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Our findings imply that reduced stability and enhanced dynamics of MBD1 (show DPEP1 ELISA Kits) or MBD6 is the origin of ATP7B dysfunction in Wilson disease patients with the G85V or G591D mutation.
single nucleotide polymorphisms in ATP7B gene is associated with copper dysmetabolism in Alzheimer's disease.
Mutation in ATP7B gene is associated with copper dysmetabolism in Wilson disease.
We here demonstrate that ATP7B confers multidrug resistance by facilitating nuclear drug efflux and late endosomal drug sequestration.
Data suggest that N-terminal segment of metal-binding domains (MBDs) 1-3 of ATOX1 (show ATOX1 ELISA Kits) interact with nucleotide-binding domain of ATP7B, thus physically coupling the domains involved in copper binding and those involved in ATP hydrolysis; interactions with MBDs 1-3 of ATOX1 (show ATOX1 ELISA Kits) activate ATP7B ATP hydrolysis. (ATOX1 (show ATOX1 ELISA Kits) = copper transport protein ATOX1 (show ATOX1 ELISA Kits); ATP7B = Cu-binding P type ATPase (show ATP7A ELISA Kits) ATP7B)
11 single-nucleotide polymorphisms (SNPs) in CTR1 (show SLC31A1 ELISA Kits), CTR2, ATP7A (show ATP7A ELISA Kits), and ATP7B were genotyped in these patients.
Wilson's disease results from mutations that cause absent or markedly diminished levels of ATP7B that can be determined in dried blood spots using a novel immune-SRM (show SRM ELISA Kits) assay.
The P-type copper ATPases ATP7A (show ATP7A ELISA Kits) and ATP7B provide an important system for acquisition, active transport, distribution and elimination of copper. Relevance of copper metabolism to human diseases and therapy is already known. It is quite certain that further studies will reveal detailed and useful information on biochemical mechanisms and relevance to diseases
the mechanism of copper-dependent regulation of ATP7B and ATP7A (show ATP7A ELISA Kits), the roles of individual MBDs, and the relationship between the regulatory and catalytic copper binding are still unknown. We describe the structure and dynamics of the MBDs, review the current knowledge about their functional roles and propose a mechanism of regulation of ATP7B by copper-dependent changes in the dynamics and conformation of the MBD (show DPEP1 ELISA Kits) chain.
ATP-dependent copper transfer in ATP7A (show ATP7A ELISA Kits)/B is not affected by varying the pH, suggesting that net proton counter-transport may not occur in copper ATPases. Platinum anticancer drugs activate ATP7A (show ATP7A ELISA Kits)/B and are subjected to ATP-dependent vectorial displacement with a mechanism analogous to that of copper
This study showed that knockout of Atp7b led to altered lipid metabolism and liver steatosis in the absence of inflammation.
ATP7B is transported from the trans-Golgi network (TGN (show TG ELISA Kits)) to the bile canaliculus by basolateral sorting and endocytosis, and microtubule-mediated transcytosis through the subapical compartment.
Data indicate that the copper-transporting ATPase (show DNAH8 ELISA Kits) gene (Atp7b) knockout mice showed a drastic, time-dependent accumulation of hepatic copper.
The aim of this study was to identify copper disturbances according to various brain compartments and further dissect the causal relationship between copper storage and neuronal damage using Atp7b(-/-) mice.
DKWSLLL sequence is essential for ATP7b sorting at the TGN (show TG ELISA Kits), transport from the TGN (show TG ELISA Kits) to the PM, endocytosis, and recycling to the TGN (show TG ELISA Kits) and PM.
Ligand-activated nuclear receptors FXR/NR1H4 (show NR1H4 ELISA Kits) and GR/NR3C1 (show NR3C1 ELISA Kits) and nuclear receptor interacting partners are less abundant in Atp7b(-/-) hepatocyte nuclei.
By performing dynamic PET, authors obtained the first real-time measurements of 64Cu distribution in the organs or tissues of Atp7b -/- mice.
Clusterin (show CLU ELISA Kits) and COMMD1 (show COMMD1 ELISA Kits) independently regulate degradation of the mammalian copper ATPases ATP7A (show ATP7A ELISA Kits) and ATP7B.
Neuroinflammatory and behavioural changes in the Atp7B mutant mouse model of Wilson's disease.
The Jackson toxic milk mouse as a model for copper loading
Data show that CD4 (show CD4 ELISA Kits)(+) and WC1(+) gammadelta T-cells were induced to produce IL-17 (show IL17A ELISA Kits) termed Th17 and gammadelta17 cells.
The endocytosis and signaling of the gamma-delta T cell coreceptor WC1 are regulated by a dileucine motif.
WC1 is a hybrid gamma-delta TCR coreceptor and pattern recognition receptor for pathogenic bacteria.
Identification of differences in the signal transduction through the endodomains of WC1 contributes to understanding the functional role of the WC1 coreceptors in the gammadelta T cell responses.
Specific receptors in the WC1 family directly participate in Leptospira recognition and/or activation of gamma-delta T cells.
These findings revealed that despite the existence of a distinct bovine CD4 (show CD4 ELISA Kits)(+)CD25 (show IL2RA ELISA Kits)(high) T cell population, which showed Foxp3 (show FOXP3 ELISA Kits) transcription/expression, natural regulatory activity did not reside in this cell population
Sudies demonstrate that WC1 molecules are encoded by a large, multi-gene family whose transcripts undergo extensive alternative splicing.
A copper-dependent ATPase (show DNAH8 ELISA Kits) hydrolysis in a native Golgi-enriched preparation from liver, was characterized.
This gene is a member of the P-type cation transport ATPase family and encodes a protein with several membrane-spanning domains, an ATPase consensus sequence, a hinge domain, a phosphorylation site, and at least 2 putative copper-binding sites. This protein functions as a monomer, exporting copper out of the cells, such as the efflux of hepatic copper into the bile. Alternate transcriptional splice variants, encoding different isoforms with distinct cellular localizations, have been characterized. Mutations in this gene have been associated with Wilson disease (WD).
ATPase, Cu(2+)- transporting, beta polypeptide
, Wilson disease-associated protein
, copper pump 2
, copper-transporting ATPase 2
, Wilson protein
, toxic milk
, wilson disease-associated protein homolog
, ATPase, Cu++ transporting, beta polypeptide (same as Wilson disease)
, PINA gene, promoter
, pineal night-specific ATPase
, ATPase, Cu++ transporting, beta polypeptide
, copper-transporting ATPase beta subunit
, ATPase 7B protein
, ATPase, Cu++ transporting, beta polypeptide (Wilson disease)
, Wilson's disease protein
, copper-transporting ATPase
, ATPase, Cu(2+)-transporting, beta polypeptide
, copper-transporting ATPase 2-like
, scavenger receptor cysteine-rich type 1 protein M160
, scavenger-receptor protein