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ATPase, Cu++ transporting, beta polypeptide

ATP7B, ATP7A, WC1, MC1, MNK
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). [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: ATPase, CAN, HAD, AGE, V1a
Papers using ATP7B antibodies
3-Hydroxykynurenine and 3-hydroxyanthranilic acid generate hydrogen peroxide and promote alpha-crystallin cross-linking by metal ion reduction.
Supplier
Gwinn-Hardy Katrina, In PLoS ONE, 1999
... Antibodies used were anti-APLP2 (Calbiochem), anti-ATP7A (Abcam), anti-ATP7B N-terminus antibody (Novus), ...
A novel trinuclear platinum complex overcomes cisplatin resistance in an osteosarcoma cell system.
Supplier
Jaehde Ulrich et al., In BMC Cancer, 1998
... Goat antibodies to ATP7A and ATP7B were from Santa Cruz Biotechnology, Inc ...
Papers on ATP7B
From the Editor's desk...: February 2016.
New
Jalan et al., In J Hepatol, Feb 2016
In this work, Murillo et al. assessed the efficacy of gene therapy by transducing the liver of the Atp7b(-/-) WD mouse model with an adenovirus encoding the human ATP7B cDNA.
D-penicillamine-induced ANA (+) ANCA (+) vasculitis in pediatric patients with Wilson's disease.
New
Cho et al., In Clin Nephrol, Feb 2016
Wilson's disease is an inborn error of copper metabolism caused by a mutation in the copper transporting gene ATP7B, and traditional treatment is based on copper chelation with agents such as D-penicillamine.
Non-Ceruloplasmin Copper Distincts Subtypes in Alzheimer's Disease: a Genetic Study of ATP7B Frequency.
New
Bonvicini et al., Roma, Italy. In Mol Neurobiol, Feb 2016
ATP7B gene variants associate with AD, modulating the size of non-Cp-Cu pool.
Augmentation of Immune Checkpoint Cancer Immunotherapy with IL-18.
New
Okamura et al., La Défense, France. In Clin Cancer Res, Feb 2016
The combination modality led to the accumulation of precursor of mature natural killer (pre-mNK) cells in the peritoneal cavity together with increased CD8+ T and decreased CD4+CD25+Foxp3+ T cells.
Copper at synapse: Release, binding and modulation of neurotransmission.
Review
New
Rossi et al., Roma, Italy. In Neurochem Int, Nov 2015
The copper pump ATP7A, which mutations are responsible for diseases with a prominent neurodegenerative component, seems to play a pivotal role in the release of copper at synapses.
Signalling to eIF4E in cancer.
Review
New
Sonenberg et al., Montréal, Canada. In Biochem Soc Trans, Nov 2015
The activity of eIF4E is regulated at many levels, most profoundly by two major signalling pathways: PI3K (phosphoinositide 3-kinase)/Akt (also known and Protein Kinase B, PKB)/mTOR (mechanistic/mammalian target of rapamycin) and Ras (rat sarcoma)/MAPK (mitogen-activated protein kinase)/Mnk (MAPK-interacting kinases).
Interferon-γ regulates cellular metabolism and mRNA translation to potentiate macrophage activation.
New
Impact
Ivashkiv et al., New York City, United States. In Nat Immunol, Aug 2015
We found that IFN-γ regulated the metabolism and mRNA translation of human macrophages by targeting the kinases mTORC1 and MNK, both of which converge on the selective regulator of translation initiation eIF4E.
Currently Clinical Views on Genetics of Wilson's Disease.
Review
New
Wang et al., Shanghai, China. In Chin Med J (engl), Aug 2015
DATA SOURCES: We searched documents from PubMed and Wanfang databases both in English and Chinese up to 2014 using the keywords WD in combination with genetic, ATP7B gene, gene mutation, genotype, phenotype.
Wilson's disease and other neurological copper disorders.
