PMID-sentid	Pub_year	Sent_text	comp_official_name	comp_offset	protein_name	organism	prot_offset
33894639-2	2021	Here we describe a family with OHS caused by a novel mutation in the ATP7A gene, including a patient with a comorbid dHMN that worsened markedly after being treated with copper histidinate.	Copper Histidine	170-188	ATPase copper transporting alpha	Homo sapiens	69-74
33894639-10	2021	The copper-induced toxicity and low levels of both ATP7A and ATP7B in our patient suggest that copper accumulation in motor neurons is the pathogenic mechanism in ATP7A-related dHMN.	Copper	4-10	ATPase copper transporting alpha	Homo sapiens	163-168
33894639-10	2021	The copper-induced toxicity and low levels of both ATP7A and ATP7B in our patient suggest that copper accumulation in motor neurons is the pathogenic mechanism in ATP7A-related dHMN.	Copper	95-101	ATPase copper transporting alpha	Homo sapiens	51-56
33894639-10	2021	The copper-induced toxicity and low levels of both ATP7A and ATP7B in our patient suggest that copper accumulation in motor neurons is the pathogenic mechanism in ATP7A-related dHMN.	Copper	95-101	ATPase copper transporting alpha	Homo sapiens	163-168
34058339-4	2021	In this review, an updated view of the current literature regarding the intracellular transport and processing of cisplatin will be presented, with special emphasis on the plasma membrane copper permease CTR1, the Cu-transporting ATPases, ATP7A and ATP7B, located in the trans-Golgi network, and the soluble copper chaperone ATOX1.	Cisplatin	114-123	ATPase copper transporting alpha	Homo sapiens	239-244
33482423-2	2021	Several inherited copper storage diseases are described of which Wilson disease (copper overload, mutations in ATP7B gene) and Menkes disease (copper deficiency, mutations in ATP7A gene) are the most prominent ones.	Copper	18-24	ATPase copper transporting alpha	Homo sapiens	175-180
33917579-2	2021	The copper pump, ATP7A is critical for whole-body, cellular, and subcellular copper homeostasis, and dysfunction due to genetic defects results in Menkes disease.	Copper	4-10	ATPase copper transporting alpha	Homo sapiens	17-22
33890175-2	2021	Downregulated dysbindin-1 expression is associated with lower expression of copper transporters ATP7A and CTR1, required for copper transport to the central nervous system.	Copper	76-82	ATPase copper transporting alpha	Homo sapiens	96-101
33890175-2	2021	Downregulated dysbindin-1 expression is associated with lower expression of copper transporters ATP7A and CTR1, required for copper transport to the central nervous system.	Copper	125-131	ATPase copper transporting alpha	Homo sapiens	96-101
20301586-0	1993	ATP7A-Related Copper Transport Disorders CLINICAL DESCRIPTION: Menkes disease, occipital horn syndrome (OHS), and ATP7A-related distal motor neuropathy (DMN) are disorders of copper transport caused by pathogenic variants in ATP7A (encoding a copper-transporting ATPase).	Copper	14-20	ATPase copper transporting alpha	Homo sapiens	0-5
20301586-0	1993	ATP7A-Related Copper Transport Disorders CLINICAL DESCRIPTION: Menkes disease, occipital horn syndrome (OHS), and ATP7A-related distal motor neuropathy (DMN) are disorders of copper transport caused by pathogenic variants in ATP7A (encoding a copper-transporting ATPase).	Copper	14-20	ATPase copper transporting alpha	Homo sapiens	114-119
20301586-0	1993	ATP7A-Related Copper Transport Disorders CLINICAL DESCRIPTION: Menkes disease, occipital horn syndrome (OHS), and ATP7A-related distal motor neuropathy (DMN) are disorders of copper transport caused by pathogenic variants in ATP7A (encoding a copper-transporting ATPase).	Copper	14-20	ATPase copper transporting alpha	Homo sapiens	114-119
33175605-4	2021	We also show that GLUT4 is retained in an element/domain of the TGN from which newly synthesized lysosomal proteins are targeted to the late endosomes and the ATP7A copper transporter is translocated to the PM by elevated copper.	Copper	165-171	ATPase copper transporting alpha	Homo sapiens	159-164
33175605-4	2021	We also show that GLUT4 is retained in an element/domain of the TGN from which newly synthesized lysosomal proteins are targeted to the late endosomes and the ATP7A copper transporter is translocated to the PM by elevated copper.	Copper	222-228	ATPase copper transporting alpha	Homo sapiens	159-164
33359068-8	2021	Suppression of MGP may reverse OXA resistance by upregulating copper transporter 1 (CTR1) and downregulating ATP7A and ATP7B.	Oxaliplatin	31-34	ATPase copper transporting alpha	Homo sapiens	109-114
33441033-4	2021	The pyridone-aminal scaffold has been utilized to generate several series of Mnk inhibitors presented in multiple patent applications and research articles.	pyridone-aminal	4-19	ATPase copper transporting alpha	Homo sapiens	77-80
33441033-7	2021	The present compilation provides a succinct review of the current state of development of pyridone-aminal-derived Mnk inhibitors through the analysis of relevant patent applications filed in the last 5 years.	pyridone-aminal	90-105	ATPase copper transporting alpha	Homo sapiens	114-117
33146201-5	2020	Here we found that expression of the Cu transporter genes ATP7A, ATP7B, SLC31A1, and SLC31A2 was significantly altered in liver cancer samples and were associated with elevated Cu levels in liver cancer tissue and cells.	Copper	37-39	ATPase copper transporting alpha	Homo sapiens	58-63
32818544-6	2020	BEZ235 declined IC50 of HCT116/L-OHP cells to L-OHP, decreased the expressions of ABCB1, ABCC1, ABCG2, ATP7A, ATP7B, MATE1, p-gp, MRP1 and BCRP, induced cell apoptosis, reduced cell proliferation, and arrested cells at G0/G1, which was reversed by GOLPH3 overexpression.	dactolisib	0-6	ATPase copper transporting alpha	Homo sapiens	103-108
33680921-8	2020	PTX treatment also decreased p65 phosphorylation, increased Pt levels, depleted GSH, and downregulated the expression of the ATP7A, ATP7B, GSR, and MGST1 genes.	Pentoxifylline	0-3	ATPase copper transporting alpha	Homo sapiens	125-130
32427278-3	2020	The main function of the enzyme ATPase copper-transporting alpha (ATP7A) is to transport copper across the membrane in order to retain copper homeostasis, which is closely associated with the onset of mental disorders and cognitive impairment.	Copper	39-45	ATPase copper transporting alpha	Homo sapiens	66-71
32427278-3	2020	The main function of the enzyme ATPase copper-transporting alpha (ATP7A) is to transport copper across the membrane in order to retain copper homeostasis, which is closely associated with the onset of mental disorders and cognitive impairment.	Copper	89-95	ATPase copper transporting alpha	Homo sapiens	32-64
32427278-3	2020	The main function of the enzyme ATPase copper-transporting alpha (ATP7A) is to transport copper across the membrane in order to retain copper homeostasis, which is closely associated with the onset of mental disorders and cognitive impairment.	Copper	89-95	ATPase copper transporting alpha	Homo sapiens	66-71
