individuals from family screening of patients with Wilson disease; 4) to confirm the diagnosis, although late, of cases with severe acute liver failure, but very important to perform family screening; 5) to identify simple heterozygotes in patients with severe acute liver failure; 6) to describe unusual cases of three different genotypes of WD patients in a same family (two different homozygous mutations and one compound heterozygous); 7) to better define that p.M645R mutation in homozigosity develops WD, although the results from in vitro studies suggested a normal function for the defective synthesized protein; 8) to define that there are patients with p.M645R mutations in compound heretozigosity with a very benign clinical picture, with late diagnosis, after the fifth decade of life, with mild liver alterations. However, there are patients with a more severe clinical evaluation, hepatic or neurologic, probably secondary to the influence of the other mutation
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Jeromson, Sarah Joy. "Development of a yeast model to distinguish missense mutations from polymorphisms in the Wilson's disease gene ATP7B." Thesis, University of Huddersfield, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.288501.

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Hercend, Claude. "Contribution de la modélisation moléculaire à l'étude de pathologies humaines : Application au transporteur ATP7B et au récepteur 5HT2B." Phd thesis, Université René Descartes - Paris V, 2012. http://tel.archives-ouvertes.fr/tel-00708236.

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Hercend, Claude. "Contribution de la modélisation moléculaire à l’étude de pathologies humaines : Application au transporteur ATP7B et au récepteur 5HT2B." Thesis, Paris 5, 2012. http://www.theses.fr/2012PA05T005/document.

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Books on the topic "ATP7B"

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Tsay, Mike J. Expression, purification and characterization of the LEC-rat n-terminal metal binding domain from Atp7b, an orthologue to ATP7B, a copper transporting P-type ATPase implicated in Wilson disease. National Library of Canada, 2001.

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Trocello, Jean-Marc, and France Woimant. Disorders of Copper and Iron Metabolism. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199972135.003.0044.

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Both copper and iron are essential metals that have a critical function in a series of biochemical pathways. This chapter describes the disorders associated with genetic abnormalities in copper and iron metabolic pathways and their manifestations in adult patients. Mutations in the genes of the copper transporting P-type ATPases, ATP7A and ATP7B are associated with Wilson disease, Menkes disease, occipital horn syndrome and ATP7A-related distal motor neuropathy. Neurodegeneration with brain iron accumulation (NBIA) is a group of disorders characterized by excess iron deposition in globus pallidus, substantia nigra pars reticulata, striata and cerebellar dentate nuclei. Several genes associated with NBIA have been identified.
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Beattie, R. Mark, Anil Dhawan, and John W.L. Puntis. Wilson's disease. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780198569862.003.0056.

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Clinical features 412Diagnosis 413Management 414Indications for liver transplantation 415• Wilson's disease (WD) is an autosomal disorder of copper metabolism. The gene ATP7B codes for a copper carrier which both exports copper from hepatocyte to bile, and enables caeruloplasmin synthesis.• WD occurs worldwide with reported incidences of 5–30 per million population. WD may present with almost any variety of liver disease in the age group 3–12 years, with psychiatric and/or neurological disease in adolescence or young adults, with combined hepatic and neurological problems, or less commonly with haemolysis or arthritis....
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Fox, Susan H. Seizures and Shakes. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190607555.003.0017.

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Wilson’s disease is an autosomal recessive, treatable heredodegenerative disorder characterized by excessive deposition of copper in the liver, brain, and other tissues including the kidneys, pancreas, and joints. Early recognition of the disorder, which can present with a variety of movement disorders and neuropsychiatric phenomena, is critical to avoid irreversible end organ damage through the initiation of copper chelating agents. Diagnosis relies first on demonstrating evidence of brain iron deposition on magnetic resonance imaging of brain and elevated urinary copper excretion in the appropriate clinical context. Genetic testing for mutations in the ATP7B gene will identify a mutation in up to 90% of cases.
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Book chapters on the topic "ATP7B"

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Safaei, Roohangiz, and Stephen B. Howell. "Regulation of the Export of Platinum-Containing Drugs by the Copper Efflux Transporters ATP7A and ATP7B." In Platinum and Other Heavy Metal Compounds in Cancer Chemotherapy. Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60327-459-3_13.

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Hosokawa, T., M. Okabe, M. Kurasaki, et al. "Distribution of Copper Transported ATP7B in Embryo and New Born Rat." In Trace Elements in Man and Animals 10. Springer US, 2002. http://dx.doi.org/10.1007/0-306-47466-2_11.

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DiDonato, Michael, Suree Narindrasorasak, and Bibudhendra Sarkar. "Expression, Purification, and Metal Binding Characteristics of the Putative Copper Binding Domain from the Wilson Disease Copper Transporting ATPase (ATP7B)." In Copper Transport and Its Disorders. Springer US, 1999. http://dx.doi.org/10.1007/978-1-4615-4859-1_14.

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Usta, Julnar, Hussein Abu Daya, Houssam Halawi, et al. "Homozygosity for Non-H1069Q Missense Mutations in ATP7B Gene and Early Severe Liver Disease: Report of Two Families and a Meta-analysis." In JIMD Reports. Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/8904_2011_91.

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Tümer, Zeynep, Lisbeth Birk Møller, and Nina Horn. "Mutation Spectrum of ATP7A, the Gene Defective in Menkes Disease." In Copper Transport and Its Disorders. Springer US, 1999. http://dx.doi.org/10.1007/978-1-4615-4859-1_7.