Review
Impact
Kaler et al., Heidelberg, Germany. In Lancet Neurol, 2015
Direct genetic testing for ATP7B mutations are increasingly available to confirm the clinical diagnosis of Wilson's disease, and results from biochemical and genetic prevalence studies suggest that Wilson's disease might be much more common than previously estimated.
Behind the Link between Copper and Angiogenesis: Established Mechanisms and an Overview on the Role of Vascular Copper Transport Systems.
Review
Maffia et al., Lecce, Italy. In J Vasc Res, 2014
Functions regulated by the major copper transport proteins (CTR1 importer, ATP7A efflux pump and metallo-chaperones) include the modulation of endothelial migration and vascular superoxide, known to activate angiogenesis within a narrow concentration range.
Mottled Mice and Non-Mammalian Models of Menkes Disease.
Review
Møller et al., Kraków, Poland. In Front Mol Neurosci, 2014
Mice with mutations in the Atp7a gene, called mottled mutants, are well-established and excellent models of Menkes disease.
Analysis and application of ATP7B gene mutations in 35 patients with hepatolenticular degeneration.
Kong et al., Zhengzhou, China. In Genet Mol Res, 2014
The polymerase chain reaction (PCR) was used to amplify the exons and exon-intron boundaries of the ATP7B gene in 35 Wilson's disease pedigrees.
A global analysis of SNX27-retromer assembly and cargo specificity reveals a function in glucose and metal ion transport.
Impact
Cullen et al., Bristol, United Kingdom. In Nat Cell Biol, 2013
Over 100 cell surface proteins, many of which interact with SNX27, including the glucose transporter GLUT1, the Menkes disease copper transporter ATP7A, various zinc and amino acid transporters, and numerous signalling receptors, require SNX27-retromer to prevent lysosomal degradation and maintain surface levels.
Disruption of copper homeostasis due to a mutation of Atp7a delays the onset of prion disease.
GeneRIF
Oldstone et al., Los Angeles, United States. In Proc Natl Acad Sci U S A, 2012
ATP7A-mediated copper homeostasis is important for the formation of pathogenic proteinase-resistant prion protein
A structural model of the copper ATPase ATP7B to facilitate analysis of Wilson disease-causing mutations and studies of the transport mechanism.
GeneRIF
Lutsenko et al., Tel Aviv-Yafo, Israel. In Metallomics, 2012
The ATP7B core (residues 643-1377) homology was modelled using the recent structure of the bacterial copper-ATPase LCopA as a template.
Multiple Menkes copper ATPase (Atp7a) transcript and protein variants are induced by iron deficiency in rat duodenal enterocytes.
GeneRIF
Collins et al., Gainesville, United States. In J Trace Elem Med Biol, 2012
Multiple Atp7a transcript and protein variants exist in rodent intestinal epithelial cells and are induced by dietary iron deprivation.
Molecular analysis of Wilson patients: direct sequencing and MLPA analysis in the ATP7B gene and Atox1 and COMMD1 gene analysis.
GeneRIF
Wilson et al., Bron, France. In J Trace Elem Med Biol, 2012
Among our 112 WD unrelated patients, 83 different ATP7B gene mutations were identified, 27 of which were novel.
Alagille syndrome and Wilson disease in siblings: a diagnostic conundrum.
GeneRIF
Tischkowitz et al., Québec, Canada. In Can J Gastroenterol, 2012
The potential implications of being a heterozygote for Wilson disease in the context of Alagille syndrome are discussed, with a mutation in the Wilson disease gene, ATP7B.
Crystal structure of a copper-transporting PIB-type ATPase.
Impact
Nissen et al., Århus, Denmark. In Nature, 2011
The structure also provides a framework to analyse missense mutations in the human ATP7A and ATP7B proteins associated with Menkes' and Wilson's diseases.
Cardiac copper deficiency activates a systemic signaling mechanism that communicates with the copper acquisition and storage organs.
Impact
Thiele et al., Durham, United States. In Cell Metab, 2010
Expression of the ATP7A Cu exporter, thought to function predominantly in intestinal Cu acquisition, was strongly increased in liver and intestine of Ctr1(hrt/hrt) mice.
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