32427278-10	2020	In addition, negative correlations were noted between the decline in mRNA expression levels of ATP7A and the increased Cho/Cr ratios of the left PWM, right PWM and right ACC in MDD patients.	Choline	119-122	ATPase copper transporting alpha	Homo sapiens	95-100
32427278-10	2020	In addition, negative correlations were noted between the decline in mRNA expression levels of ATP7A and the increased Cho/Cr ratios of the left PWM, right PWM and right ACC in MDD patients.	Creatine	123-125	ATPase copper transporting alpha	Homo sapiens	95-100
33142854-2	2020	The variation of hepatic copper levels in Labrador retrievers has been partly explained by mutations in ATP7A c.980C>T and ATP7B c.4358G>A.	Copper	25-31	ATPase copper transporting alpha	Homo sapiens	104-109
32506322-5	2020	After incorporation, cuprous ions are delivered to ATP7A, which pumps Cu+ from enterocytes into the blood.	Copper	70-73	ATPase copper transporting alpha	Homo sapiens	51-56
32967084-0	2020	Design, Synthesis and Bioactivity Evaluation of 4,6-Disubstituted Pyrido[3,2-d]pyrimidine Derivatives as Mnk and HDAC Inhibitors.	4,6-disubstituted	48-65	ATPase copper transporting alpha	Homo sapiens	105-108
32967084-0	2020	Design, Synthesis and Bioactivity Evaluation of 4,6-Disubstituted Pyrido[3,2-d]pyrimidine Derivatives as Mnk and HDAC Inhibitors.	pyrido(3,2-d)pyrimidine	66-89	ATPase copper transporting alpha	Homo sapiens	105-108
32967084-3	2020	Based on the previous work and the merge pharmacophore method; we designed and synthesized a series of 4,6-disubstituted pyrido[3,2-d]pyrimidine derivatives as HDAC and Mnk dual inhibitors.	4,6-disubstituted	103-120	ATPase copper transporting alpha	Homo sapiens	169-172
32967084-3	2020	Based on the previous work and the merge pharmacophore method; we designed and synthesized a series of 4,6-disubstituted pyrido[3,2-d]pyrimidine derivatives as HDAC and Mnk dual inhibitors.	pyrido(3,2-d)pyrimidine	121-144	ATPase copper transporting alpha	Homo sapiens	169-172
32967084-6	2020	Docking study revealed that the pyrido[3,2-d]pyrimidine framework and hydroxamic acid motif of compound A12 were essential for maintaining the activity of HDAC and Mnk.	pyrido(3,2-d)pyrimidine	32-55	ATPase copper transporting alpha	Homo sapiens	164-167
32967084-6	2020	Docking study revealed that the pyrido[3,2-d]pyrimidine framework and hydroxamic acid motif of compound A12 were essential for maintaining the activity of HDAC and Mnk.	Hydroxamic Acids	70-85	ATPase copper transporting alpha	Homo sapiens	164-167
32967084-7	2020	These result indicated that A12 was a potent Mnk /HDAC inhibitor and will be further researched.	compound A 12	28-31	ATPase copper transporting alpha	Homo sapiens	45-48
32828276-0	2020	Preclinical evidence that MNK/eIF4E inhibition by cercosporamide enhances the response to antiangiogenic TKI and mTOR inhibitor in renal cell carcinoma.	cercosporamide	50-64	ATPase copper transporting alpha	Homo sapiens	26-29
32828276-2	2020	In this study, we investigated the anti-RCC potential of a unique Mnk inhibitor cercosporamide.	cercosporamide	80-94	ATPase copper transporting alpha	Homo sapiens	66-69
32843536-3	2020	Cellular copper homeostasis is regulated primarily by two transporters: the copper influx transporter copper transporter 1 (CTR1; also known as SLC31A1), which controls the uptake of copper, and the copper-extruding ATPase ATP7A, a recognised retromer cargo.	Copper	9-15	ATPase copper transporting alpha	Homo sapiens	223-228
32994893-1	2020	ATP7A is a critical copper transporter involved in Menkes Disease, Occipital horn Syndrome and X-linked distal spinal muscular atrophy type 3 which are X linked genetic disorders.	Copper	20-26	ATPase copper transporting alpha	Homo sapiens	0-5
32570116-0	2020	The contribution of copper efflux transporters ATP7A and ATP7B to chemoresistance and personalized medicine in ovarian cancer.	Copper	20-26	ATPase copper transporting alpha	Homo sapiens	47-52
32570116-4	2020	Recent studies suggest that the copper efflux transporters ATP7A and ATP7B play an important role in platinum resistance.	Platinum	101-109	ATPase copper transporting alpha	Homo sapiens	59-64
32570116-7	2020	It then presents clinical studies showing a significant association of ATP7A and ATP7B with response to cisplatin/carboplatin and prognosis.	Cisplatin	104-113	ATPase copper transporting alpha	Homo sapiens	71-76
32570116-7	2020	It then presents clinical studies showing a significant association of ATP7A and ATP7B with response to cisplatin/carboplatin and prognosis.	Carboplatin	114-125	ATPase copper transporting alpha	Homo sapiens	71-76
32437713-14	2020	The luciferase assay findings showed that miR-30a-3p binds to ERCC1 and ATP7A which are the key regulators for DNA repair and cisplatin transportation.	Cisplatin	126-135	ATPase copper transporting alpha	Homo sapiens	72-77
32053088-1	2020	Sialuria is a rare inborn error of metabolism caused by excessive synthesis of sialic acid due to the mutation in the binding site of the cytidine monophosphate-sialic acid of UDP-GlcNAc 2-epimerase/ManNAc kinase (GNE/MNK).	Sialic Acids	79-90	ATPase copper transporting alpha	Homo sapiens	218-221
32278528-1	2020	Copper (Cu) is an essential element regulated by four genes (hCTR1, hATOX1, hATP7A, and hATP7B in humans and zctr1, zatox1, zatp7a, and zatp7b in zebrafish) in copper uptake, distribution, and transport in animal cells.	Copper	0-6	ATPase copper transporting alpha	Homo sapiens	76-82
32278528-1	2020	Copper (Cu) is an essential element regulated by four genes (hCTR1, hATOX1, hATP7A, and hATP7B in humans and zctr1, zatox1, zatp7a, and zatp7b in zebrafish) in copper uptake, distribution, and transport in animal cells.	Copper	8-10	ATPase copper transporting alpha	Homo sapiens	76-82
32709883-4	2020	Cell surface-based loss-of-function screens reveal that ATP7A, a copper-exporter upregulated by mutant KRAS, is essential for neoplastic growth.	Copper	65-71	ATPase copper transporting alpha	Homo sapiens	56-61
32709883-5	2020	ATP7A is upregulated at the surface of KRAS-mutated CRC, and protects cells from excess copper-ion toxicity.	Copper	88-94	ATPase copper transporting alpha	Homo sapiens	0-5
32315022-12	2020	Moreover, Cu/NaHS markedly suppressed the level of the Cu exporter ATP7A, but not ATP7B, protein, whereas the combination did not affect that of the Cu importer CTR1 protein.	Copper	10-12	ATPase copper transporting alpha	Homo sapiens	67-72
32315022-12	2020	Moreover, Cu/NaHS markedly suppressed the level of the Cu exporter ATP7A, but not ATP7B, protein, whereas the combination did not affect that of the Cu importer CTR1 protein.	sodium bisulfide	13-17	ATPase copper transporting alpha	Homo sapiens	67-72
