Browse our anti-ATP7B (ATP7B) Antibodies

Human ATPase, Cu++ Transporting, beta Polypeptide (ATP7B) interaction partners

1. for ATP7B mutations, the more severe impact on ATP7B protein was, the younger onset age and lower Cp level presented. The feasibility of presymptomatic DNA diagnosis and predicting clinical manifestation or severity of Wilson disease (WD) would be facilitated with identified mutations and genotype-phenotype correlation precisely revealed in the study.

2. Among those >800 reported mutations of the ATP7B gene missense/nonsense mutations are very rare. A874V-ATP7B protein mutant showed apparent destabilization and endoplasmic reticulum retention, and lost copper transport activity, thus likely causing Wilson disease phenotype.

3. Our findings imply that reduced stability and enhanced dynamics of MBD1 (show DPEP1 Antibodies) or MBD6 (show MBD6 Antibodies) is the origin of ATP7B dysfunction in Wilson disease patients with the G85V or G591D mutation.

4. single nucleotide polymorphisms in ATP7B gene is associated with copper dysmetabolism in Alzheimer's disease.

5. Mutation in ATP7B gene is associated with copper dysmetabolism in Wilson disease.

6. We here demonstrate that ATP7B confers multidrug resistance by facilitating nuclear drug efflux and late endosomal drug sequestration.

7. Data suggest that N-terminal segment of metal-binding domains (MBDs) 1-3 of ATOX1 (show ATOX1 Antibodies) 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 Antibodies) activate ATP7B ATP hydrolysis. (ATOX1 (show ATOX1 Antibodies) = copper transport protein ATOX1 (show ATOX1 Antibodies); ATP7B = Cu-binding P type ATPase (show ATP7A Antibodies) ATP7B)

8. 11 single-nucleotide polymorphisms (SNPs) in CTR1 (show SLC31A1 Antibodies), CTR2 (show SLC31A2 Antibodies), ATP7A (show ATP7A Antibodies), and ATP7B were genotyped in these patients.

9. 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 Antibodies) assay.

10. The P-type copper ATPases ATP7A (show ATP7A Antibodies) 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

Mouse (Murine) ATPase, Cu++ Transporting, beta Polypeptide (ATP7B) interaction partners

1. This study showed that knockout of Atp7b led to altered lipid metabolism and liver steatosis in the absence of inflammation.

2. ATP7B is transported from the trans-Golgi network (TGN (show TG Antibodies)) to the bile canaliculus by basolateral sorting and endocytosis, and microtubule-mediated transcytosis through the subapical compartment.

3. Data indicate that the copper-transporting ATPase (show DNAH8 Antibodies) gene (Atp7b) knockout mice showed a drastic, time-dependent accumulation of hepatic copper.

4. 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.

5. DKWSLLL sequence is essential for ATP7b sorting at the TGN (show TG Antibodies), transport from the TGN (show TG Antibodies) to the PM, endocytosis, and recycling to the TGN (show TG Antibodies) and PM.

6. Ligand-activated nuclear receptors FXR/NR1H4 (show NR1H4 Antibodies) and GR/NR3C1 (show NR3C1 Antibodies) and nuclear receptor interacting partners are less abundant in Atp7b(-/-) hepatocyte nuclei.

7. By performing dynamic PET, authors obtained the first real-time measurements of 64Cu distribution in the organs or tissues of Atp7b -/- mice.

8. Clusterin (show CLU Antibodies) and COMMD1 (show COMMD1 Antibodies) independently regulate degradation of the mammalian copper ATPases ATP7A (show ATP7A Antibodies) and ATP7B.

9. Neuroinflammatory and behavioural changes in the Atp7B mutant mouse model of Wilson's disease.

10. The Jackson toxic milk mouse as a model for copper loading

Cow (Bovine) ATPase, Cu++ Transporting, beta Polypeptide (ATP7B) interaction partners

1. Data show that CD4 (show CD4 Antibodies)(+) and WC1(+) gammadelta T-cells were induced to produce IL-17 (show IL17A Antibodies) termed Th17 and gammadelta17 cells.

2. The endocytosis and signaling of the gamma-delta T cell coreceptor WC1 are regulated by a dileucine motif.

3. WC1 is a hybrid gamma-delta TCR coreceptor and pattern recognition receptor for pathogenic bacteria.

4. 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.

5. Specific receptors in the WC1 family directly participate in Leptospira recognition and/or activation of gamma-delta T cells.

6. These findings revealed that despite the existence of a distinct bovine CD4 (show CD4 Antibodies)(+)CD25 (show IL2RA Antibodies)(high) T cell population, which showed Foxp3 (show FOXP3 Antibodies) transcription/expression, natural regulatory activity did not reside in this cell population

7. Sudies demonstrate that WC1 molecules are encoded by a large, multi-gene family whose transcripts undergo extensive alternative splicing.

Pig (Porcine) ATPase, Cu++ Transporting, beta Polypeptide (ATP7B) interaction partners

1. A copper-dependent ATPase (show DNAH8 Antibodies) hydrolysis in a native Golgi-enriched preparation from liver, was characterized.