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anti-Human ATP7A Antibodies:
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Human Polyclonal ATP7A Primary Antibody for IF (p), IHC (p) - ABIN731513
Wang, Zhu, Zhao, Wang: miR-133a enhances the sensitivity of Hep-2 cells and vincristine-resistant Hep-2v cells to cisplatin by downregulating ATP7B expression. in International journal of molecular medicine 2016
Human Polyclonal ATP7A Primary Antibody for ELISA - ABIN449703
Schlief, West, Craig, Holtzman, Gitlin: Role of the Menkes copper-transporting ATPase in NMDA receptor-mediated neuronal toxicity. in Proceedings of the National Academy of Sciences of the United States of America 2006
Mouse (Murine) Polyclonal ATP7A Primary Antibody for FACS, IHC (p) - ABIN2192174
Steveson, Ciccotosto, Ma, Mueller, Mains, Eipper: Menkes protein contributes to the function of peptidylglycine alpha-amidating monooxygenase. in Endocrinology 2002
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).
The authors conclude that the ATP7A interactome encompasses a novel Golgi-localized conserved oligomeric Golgi (COG (show TG Antibodies)) complex-dependent mechanism to specify neuronal development and survival.
Mutation in ATP7A gene is associated with X-linked distal hereditary motor neuropathy.
MNK orchestrates counterbalancing forces that regulate mTORC1 enzymatic activity.
11 single-nucleotide polymorphisms (SNPs) in CTR1 (show SLC31A1 Antibodies), CTR2 (show SLC31A2 Antibodies), ATP7A, and ATP7B (show ATP7B Antibodies) were genotyped in these patients.
The P-type copper ATPases ATP7A and ATP7B (show ATP7B Antibodies) 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 (show ATP7B Antibodies) and ATP7A, 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 (show ATP7B Antibodies) by copper-dependent changes in the dynamics and conformation of the MBD (show DPEP1 Antibodies) chain.
Deletion spanning exons 8 to 12 of the ATP7A gene is associated with a family affected with Menkes disease.
ATP-dependent copper transfer in ATP7A/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/B and are subjected to ATP-dependent vectorial displacement with a mechanism analogous to that of copper
studies show that merestinib effectively blocks eIF4E (show EIF4E Antibodies) phosphorylation in AML (show RUNX1 Antibodies) cells and suppresses primitive leukemic progenitors from AML (show RUNX1 Antibodies) patients in vitro and in an AML (show RUNX1 Antibodies) xenograft model in vivo.
It has been demonstrated in ovarian cancer cells that cisplatin resistance and uptake correlates with reduced CTR1 (show SLC31A1 Antibodies) and LRRC8A (show LRRC8A Antibodies) protein expression/activity and a concomitant upregulation in cisplatin exporting transporters (ATP7A, ATP7B (show ATP7B Antibodies)), which implies that the resistant cells have a reduced ability to accumulate cisplatin and activate proapoptotic transporters for osmolytes.
Atp7a(T985I/Y) mice have reduced Atp7a protein levels and recapitulate the defective trafficking and altered post-translational regulatory mechanisms observed in the human ATP7A(T994I) patient fibroblasts
Thus, ATP7A activity protects mitochondria from excessive copper entry, which is deleterious to redox buffers. Mitochondrial redox misbalance could significantly contribute to pathologies associated with ATP7A inactivation in tissues with paradoxical accumulation of copper
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).
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.
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.
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