32315022-12	2020	Moreover, Cu/NaHS markedly suppressed the level of the Cu exporter ATP7A, but not ATP7B, protein, whereas the combination did not affect that of the Cu importer CTR1 protein.	Copper	55-57	ATPase copper transporting alpha	Homo sapiens	67-72
32315022-12	2020	Moreover, Cu/NaHS markedly suppressed the level of the Cu exporter ATP7A, but not ATP7B, protein, whereas the combination did not affect that of the Cu importer CTR1 protein.	Copper	55-57	ATPase copper transporting alpha	Homo sapiens	67-72
32315022-13	2020	Taken together, we conclude that the marked decrease in the ATP7A protein level by Cu/NaHS promotes intracellular Cu accumulation and leads to increased Cu cytotoxicity.	Copper	83-85	ATPase copper transporting alpha	Homo sapiens	60-65
32315022-13	2020	Taken together, we conclude that the marked decrease in the ATP7A protein level by Cu/NaHS promotes intracellular Cu accumulation and leads to increased Cu cytotoxicity.	sodium bisulfide	86-90	ATPase copper transporting alpha	Homo sapiens	60-65
32315022-13	2020	Taken together, we conclude that the marked decrease in the ATP7A protein level by Cu/NaHS promotes intracellular Cu accumulation and leads to increased Cu cytotoxicity.	Copper	114-116	ATPase copper transporting alpha	Homo sapiens	60-65
32315022-13	2020	Taken together, we conclude that the marked decrease in the ATP7A protein level by Cu/NaHS promotes intracellular Cu accumulation and leads to increased Cu cytotoxicity.	Copper	114-116	ATPase copper transporting alpha	Homo sapiens	60-65
32398691-2	2020	Elevated expression of the ATP7A Cu exporter is known to confer copper tolerance, however, the contribution of metal-binding metallothioneins is less clear.	Copper	64-70	ATPase copper transporting alpha	Homo sapiens	27-32
32398691-4	2020	Although the loss of ATP7A increased sensitivity to low Cu concentrations, the absence of MTs did not significantly affect Cu tolerance.	Copper	56-58	ATPase copper transporting alpha	Homo sapiens	21-26
32398691-6	2020	A lack of MTs resulted in the trafficking of ATP7A from the trans-Golgi complex in a Cu-dependent manner, suggesting that MTs regulate the delivery of Cu to ATP7A.	Copper	85-87	ATPase copper transporting alpha	Homo sapiens	45-50
32398691-6	2020	A lack of MTs resulted in the trafficking of ATP7A from the trans-Golgi complex in a Cu-dependent manner, suggesting that MTs regulate the delivery of Cu to ATP7A.	Copper	85-87	ATPase copper transporting alpha	Homo sapiens	157-162
32398691-6	2020	A lack of MTs resulted in the trafficking of ATP7A from the trans-Golgi complex in a Cu-dependent manner, suggesting that MTs regulate the delivery of Cu to ATP7A.	Copper	151-153	ATPase copper transporting alpha	Homo sapiens	45-50
32398691-6	2020	A lack of MTs resulted in the trafficking of ATP7A from the trans-Golgi complex in a Cu-dependent manner, suggesting that MTs regulate the delivery of Cu to ATP7A.	Copper	151-153	ATPase copper transporting alpha	Homo sapiens	157-162
32398691-7	2020	Under Cu deficiency conditions, the absence of MTs and / or ATP7A enhanced cell proliferation compared to wild type cells, suggesting that these proteins compete with essential Cu-dependent pathways when Cu is scarce.	Copper	6-8	ATPase copper transporting alpha	Homo sapiens	60-65
32398691-7	2020	Under Cu deficiency conditions, the absence of MTs and / or ATP7A enhanced cell proliferation compared to wild type cells, suggesting that these proteins compete with essential Cu-dependent pathways when Cu is scarce.	Copper	177-179	ATPase copper transporting alpha	Homo sapiens	60-65
31932435-6	2020	Because silencing of the copper transporter ATP7A also reduced cell migration, these proteins appear to be on the same pathway, suggesting that their well-known copper transport activity is involved.	Copper	25-31	ATPase copper transporting alpha	Homo sapiens	44-49
31932435-6	2020	Because silencing of the copper transporter ATP7A also reduced cell migration, these proteins appear to be on the same pathway, suggesting that their well-known copper transport activity is involved.	Copper	161-167	ATPase copper transporting alpha	Homo sapiens	44-49
31932435-7	2020	In-cell proximity ligation assays demonstrated that Atox1, ATP7A, and the proenzyme of lysyl oxidase (LOX; copper-loaded via ATP7A) are all in close proximity and that LOX activity is reduced upon Atox1 silencing in the cells.	Copper	107-113	ATPase copper transporting alpha	Homo sapiens	125-130
31932435-8	2020	Since LOX is an established player in cancer cell migration, our results imply that Atox1 mediates breast cancer cell migration via coordinated copper transport in the ATP7A-LOX axis.	Copper	144-150	ATPase copper transporting alpha	Homo sapiens	168-173
31969342-1	2020	ATP7A encodes a copper-transporting P-type ATPase and is one of 23 genes in which mutations produce distal hereditary motor neuropathy (dHMN), a group of diseases characterized by length-dependent axonal degeneration of motor neurons.	Copper	16-22	ATPase copper transporting alpha	Homo sapiens	0-5
31921404-0	2020	TSC patient-derived isogenic neural progenitor cells reveal altered early neurodevelopmental phenotypes and rapamycin-induced MNK-eIF4E signaling.	Sirolimus	108-117	ATPase copper transporting alpha	Homo sapiens	126-129
31921404-12	2020	Our data showing upregulation of these signaling pathways by rapamycin support a strategy to combine a MEK or a MNK inhibitor with rapamycin that may be superior for TSC-associated CNS defects.	Sirolimus	61-70	ATPase copper transporting alpha	Homo sapiens	112-115
32508020-7	2020	RESULTS: In this current study, we identified knocking-down ATP7A could enhance cytotoxicity treatment of cisplatin in breast cancer cells.	Cisplatin	106-115	ATPase copper transporting alpha	Homo sapiens	60-65
32396355-1	2020	Atox1 is a human copper metallochaperone that is responsible for transferring copper ions from the main human copper transporter, hCtr1, to ATP7A/B in the Golgi apparatus.	Copper	17-23	ATPase copper transporting alpha	Homo sapiens	140-147
32396355-1	2020	Atox1 is a human copper metallochaperone that is responsible for transferring copper ions from the main human copper transporter, hCtr1, to ATP7A/B in the Golgi apparatus.	Copper	78-84	ATPase copper transporting alpha	Homo sapiens	140-147
32396355-1	2020	Atox1 is a human copper metallochaperone that is responsible for transferring copper ions from the main human copper transporter, hCtr1, to ATP7A/B in the Golgi apparatus.	Copper	78-84	ATPase copper transporting alpha	Homo sapiens	140-147
32006874-6	2020	METHODS: We studied the expression of copper transporters CTR1, ATP7A and ATP7B which are presumably involved in the uptake, cellular transport and efflux of platinum compounds by immunofluorescence microscopy and flow-cytometry.	Copper	38-44	ATPase copper transporting alpha	Homo sapiens	64-69
