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ATP7A encodes a transmembrane protein that functions in copper transport across membranes. Additionally we are shipping ATP7A Proteins (9) and ATP7A Kits (6) and many more products for this protein.
Showing 10 out of 100 products:
Human Monoclonal ATP7A Primary Antibody for IP, IHC - ABIN1027714
Samimi, Varki, Wilczynski, Safaei, Alberts, Howell: Increase in expression of the copper transporter ATP7A during platinum drug-based treatment is associated with poor survival in ovarian cancer patients. in Clinical cancer research : an official journal of the American Association for Cancer Research 2003
Show all 6 references for ABIN1027714
Mouse (Murine) Polyclonal ATP7A Primary Antibody for IHC (fro), IF - ABIN1105467
Steveson, Ciccotosto, Ma, Mueller, Mains, Eipper: Menkes protein contributes to the function of peptidylglycine alpha-amidating monooxygenase. in Endocrinology 2002
Dog (Canine) Polyclonal ATP7A Primary Antibody for WB - ABIN2778126
Zhang, Lü, Wang, Zou: A novel deletion mutation of ATP7A gene in a Chinese family with Menkes disease. in Chinese medical journal 2008
A hierarchic gene expression of copper homeostatic genes was demonstrated between atp7a, sp1 (show SP1 Antibodies) and sod1 (show SOD1 Antibodies) in zebrafish.
The investigators interrogated a genetic screen for embryos phenocopied by copper deficiency, identifying calamity, a mutant defective in the zebrafish ortholog of the Menkes disease gene (atp7a).
Cu chaperone function of Atox1 (show ATOX1 Antibodies) mediated through Cu transporter ATP7A is required for VEGF (show VEGFA Antibodies)-induced angiogenesis via activation of Cu enzyme lysyl oxidase (show LOX Antibodies).
Upon neuronal differentiation, transitions in redox states upregulates expression of ATOX1 (show ATOX1 Antibodies) and its partner ATP7A, producing higher flux of copper through the secretory pathway.
CTR1 (show SLC31A1 Antibodies), ATP7A, and lysyl oxidase (show LOX Antibodies) were upregulated in the lung tissues and pulmonary arteries of mice with hypoxia-induced pulmonary hypertension and pulmonary arterial smooth muscle cells.
A total of 11 different ATP7A mutations were identified in the 11 Korean families tested: 3 frameshift, 2 nonsense, 3 large deletions, 2 splice-site, and 1 missense mutation.
Data suggest that even small amounts of functional ATP7A in subjects with genetic diseases associated with mutant ATP7A result in milder phenotypes; this includes Menkes disease, occipital horn syndrome, and X-linked distal motor neuropathy. [REVIEW]
we demonstrate here that (1) AP complexes 1 and 2 of the CCV traffic machinery physically interact with ATP7A.
Twenty-five novel mutations including duplications, missense, and splice site variants enable us to confirm the pathogenic role of ATP7A mutations in Menkes disease and occipital horn syndrome.
Depletion of CCC complex components leads to lack of copper-dependent movement of the copper transporter ATP7A from endosomes, resulting in intracellular copper accumulation and modest alterations in copper homeostasis in humans with CCDC22 (show CCDC22 Antibodies) mutations.
This is the first time the activation of pseudo-exons is demonstrated in the ATP7A gene, and it demonstrates the usefulness of RNA analysis, in terms of revealing disease-causing mutations in noncoding regions.
Normal male karyotypes without c.3914A>G mutation on ATP7A gene was showed. Postnatal genetic analysis and normal development confirmed the prenatal diagnosis.
study characterized the Mottled-dappled deletion in C3H101H carrier females
Results from experiments in mouse model of Menkes disease harboring ATP5a (show ATP5G1 Antibodies) mutation, show increase expression of SOD1 (show SOD1 Antibodies) and induction of HO-1 (show HMOX1 Antibodies) causing iron metabolism disruption and hemolysis due to copper deficiency.
The MPhi ATP7A selectively regulates LPS (show TLR4 Antibodies)-induced inflammatory mediators, in part, via modulation of cellular copper availability, whereas neocuproine generally inhibits the production of inflammatory mediators.
a decrease in ATP7A protein expression contributes to impaired SOD3 (show SOD3 Antibodies) activity, resulting in O2(*-) overproduction and endothelial dysfunction in blood vessels of type 1 diabetes mellitus.
ATP7A mutations leading to Menkes disease and occipital horn syndrome in human and animal models [Review]
These studies demonstrate the essential role of the Atp7a gene in mouse embryonic development and establish a powerful model for understanding the tissue-specific roles of ATP7A in copper metabolism and disease.
ATP7A-mediated copper homeostasis is important for the formation of pathogenic proteinase-resistant prion protein (show PRNP Antibodies)
In the present study we identified a G to C nucleotide exchange in exon 15 of the Atp7a gene in mosaic mutants, which resulted in an arginine to proline substitution in the highly conserved 6th transmembrane domain of the ATP7A protein.
This gene encodes a transmembrane protein that functions in copper transport across membranes. This protein is localized to the trans-Golgi network, where it is predicted to supply copper to copper-dependent enzymes in the secretory pathway. It relocalizes to the plasma membrane under conditions of elevated extracellular copper, and functions in the efflux of copper from cells. Mutations in this gene are associated with Menkes disease, X-linked cutis laxa, and occipital horn syndrome.
ATPase, Cu++ transporting, alpha polypeptide (Menkes syndrome)
, ATPase, Cu++ transporting, alpha polypeptide
, Menkes disease ATPase
, copper-transporting ATPase 1
, copper-transporting P-type ATPase
, copper-transporting ATPase
, ATPase protein
, Copper-transporting ATPase 1
, copper-transporting ATPase 1-like
, Cu++-transporting P-type ATPase
, Menkes disease-associated protein
, copper pump 1
, Menkes protein
, menkes disease-associated protein homolog
, copper transporting ATPase