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anti-Human ATP7A Antikörper:
anti-Mouse (Murine) ATP7A Antikörper:
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Mouse (Murine) Polyclonal ATP7A Primary Antibody für FACS, IHC (p) - ABIN2192174
Steveson, Ciccotosto, Ma, Mueller, Mains, Eipper: Menkes protein contributes to the function of peptidylglycine alpha-amidating monooxygenase. in Endocrinology 2002
Human Polyclonal ATP7A Primary Antibody für 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
Polyclonal ATP7A Primary Antibody für ELISA, WB - ABIN539740
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
A hierarchic gene expression of copper homeostatic genes was demonstrated between atp7a, sp1 and sod1 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).
In our review, we highlight the roles of ATP7A/7B in platinum drug resistance and cancer progression. We also discuss the possible mechanisms of platinum drug resistance mediated by ATP7A/7B and provide novel strategies for overcoming resistance. This review may be helpful for understanding the roles of ATP7A and ATP7B in platinum drug resistance
we demonstrated that the restoration/preservation of autophagic-lysosomal degradation in senescent MEFs following rapamycin treatment correlated with attenuation of copper accumulation in these cells despite a further decrease in Atp7a levels. This study for the first time establishes a link between Atp7a and the autophagic-lysosomal pathway, and a requirement for both to effect efficient copper export
the severity of MD correlate with cellular localization of ATP7A and support previous studies indicating that phosphorylation is crucial for the exit of ATP7A from TGN, while dephosphorylation is crucial for recycling back to TGN.
We determined in silico that all the mutations leading to the classical Menkes disease leave no residual activity of ATP7A including the apparently less severe in-frame deletions. Whereas milder forms of the disease are characterized by mutations that allow a limited residual activity of ATP7A, including the nonsense mutation observed.
Candidate RNAi screen revealed copper-transporting ATPase (ATP7A) as a target for inducing cisplatin sensitivity.
Mnk inhibition enhances apoptotic activity of cytarabine in acute myeloid leukemia cells
The authors conclude that the ATP7A interactome encompasses a novel Golgi-localized conserved oligomeric Golgi (COG) 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, CTR2, ATP7A, and ATP7B were genotyped in these patients.
The P-type copper ATPases ATP7A 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, 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 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 phosphorylation in AML cells and suppresses primitive leukemic progenitors from AML patients in vitro and in an AML xenograft model in vivo.
It has been demonstrated in ovarian cancer cells that cisplatin resistance and uptake correlates with reduced CTR1 and LRRC8A protein expression/activity and a concomitant upregulation in cisplatin exporting transporters (ATP7A, ATP7B), which implies that the resistant cells have a reduced ability to accumulate cisplatin and activate proapoptotic transporters for osmolytes.
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 mediated through Cu transporter ATP7A is required for VEGF-induced angiogenesis via activation of Cu enzyme lysyl oxidase.
Upon neuronal differentiation, transitions in redox states upregulates expression of ATOX1 and its partner ATP7A, producing higher flux of copper through the secretory pathway.
CTR1, ATP7A, and lysyl oxidase were upregulated in the lung tissues and pulmonary arteries of mice with hypoxia-induced pulmonary hypertension and pulmonary arterial smooth muscle cells.
A key copper homeostasis gene, Atp7a, undergoes dynamic changes in expression during myogenic differentiation.
Akt2 plays a critical role in ATP7A protein stabilization and translocation to plasma membrane in vascular smooth muscle cells, which contributes to full activation of vascular SOD3 that protects against endothelial dysfunction in T2DM.
Copper therapy reduces intravascular hemolysis and derepresses ferroportin in mice with mosaic mutation (Atp7a(mo-ms)): An implication for copper-mediated regulation of the Slc40a1 gene expression.
Copper homeostasis in the testes is closely controlled by copper-transporting ATPases ATP7A and ATP7B proteins.
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
study characterized the Mottled-dappled deletion in C3H101H carrier females
Results from experiments in mouse model of Menkes disease harboring ATP5a mutation, show increase expression of SOD1 and induction of HO-1 causing iron metabolism disruption and hemolysis due to copper deficiency.
The MPhi ATP7A selectively regulates LPS-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 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
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.
macrophage ATP7A is localized in the trans-Golgi apparatus, regulates intracellular copper levels, and mediates macrophage responses to a dermal wound
Mutations in ATP7A is associated with lethal infantile neurodegenerative disorder of copper metabolism
Clusterin and COMMD1 independently regulate degradation of the mammalian copper ATPases ATP7A and ATP7B.
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