32006874-6	2020	METHODS: We studied the expression of copper transporters CTR1, ATP7A and ATP7B which are presumably involved in the uptake, cellular transport and efflux of platinum compounds by immunofluorescence microscopy and flow-cytometry.	Platinum	158-166	ATPase copper transporting alpha	Homo sapiens	64-69
32508020-11	2020	CONCLUSIONS: Our results highlight that inhibition of ATP7A is a potential strategy for targeting breast cancer resistant to cisplatin, and we provided an interesting method to compare the involvement of various genes in the assessment of cisplatin resistance.	Cisplatin	125-134	ATPase copper transporting alpha	Homo sapiens	54-59
32508020-11	2020	CONCLUSIONS: Our results highlight that inhibition of ATP7A is a potential strategy for targeting breast cancer resistant to cisplatin, and we provided an interesting method to compare the involvement of various genes in the assessment of cisplatin resistance.	Cisplatin	239-248	ATPase copper transporting alpha	Homo sapiens	54-59
32053088-1	2020	Sialuria is a rare inborn error of metabolism caused by excessive synthesis of sialic acid due to the mutation in the binding site of the cytidine monophosphate-sialic acid of UDP-GlcNAc 2-epimerase/ManNAc kinase (GNE/MNK).	Cytidine Monophosphate	138-172	ATPase copper transporting alpha	Homo sapiens	218-221
32053088-1	2020	Sialuria is a rare inborn error of metabolism caused by excessive synthesis of sialic acid due to the mutation in the binding site of the cytidine monophosphate-sialic acid of UDP-GlcNAc 2-epimerase/ManNAc kinase (GNE/MNK).	Uridine Diphosphate	176-179	ATPase copper transporting alpha	Homo sapiens	218-221
32053088-1	2020	Sialuria is a rare inborn error of metabolism caused by excessive synthesis of sialic acid due to the mutation in the binding site of the cytidine monophosphate-sialic acid of UDP-GlcNAc 2-epimerase/ManNAc kinase (GNE/MNK).	2-acetamido-2-deoxy-4-O-(beta-2-acetamid-2-deoxyglucopyranosyl)glucopyranose	180-186	ATPase copper transporting alpha	Homo sapiens	218-221
30230404-5	2020	We characterised specific protein domains of copper transporters ATP7A, CTR1, ATP7B and dysbindin isoforms 1 A and 1B/C in SZP (n = 15) and matched controls (n = 11), and SN copper content in SZP (n = 14) and matched controls (n = 11).	Copper	45-51	ATPase copper transporting alpha	Homo sapiens	65-70
32435310-1	2020	Background: Menkes disease is an X-linked neurodegenerative disease caused by mutation in ATP7A gene, which codes for copper-transporting ATPase.	Copper	118-124	ATPase copper transporting alpha	Homo sapiens	90-95
31558336-8	2019	Mutations in the ATP7A gene, encoding for a copper-transporting ATPase, have been associated with the severe infantile neurodegenerative Menkes disease and in its milder variant, the Occipital Horn Syndrome.	Copper	44-50	ATPase copper transporting alpha	Homo sapiens	17-22
31553923-4	2019	The results showed that Cu2+ supplemented directly into the culture medium or released from Cu-Hier-Ti surface could polarize macrophages to pro-inflammatory M1 phenotype by activating Cu-transport signaling (copper transporter 1 (CTR1) and ATP7A) in macrophages, while the material characteristics exhibited anti-inflammatory effect to some extent by regulating integrin (alpha5, alphaM, beta1 and beta2) and TLR (TLR-3, TLR-4, Myd88 and Ticam-1/2) signaling.	Copper	24-28	ATPase copper transporting alpha	Homo sapiens	241-246
31553923-4	2019	The results showed that Cu2+ supplemented directly into the culture medium or released from Cu-Hier-Ti surface could polarize macrophages to pro-inflammatory M1 phenotype by activating Cu-transport signaling (copper transporter 1 (CTR1) and ATP7A) in macrophages, while the material characteristics exhibited anti-inflammatory effect to some extent by regulating integrin (alpha5, alphaM, beta1 and beta2) and TLR (TLR-3, TLR-4, Myd88 and Ticam-1/2) signaling.	Copper	24-26	ATPase copper transporting alpha	Homo sapiens	241-246
31553923-4	2019	The results showed that Cu2+ supplemented directly into the culture medium or released from Cu-Hier-Ti surface could polarize macrophages to pro-inflammatory M1 phenotype by activating Cu-transport signaling (copper transporter 1 (CTR1) and ATP7A) in macrophages, while the material characteristics exhibited anti-inflammatory effect to some extent by regulating integrin (alpha5, alphaM, beta1 and beta2) and TLR (TLR-3, TLR-4, Myd88 and Ticam-1/2) signaling.	Titanium	100-102	ATPase copper transporting alpha	Homo sapiens	241-246
31630791-5	2019	Functional characterization of fibroblasts derived from affected individuals closely resembles the abnormal ATP7A trafficking described in MEDNIK syndrome both at baseline and in response to copper treatment.	Copper	191-197	ATPase copper transporting alpha	Homo sapiens	108-113
31684984-10	2019	FL3 induced apoptosis of DLBCL cell lines that was associated with inhibition of the ERK-MNK-eIF4E signaling pathway, including aggressive double/triple-hit DLBCL cell lines.	fl3	0-3	ATPase copper transporting alpha	Homo sapiens	89-92
31601252-2	2019	Previously we reported that treatment of Mnk inhibitor CGP57380 resulted in decreased Mcl-1 expression while increased c-PARP expression in non-small cell lung cancer (NSCLC) cells.	CGP 57380	55-63	ATPase copper transporting alpha	Homo sapiens	41-44
31673101-5	2019	Co-administration of DSF with GC affected cellular localisation of a cisplatin efflux transporter ATP7A, increased DNA-platinum adducts and promoted apoptosis.	Disulfiram	21-24	ATPase copper transporting alpha	Homo sapiens	98-103
31673101-5	2019	Co-administration of DSF with GC affected cellular localisation of a cisplatin efflux transporter ATP7A, increased DNA-platinum adducts and promoted apoptosis.	Cisplatin	69-78	ATPase copper transporting alpha	Homo sapiens	98-103
31176065-2	2019	This review provides a compendium of current knowledge regarding the mechanism of copper transfer from the blood system to the Golgi apparatus; this mechanism involves the copper transporter hCtr1, the metallochaperone Atox1, and the ATPases ATP7A/B.	Copper	82-88	ATPase copper transporting alpha	Homo sapiens	242-249
31327462-6	2019	We found that eIF4E phosphorylation was upregulated in cervical cancer cells and tissues but not normal cervical counterparts, and its phosphorylation at Ser 209 activates Wnt/beta-catenin signaling, promotes growth and migration in cervical cancer, in an MNK-dependent manner.	Serine	154-157	ATPase copper transporting alpha	Homo sapiens	256-259
31540259-2	2019	One of these is the maintenance of copper (Cu) homeostasis operated by the Golgi-localized Cu-transporting ATPases ATP7A and ATP7B.	Copper	35-41	ATPase copper transporting alpha	Homo sapiens	115-120
31540259-2	2019	One of these is the maintenance of copper (Cu) homeostasis operated by the Golgi-localized Cu-transporting ATPases ATP7A and ATP7B.	Copper	43-45	ATPase copper transporting alpha	Homo sapiens	115-120
