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Wilson disease protein
Molecular Mechanisms Regulating Copper Balance in Human Cells
( 12 ) United States Patent
Cisplatin Inhibits MEK1/2
Biophysical Characterization of the First Four Metal-Binding Domains of Human Wilson Disease Protein
Benchmarking Computational Methods for Estimating the Pathogenicity of Wilson’S
Hepatic Presentation of Wilson's Disease in Children
Structural Models of the Human Copper P-‐Type Atpases ATP7A
Copper Transporter 2 (CTR2) As a Regulator of Cisplatin Accumulation and Sensitivity
Bhuiyan Et Al., 2018 Supplementary Data: Systematic Evaluation of Isoform Function
Inhibition of Copper Transport Induces Apoptosis in Triple Negative Breast Cancer Cells and Suppresses Tumor Angiogenesis
ATP7A-Regulated Enzyme Metalation and Trafficking in the Menkes
Cloning and Expression of the Two Isoforms of Copper Atpase in a Fish
Mutational Analysis of ATP7B in North Chinese Patients with Wilson Disease
Structural and Functional Hepatocyte Polarity and Liver Disease
Copper Accumulation in Senescent Cells: Interplay Between Copper Transporters and Impaired Autophagy
Endometriose Og Type I Interferon
Mitochondrial Copper Overload in a Rat Model for Wilson Disease Is Paralleled by Upregulated COX17 and Can Be Restored Using the Bacterial Peptide Methanobactin
Cloning and Expression of the Two Isoforms of Copper Atpase
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Solution Structure of the N-Domain of Wilson Disease Protein: Distinct Nucleotide-Binding Environment and Effects of Disease Mutations
University of Florida Thesis Or Dissertation Formatting Template
Journal of Trace Elements in Medicine and Biology Copper Homeostasis
Wilson Disease-3
Structural and Functional Studies of ATP7B, the Copper(I)-Transporting P-Type Atpase Implicated in Wilson Disease
Wilson's Disease Protein Binds Nucleotides and Interacts with the N
Structures of P-Type Transporting Atpasesand
1. Introduction
Pharmacoproteomics Pinpoints HSP70 Interaction for Correction of the Most Frequent Wilson Disease-Causing Mutant of ATP7B
Inhibition of Copper Transport Induces Apoptosis in Triple-Negative Breast Cancer Cells and Suppresses Tumor Angiogenesis Olga Karginova1, Claire M
Characterization of the N-Terminal Domains and Disease-Causing Mutations of the Human Wilson Protein
Structure and Function of KH Domain in DDX43 and DDX53 Cancer Antigen Helicases