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Blumenstein, Sarah, Stefan Leu, Eahab Abu-Much, Dudy Bar-Zvi, Noun Shavit, and Allan Michaels. "Expression of the Chloroplast atpB Gene of Chlamydomonas reinhardtii in E. coli." In Current Research in Photosynthesis. Springer Netherlands, 1990. http://dx.doi.org/10.1007/978-94-009-0511-5_482.

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Choi, Eun-Young, Keyur Patel, Marie Reine Haddad, et al. "Tandem Duplication of Exons 1–7 Neither Impairs ATP7A Expression Nor Causes a Menkes Disease Phenotype." In JIMD Reports. Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/8904_2014_391.

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Strehler, Emanuel E. "The ATP2B Plasma Membrane Ca2+ ATPase Family: Regulation in Response to Changing Demands of Cellular Calcium Transport." In Regulation of Ca2+-ATPases,V-ATPases and F-ATPases. Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-24780-9_5.

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Hoot, Sara B. "Phylogeny of the Ranunculaceae based on preliminary atpB, rbcL and 18S nuclear ribosomal DNA sequence data." In Systematics and Evolution of the Ranunculiflorae. Springer Vienna, 1995. http://dx.doi.org/10.1007/978-3-7091-6612-3_24.

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Leu, S., J. Schlesinger, Hu Dongli, H. R. Fiedler, H. Strotmann, and N. Shavit. "Molecular Characterization of atpA and atpB Deletion Mutants Induced in Chlamydomonas Reinhardth CW15 by Chloroplast Transformation." In Photosynthesis: from Light to Biosphere. Springer Netherlands, 1995. http://dx.doi.org/10.1007/978-94-009-0173-5_499.

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Conference papers on the topic "ATP7B"

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Guttmann, S., and H. Schmidt. "ATP7B Knockout in einer intestinalen Zelllinie." In Viszeralmedizin 2019. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1695588.

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Zibert, A., S. Guttmann, and HH Schmidt. "New role of copper transporter ATP7B in lipid metabolism of enterocytes." In 36. Jahrestagung der Deutschen Arbeitsgemeinschaft zum Studium der Leber. Georg Thieme Verlag KG, 2020. http://dx.doi.org/10.1055/s-0039-3402196.

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Kakuda, Mamoru. "Abstract 2153: ATP7B is a promising therapeutic target for uterine leiomyosarcoma." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-2153.

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Kakuda, Mamoru, Shinya Matsuzaki, Ruriko Nakae, et al. "Abstract 1200: Novel strategy to overcome platinum resistance in uterine leiomyosarcoma; blocking ATP7B by copper ion." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-1200.

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Safaei, Roohangiz, Preston L. Adams, Ryan A. Mathews, and Stephen B. Howell. "Abstract 833: The CXXC motifs in the metal binding domains are required for ATP7B to mediate resistance to cisplatin." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-833.

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Filpo, Alessandra, Caio Disserol, Bernardo Corrêa de Almeida Teixeira, Kenzo Hokazono, and Hélio A. G. Teive. "An Unexpected Smile: risus sardonicus and wing-beating tremor in a first office visit." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.505.

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Context: We present a noteworthy reminder of Wilson disease’s classical manifestations, which may become rarer in clinical practice as availability of genetic tests increases, allowing timely diagnosis and treatment. Case report: A 29 year-old woman developed progressive and asymmetric upper limb tremor and dystonia over 1 year, along with speech and feeding impairment in the last two weeks. Examination revealed segmental dystonia with risus sardonicus, open-jaw oromandibular and severe left arm dystonia, along with wing-beating tremor. Bilateral Kayser-Fleischer ring, low serum ceruloplasmin level, high urinary copper level, bilateral putaminal lesions on brain MRI and detection of ATP7B mutation confirmed Wilson disease (WD). A nasoenteric tube was inserted and D-penicillamine was started. Conclusion: This case illustrates the hallmark neuro-ophtalmological signs of WD: wing-beating tremor, risus sardonicus and Kayser-Fleischer ring. The former is probably associated with lesions in the dentato-rubro-thalamic pathway¹ and means a low frequency, high amplitude, posture-induced proximal arm tremor. Risus sardonicus means a fixed smile due to risorius muscle dystonia². Although it is a well-known manifestation of cephalic tetanus, it is also frequent in WD¹. Finally, the Kayser-Fleischer ring is caused by copper accumulation in the Descemet membrane and occurs in almost 100% of patients with neurological WD².
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Zhu, Sha, and Michael J. Petris. "Abstract 1000: ATP7A mutation reduces resistance to chemotherapy agentsin vitroandin vivo." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-1000.

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Shanbhag, Vinit, and Nikita Gudekar. "Abstract 246: Role for ATP7A copper transporter in cisplatin resistance, tumorigenesis and metastasis." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-246.

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Matsuzaki, Shinya, Akiko Morimoto, Satoshi Serada, et al. "Abstract 4059: Annexin A4-conferred platinum resistance is mediated by the copper transporter ATP7A." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-4059.

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Almeida, Vitor H., Luiz H. de Araújo Lima, Mauricio S. Caetano, et al. "Abstract 1731: Correlation between XIAP, pAkt, and ATP7A expression and cisplatin resistance in non-small cell lung cancer." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-1731.

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