31540259-4	2019	However, in response to elevated Cu, the Golgi exports ATP7A/B to post-Golgi sites where they promote sequestration and efflux of excess Cu to limit its potential toxicity.	Copper	33-35	ATPase copper transporting alpha	Homo sapiens	55-60
31540259-4	2019	However, in response to elevated Cu, the Golgi exports ATP7A/B to post-Golgi sites where they promote sequestration and efflux of excess Cu to limit its potential toxicity.	Copper	137-139	ATPase copper transporting alpha	Homo sapiens	55-60
31540259-5	2019	Growing tumors actively consume Cu and employ ATP7A/B to regulate the availability of this metal for oncogenic enzymes such as LOX and LOX-like proteins, which confer higher invasiveness to malignant cells.	Metals	91-96	ATPase copper transporting alpha	Homo sapiens	46-51
31540259-6	2019	Furthermore, ATP7A/B activity and trafficking allow tumor cells to detoxify platinum (Pt)-based drugs (like cisplatin), which are used for the chemotherapy of different solid tumors.	Platinum	76-84	ATPase copper transporting alpha	Homo sapiens	13-18
31540259-6	2019	Furthermore, ATP7A/B activity and trafficking allow tumor cells to detoxify platinum (Pt)-based drugs (like cisplatin), which are used for the chemotherapy of different solid tumors.	Platinum	86-88	ATPase copper transporting alpha	Homo sapiens	13-18
31540259-6	2019	Furthermore, ATP7A/B activity and trafficking allow tumor cells to detoxify platinum (Pt)-based drugs (like cisplatin), which are used for the chemotherapy of different solid tumors.	Cisplatin	108-117	ATPase copper transporting alpha	Homo sapiens	13-18
31327462-9	2019	The combination of MNK kinase inhibitor with paclitaxel achieved greater efficacy in cervical cancer cells than paclitaxel alone.	Paclitaxel	112-122	ATPase copper transporting alpha	Homo sapiens	19-22
31934199-1	2019	OBJECTIVE: This study investigated the expression of P-type copper transporting adenosine triphosphatase ATP7A in the tumor tissues of patients with advanced esophageal squamous cell carcinoma (ESCC), and analyzed its correlation to clinicopathologic features and prognosis of advanced ESCC patients.	Copper	60-66	ATPase copper transporting alpha	Homo sapiens	105-110
31934199-1	2019	OBJECTIVE: This study investigated the expression of P-type copper transporting adenosine triphosphatase ATP7A in the tumor tissues of patients with advanced esophageal squamous cell carcinoma (ESCC), and analyzed its correlation to clinicopathologic features and prognosis of advanced ESCC patients.	Adenosine	80-89	ATPase copper transporting alpha	Homo sapiens	105-110
31934199-2	2019	METHODS: The expression of ATP7A protein in 49 specimens of advanced ESCC patients who were treated with first line cisplatin-based chemotherapy without surgery or radiotherapy, was detected by immunohistochemistry.	Cisplatin	116-125	ATPase copper transporting alpha	Homo sapiens	27-32
31934199-5	2019	ATP7A expression status was correlated with response to histologic grade and cisplatin-based chemotherapy (P values 0.02, 0.028 respectively).	Cisplatin	77-86	ATPase copper transporting alpha	Homo sapiens	0-5
31934199-10	2019	The expression level of ATP7A was an important factor affecting tumor tissue"s histologic grade, the response to platinum-based chemotherapy and the prognosis of advanced ESCC patients.	Platinum	113-121	ATPase copper transporting alpha	Homo sapiens	24-29
31934199-11	2019	This indicates that ATP7A might be involved in the genesis and development of ESCC, and could be a resistance marker for platinum-based chemotherapy, and a prognostic factor for survival in patients with ESCC treated by Pt-based chemotherapy.	Platinum	121-129	ATPase copper transporting alpha	Homo sapiens	20-25
31934199-11	2019	This indicates that ATP7A might be involved in the genesis and development of ESCC, and could be a resistance marker for platinum-based chemotherapy, and a prognostic factor for survival in patients with ESCC treated by Pt-based chemotherapy.	Platinum	220-222	ATPase copper transporting alpha	Homo sapiens	20-25
31283225-2	2019	In humans, the Cu chaperone Atox1 mediates Cu(I) delivery to P-type ATPases Atp7a and Atp7b (the Menkes and Wilson disease proteins, respectively), which are responsible for Cu release to the secretory pathway and excess Cu efflux.	Copper	15-17	ATPase copper transporting alpha	Homo sapiens	76-81
30928671-3	2019	The P-type ATPase transporters, ATP7A and ATP7B, regulate cytoplasmic copper by pumping copper out of cells or into the endomembrane system.	Copper	70-76	ATPase copper transporting alpha	Homo sapiens	32-37
30928671-3	2019	The P-type ATPase transporters, ATP7A and ATP7B, regulate cytoplasmic copper by pumping copper out of cells or into the endomembrane system.	Copper	88-94	ATPase copper transporting alpha	Homo sapiens	32-37
31283225-6	2019	We show that cisplatin and an oxaliplatin analogue can specifically bind to the heterodimeric complex Atox1-Cu(I)-Mnk1 (Mnk1 is the first soluble domain of Atp7a), thus leading to a kinetically stable adduct that has been structurally characterized by solution NMR and X-ray crystallography.	Cisplatin	13-22	ATPase copper transporting alpha	Homo sapiens	156-161
31283225-2	2019	In humans, the Cu chaperone Atox1 mediates Cu(I) delivery to P-type ATPases Atp7a and Atp7b (the Menkes and Wilson disease proteins, respectively), which are responsible for Cu release to the secretory pathway and excess Cu efflux.	Copper	43-45	ATPase copper transporting alpha	Homo sapiens	76-81
30569866-10	2019	CONCLUSION: This work proposes that exploration of the structural diversity in the context of Nphenyl- 4-(1H-pyrrol-3-yl)pyrimidin-2-amine would offer potent and selective Mnk inhibitors.	nphenyl- 4-(1h-pyrrol-3-yl)pyrimidin-2-amine	94-138	ATPase copper transporting alpha	Homo sapiens	172-175
31283225-6	2019	We show that cisplatin and an oxaliplatin analogue can specifically bind to the heterodimeric complex Atox1-Cu(I)-Mnk1 (Mnk1 is the first soluble domain of Atp7a), thus leading to a kinetically stable adduct that has been structurally characterized by solution NMR and X-ray crystallography.	Oxaliplatin	30-41	ATPase copper transporting alpha	Homo sapiens	156-161
31344863-4	2019	Cellular oxaliplatin accumulation and DNA-adduct formation were decreased and related to OCT1-3 and ATP7A expression.	Oxaliplatin	9-20	ATPase copper transporting alpha	Homo sapiens	100-105
30341172-4	2018	Dopamine is converted to norepinephrine by dopamine-beta-hydroxylase (DBH), which acquires its essential Cu cofactor from ATP7A.	Dopamine	0-8	ATPase copper transporting alpha	Homo sapiens	122-127
30341172-4	2018	Dopamine is converted to norepinephrine by dopamine-beta-hydroxylase (DBH), which acquires its essential Cu cofactor from ATP7A.	Norepinephrine	25-39	ATPase copper transporting alpha	Homo sapiens	122-127
29112372-6	2018	We demonstrate the ability of the carbon-rhodol based congener, Copper Carbo Fluor 1 (CCF1), to identify elevations in labile copper pools in the Atp7a-/- fibroblast cell model of the genetic copper disorder Menkes disease.	carbon-rhodol	34-47	ATPase copper transporting alpha	Homo sapiens	146-151
30455854-3	2018	We here show that the copper chaperone Atox1, known for shuttling copper in the cytoplasm from Ctr1 to ATP7A/B in the secretory pathway, interacts with several APC subunits.	Copper	22-28	ATPase copper transporting alpha	Homo sapiens	103-110
30455854-3	2018	We here show that the copper chaperone Atox1, known for shuttling copper in the cytoplasm from Ctr1 to ATP7A/B in the secretory pathway, interacts with several APC subunits.	Copper	66-72	ATPase copper transporting alpha	Homo sapiens	103-110
30008940-13	2018	Downregulated hCTP1 and upregulated ATP7A and ATP7B were associated with L-OHP resistance, and GA reversed the resistance by increasing levels of hCTR1 and decreasing levels of ATP7A and ATP7B.	Oxaliplatin	73-78	ATPase copper transporting alpha	Homo sapiens	36-41
30199530-4	2018	Differentiating adipocytes increase their Cu uptake along with the ATP7A-dependent transport of Cu into the secretory pathway to activate a highly up-regulated amino-oxidase copper-containing 3 (AOC3)/semicarbazide-sensitive amine oxidase (SSAO); in vivo, the activity of SSAO depends on the organism"s Cu status.	Copper	96-98	ATPase copper transporting alpha	Homo sapiens	67-72
29959467-4	2018	Copper is excreted from enterocytes into the blood via the Cu-ATPase, ATP7A, by trafficking the transporter towards the basolateral membrane.	Copper	0-6	ATPase copper transporting alpha	Homo sapiens	70-75
30142961-0	2018	Probing the Anticancer Action of Novel Ferrocene Analogues of MNK Inhibitors.	ferrocene	39-48	ATPase copper transporting alpha	Homo sapiens	62-65
29112372-6	2018	We demonstrate the ability of the carbon-rhodol based congener, Copper Carbo Fluor 1 (CCF1), to identify elevations in labile copper pools in the Atp7a-/- fibroblast cell model of the genetic copper disorder Menkes disease.	copper carbo fluor 1	64-84	ATPase copper transporting alpha	Homo sapiens	146-151
29112372-6	2018	We demonstrate the ability of the carbon-rhodol based congener, Copper Carbo Fluor 1 (CCF1), to identify elevations in labile copper pools in the Atp7a-/- fibroblast cell model of the genetic copper disorder Menkes disease.	Copper	126-132	ATPase copper transporting alpha	Homo sapiens	146-151
29579719-8	2018	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.	Copper	148-154	ATPase copper transporting alpha	Homo sapiens	57-62
29627895-0	2018	Toosendanin mediates cisplatin sensitization through targeting Annexin A4/ATP7A in non-small cell lung cancer cells.	Cisplatin	21-30	ATPase copper transporting alpha	Homo sapiens	74-79
29627895-13	2018	The adjustment of CDDP concentration regulated by TSN disappeared in Anxa4 or ATP7A-silenced cells.	Cisplatin	18-22	ATPase copper transporting alpha	Homo sapiens	78-83
29579719-5	2018	Elevated copper in senescent MEFs was accompanied by elevated levels of high-affinity copper uptake protein 1 (Ctr1), diminished levels of copper-transporting ATPase 1 (Atp7a) (copper export) and enhanced antioxidant defence reflected by elevated levels of glutathione (GSH), superoxide dismutase 1 (SOD1) and glutaredoxin 1 (Grx1).	Copper	9-15	ATPase copper transporting alpha	Homo sapiens	139-167
29772714-2	2018	Drug importing, intracellular shuffling, and exporting-carried out by the high-affinity copper (Cu) transporter (hCtr1), Cu chaperone (Ato x1), and Cu exporters (ATP7A and ATP7B), respectively-cumulatively contribute to the chemosensitivity of Pt drugs including cisplatin and carboplatin, but not oxaliplatin.	Cisplatin	263-272	ATPase copper transporting alpha	Homo sapiens	162-167
29579719-5	2018	Elevated copper in senescent MEFs was accompanied by elevated levels of high-affinity copper uptake protein 1 (Ctr1), diminished levels of copper-transporting ATPase 1 (Atp7a) (copper export) and enhanced antioxidant defence reflected by elevated levels of glutathione (GSH), superoxide dismutase 1 (SOD1) and glutaredoxin 1 (Grx1).	Copper	9-15	ATPase copper transporting alpha	Homo sapiens	169-174
29579719-6	2018	The levels of intracellular copper were further increased in senescent MEFs cultured in copper supplemented medium and in senescent Mottled Brindled (Mobr) MEFs lacking functional Atp7a.	Copper	28-34	ATPase copper transporting alpha	Homo sapiens	180-185
29579719-7	2018	Finally, 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.	Sirolimus	123-132	ATPase copper transporting alpha	Homo sapiens	239-244
29789304-2	2018	It occurs due to mutations in ATP7A gene located on X-chromosome leading to deficiency of several copper-containing enzymes.	Copper	98-104	ATPase copper transporting alpha	Homo sapiens	30-35
29599289-1	2018	The copper-transporting ATPase ATP7A contains eight transmembrane domains and is required for normal human copper homeostasis.	Copper	4-10	ATPase copper transporting alpha	Homo sapiens	31-36
29599289-4	2018	In this study, we further characterized this interaction and discovered a concealed UBX domain in the third lumenal loop of ATP7A, between its fifth and sixth transmembrane domains.	N-[(S)-({[(Benzyloxy)carbonyl]amino}methyl)(Hydroxy)phosphoryl]-N-Methyl-L-Leucinamide	84-87	ATPase copper transporting alpha	Homo sapiens	124-129
29599289-7	2018	The UBX domain has a conserved hydrophobic FP (Phe-Pro) motif, and substitution with di-alanine abrogated the interaction and restored the proper intracellular localization of ATP7A in the trans-Golgi network.	N-[(S)-({[(Benzyloxy)carbonyl]amino}methyl)(Hydroxy)phosphoryl]-N-Methyl-L-Leucinamide	4-7	ATPase copper transporting alpha	Homo sapiens	176-181
29599289-7	2018	The UBX domain has a conserved hydrophobic FP (Phe-Pro) motif, and substitution with di-alanine abrogated the interaction and restored the proper intracellular localization of ATP7A in the trans-Golgi network.	Phenylalanine	47-50	ATPase copper transporting alpha	Homo sapiens	176-181
29599289-7	2018	The UBX domain has a conserved hydrophobic FP (Phe-Pro) motif, and substitution with di-alanine abrogated the interaction and restored the proper intracellular localization of ATP7A in the trans-Golgi network.	alanylalanine	85-95	ATPase copper transporting alpha	Homo sapiens	176-181
29772714-2	2018	Drug importing, intracellular shuffling, and exporting-carried out by the high-affinity copper (Cu) transporter (hCtr1), Cu chaperone (Ato x1), and Cu exporters (ATP7A and ATP7B), respectively-cumulatively contribute to the chemosensitivity of Pt drugs including cisplatin and carboplatin, but not oxaliplatin.	Carboplatin	277-288	ATPase copper transporting alpha	Homo sapiens	162-167
29772714-2	2018	Drug importing, intracellular shuffling, and exporting-carried out by the high-affinity copper (Cu) transporter (hCtr1), Cu chaperone (Ato x1), and Cu exporters (ATP7A and ATP7B), respectively-cumulatively contribute to the chemosensitivity of Pt drugs including cisplatin and carboplatin, but not oxaliplatin.	Oxaliplatin	298-309	ATPase copper transporting alpha	Homo sapiens	162-167
29594361-0	2018	MircroRNA-139 sensitizes ovarian cancer cell to cisplatin-based chemotherapy through regulation of ATP7A/B.	mircrorna-139	0-13	ATPase copper transporting alpha	Homo sapiens	99-106
29594361-0	2018	MircroRNA-139 sensitizes ovarian cancer cell to cisplatin-based chemotherapy through regulation of ATP7A/B.	Cisplatin	48-57	ATPase copper transporting alpha	Homo sapiens	99-106
29594361-7	2018	RESULTS: miR-139 expression was down-regulated in cisplatin-resistant ovarian cancer tissues (**P < 0.01) and reduced by cisplatin treatment in ovarian cell lines (*P < 0.05, **P < 0.01); miR-139 could enhance cisplatin-induced suppression on ovarian cancer cell viability, shown as reduced lC50 values; ATP7A and ATP7B protein levesincreased approximately 2 ~ fold-changein cisplatin-resistant cell lines.	Cisplatin	124-133	ATPase copper transporting alpha	Homo sapiens	313-318
29594361-7	2018	RESULTS: miR-139 expression was down-regulated in cisplatin-resistant ovarian cancer tissues (**P < 0.01) and reduced by cisplatin treatment in ovarian cell lines (*P < 0.05, **P < 0.01); miR-139 could enhance cisplatin-induced suppression on ovarian cancer cell viability, shown as reduced lC50 values; ATP7A and ATP7B protein levesincreased approximately 2 ~ fold-changein cisplatin-resistant cell lines.	Cisplatin	50-59	ATPase copper transporting alpha	Homo sapiens	313-318
29594361-7	2018	RESULTS: miR-139 expression was down-regulated in cisplatin-resistant ovarian cancer tissues (**P < 0.01) and reduced by cisplatin treatment in ovarian cell lines (*P < 0.05, **P < 0.01); miR-139 could enhance cisplatin-induced suppression on ovarian cancer cell viability, shown as reduced lC50 values; ATP7A and ATP7B protein levesincreased approximately 2 ~ fold-changein cisplatin-resistant cell lines.	Cisplatin	124-133	ATPase copper transporting alpha	Homo sapiens	313-318
29594361-7	2018	RESULTS: miR-139 expression was down-regulated in cisplatin-resistant ovarian cancer tissues (**P < 0.01) and reduced by cisplatin treatment in ovarian cell lines (*P < 0.05, **P < 0.01); miR-139 could enhance cisplatin-induced suppression on ovarian cancer cell viability, shown as reduced lC50 values; ATP7A and ATP7B protein levesincreased approximately 2 ~ fold-changein cisplatin-resistant cell lines.	Cisplatin	124-133	ATPase copper transporting alpha	Homo sapiens	313-318
29594361-9	2018	CONCLUSIONS: MiR-139/ATP7A/B axis can be a reliable biomarker for ovarian cancer diagnosis, and may affect the chemoresistance of ovarian cancer to cisplatin-based chemotherapy; rescuing miR-139 expression thus to inhibit ATP7A/B might contribute to dealing with the chemoresistance of ovarian cancer.	Cisplatin	148-157	ATPase copper transporting alpha	Homo sapiens	21-26
29594361-9	2018	CONCLUSIONS: MiR-139/ATP7A/B axis can be a reliable biomarker for ovarian cancer diagnosis, and may affect the chemoresistance of ovarian cancer to cisplatin-based chemotherapy; rescuing miR-139 expression thus to inhibit ATP7A/B might contribute to dealing with the chemoresistance of ovarian cancer.	Cisplatin	148-157	ATPase copper transporting alpha	Homo sapiens	222-227
29526098-5	2018	The crystal structure-guided design leverages stereoelectronic interactions unique to MNK culminating in a novel pyridone-aminal structure described for the first time in the kinase literature.	Pyridones	113-121	ATPase copper transporting alpha	Homo sapiens	86-89
29397366-4	2018	We use triple-SILAC mass spectrometry to quantify proteomes from human pedigrees affected by mutations in ATP7A, which cause Menkes disease, a rare neurodegenerative and neurodevelopmental disorder stemming from systemic copper depletion.	Copper	221-227	ATPase copper transporting alpha	Homo sapiens	106-111
29325617-9	2018	Mutations in a second, closely related copper-transporting ATPase, ATP7A, cause a spectrum of copper deficiency disorders that include Menkes disease, occipital horn syndrome, and ATP7A-related distal motor neuropathy.	Copper	39-45	ATPase copper transporting alpha	Homo sapiens	67-72
29351582-7	2018	Given that another Charcot-Marie-Tooth disease gene, ATP7A, is a known copper transporter, our findings further underline the relevance of copper metabolism in Charcot-Marie-Tooth disease.	Copper	71-77	ATPase copper transporting alpha	Homo sapiens	53-58
29351582-7	2018	Given that another Charcot-Marie-Tooth disease gene, ATP7A, is a known copper transporter, our findings further underline the relevance of copper metabolism in Charcot-Marie-Tooth disease.	Copper	139-145	ATPase copper transporting alpha	Homo sapiens	53-58
29394468-0	2018	Copper efflux transporters ATP7A and ATP7B: Novel biomarkers for platinum drug resistance and targets for therapy.	Platinum	65-73	ATPase copper transporting alpha	Homo sapiens	27-32
29394468-3	2018	Recent studies suggest that copper efflux transporters, which are encoded by ATP7A and ATP7B, play an important role in platinum drug resistance.	Platinum	120-128	ATPase copper transporting alpha	Homo sapiens	77-82
29394468-7	2018	We also discuss the possible mechanisms of platinum drug resistance mediated by ATP7A/7B and provide novel strategies for overcoming resistance.	Platinum	43-51	ATPase copper transporting alpha	Homo sapiens	80-85
29168020-3	2018	A treatment with 12-O-tetradecanoylphorbol-13-acetate (TPA) induced the expression of the Cu transport protein ATP7A in THP-1 cells.	Tetradecanoylphorbol Acetate	17-53	ATPase copper transporting alpha	Homo sapiens	111-116
29168020-3	2018	A treatment with 12-O-tetradecanoylphorbol-13-acetate (TPA) induced the expression of the Cu transport protein ATP7A in THP-1 cells.	Tetradecanoylphorbol Acetate	55-58	ATPase copper transporting alpha	Homo sapiens	111-116
29232129-4	2018	Treatment of SKOV-3 cells with low concentrations (muM) of two of the copper complexes led to trafficking of the endogenous copper transporter ATP7A from the Golgi network to the cell membrane.	Copper	70-76	ATPase copper transporting alpha	Homo sapiens	143-148
29325617-9	2018	Mutations in a second, closely related copper-transporting ATPase, ATP7A, cause a spectrum of copper deficiency disorders that include Menkes disease, occipital horn syndrome, and ATP7A-related distal motor neuropathy.	Copper	39-45	ATPase copper transporting alpha	Homo sapiens	180-185
29970670-3	2018	The two P-type ATPases ATP7A and ATP7B have been identified to play an essential role in the transport of platinum.	Platinum	106-114	ATPase copper transporting alpha	Homo sapiens	23-28
29970670-5	2018	In this study, we aimed to investigate the association of ATP7A and ATP7B genetic polymorphisms with clinical outcome and toxicity of platinum-based chemotherapy in NSCLC patients.	Platinum	134-142	ATPase copper transporting alpha	Homo sapiens	58-63
29042487-9	2018	Additionally, it was determined that MNK inhibition sensitized MES GSCs to ATO in neurosphere and apoptosis assays.	2-(N-morpholino)ethanesulfonic acid	63-66	ATPase copper transporting alpha	Homo sapiens	37-40
29042487-9	2018	Additionally, it was determined that MNK inhibition sensitized MES GSCs to ATO in neurosphere and apoptosis assays.	Arsenic Trioxide	75-78	ATPase copper transporting alpha	Homo sapiens	37-40
28657131-4	2017	He has few neurological symptoms without connective tissue disturbances; and a missense ATP7A variant, p.(Pro852Leu), which results in impaired protein trafficking while the copper transport function is spared.	Copper	174-180	ATPase copper transporting alpha	Homo sapiens	88-93
29058724-3	2017	Our screen uncovered three genes, POR (cytochrome P450 oxidoreductase), ATP7A (copper transporter), and SLC45A4 (sucrose transporter), required for paraquat-induced cell death.	Paraquat	148-156	ATPase copper transporting alpha	Homo sapiens	72-77
29269484-4	2017	Tamoxifen-resistant translational reprogramming is shown to be mediated by increased expression of eIF4E and its increased availability by hyperactive mTOR and to require phosphorylation of eIF4E at Ser209 by increased MNK activity.	Tamoxifen	0-9	ATPase copper transporting alpha	Homo sapiens	219-222
29269484-8	2017	Tamoxifen-resistant but not tamoxifen-sensitive patient ER+ breast cancer specimens also demonstrate strongly increased MNK phosphorylation of eIF4E.	Tamoxifen	0-9	ATPase copper transporting alpha	Homo sapiens	120-123
28657131-5	2017	These findings suggest that some cuproenzymes maintain their function when sufficient copper is provided to the cells; and underline the importance of early initiated copper treatment, efficiency of which is likely to be dependent on the mutant ATP7A function.	Copper	167-173	ATPase copper transporting alpha	Homo sapiens	245-250
28652309-2	2017	A key regulator of copper homeostasis in mammalian cells is the copper-transporting P-type ATPase ATP7A, which mediates copper transport from the cytoplasm into the secretory pathway, as well as copper export across the plasma membrane.	Copper	19-25	ATPase copper transporting alpha	Homo sapiens	98-103
28737129-6	2017	In addition, we found that <italic>ATP7A</italic> rs2227291 was associated with cisplatin resistance and that carriers of the C allele were more sensitive to cisplatin (OR = 0.40, 95% CI: 0.17 - 0.94, p = 0.03).	Cisplatin	92-101	ATPase copper transporting alpha	Homo sapiens	41-46
28737129-6	2017	In addition, we found that <italic>ATP7A</italic> rs2227291 was associated with cisplatin resistance and that carriers of the C allele were more sensitive to cisplatin (OR = 0.40, 95% CI: 0.17 - 0.94, p = 0.03).	Cisplatin	170-179	ATPase copper transporting alpha	Homo sapiens	41-46
28737129-7	2017	Our findings suggest that the <italic>CTR1</italic> and <italic>ATP7A</italic> genetic polymorphisms could affect platinum resistance.	Platinum	138-146	ATPase copper transporting alpha	Homo sapiens	82-87
28737129-8	2017	The <italic>CTR1</italic> and <italic>ATP7A</italic> genes might be considered a predictive marker for carboplatin and cisplatin resistance, respectively.	Carboplatin	127-138	ATPase copper transporting alpha	Homo sapiens	56-61
28737129-8	2017	The <italic>CTR1</italic> and <italic>ATP7A</italic> genes might be considered a predictive marker for carboplatin and cisplatin resistance, respectively.	Cisplatin	143-152	ATPase copper transporting alpha	Homo sapiens	56-61
28652309-2	2017	A key regulator of copper homeostasis in mammalian cells is the copper-transporting P-type ATPase ATP7A, which mediates copper transport from the cytoplasm into the secretory pathway, as well as copper export across the plasma membrane.	Copper	64-70	ATPase copper transporting alpha	Homo sapiens	98-103
28652309-2	2017	A key regulator of copper homeostasis in mammalian cells is the copper-transporting P-type ATPase ATP7A, which mediates copper transport from the cytoplasm into the secretory pathway, as well as copper export across the plasma membrane.	Copper	64-70	ATPase copper transporting alpha	Homo sapiens	98-103
28636017-3	2017	It has been shown that cisplatin can interact with P-type ATPases, e.g., Cu+-ATPases (ATP7A and ATP7B) and Na+,K+-ATPase.	Cisplatin	23-32	ATPase copper transporting alpha	Homo sapiens	86-91
28665070-8	2017	In an ATP7A knock-out model, rapamycin treatment synergistically inhibited cell viability, wound healing, and invasion ability compared to rapamycin only.	Sirolimus	29-38	ATPase copper transporting alpha	Homo sapiens	6-11
28271598-0	2017	Dynamics of the metal binding domains and regulation of the human copper transporters ATP7B and ATP7A.	Metals	16-21	ATPase copper transporting alpha	Homo sapiens	96-101
28389643-1	2017	Menkes disease (MD) is caused by mutations in ATP7A, encoding a copper-transporting P-type ATPase which exhibits copper-dependent trafficking.	Copper	64-70	ATPase copper transporting alpha	Homo sapiens	46-51
28389643-2	2017	ATP7A is found in the Trans-Golgi Network (TGN) at low copper concentrations, and in the post-Golgi compartments and the plasma membrane at higher concentrations.	Copper	55-61	ATPase copper transporting alpha	Homo sapiens	0-5
28271598-1	2017	Copper transporters ATP7A and ATP7B regulate copper levels in the human cells and deliver copper to the biosynthetic pathways.	Copper	45-51	ATPase copper transporting alpha	Homo sapiens	20-25
28271598-1	2017	Copper transporters ATP7A and ATP7B regulate copper levels in the human cells and deliver copper to the biosynthetic pathways.	Copper	90-96	ATPase copper transporting alpha	Homo sapiens	20-25
28271598-4	2017	Although the structures of all the MBDs have been solved, 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.	Copper	75-81	ATPase copper transporting alpha	Homo sapiens	116-121
28271632-3	2017	The severe consequences of insufficient copper supply are illustrated by Menkes disease, caused by mutation in the X-linked ATP7A gene encoding a protein that transports copper from intestinal epithelia into the bloodstream and across the blood-brain barrier.	Copper	40-46	ATPase copper transporting alpha	Homo sapiens	124-129
28271632-3	2017	The severe consequences of insufficient copper supply are illustrated by Menkes disease, caused by mutation in the X-linked ATP7A gene encoding a protein that transports copper from intestinal epithelia into the bloodstream and across the blood-brain barrier.	Copper	170-176	ATPase copper transporting alpha	Homo sapiens	124-129
27980217-1	2017	Copper transporter 1 (CTR1), copper transporter 2 (CTR2), copper-transporting p-type adenosine triphosphatase 1 and 2 (ATP7A and ATP7B) are key mediators of cellular cisplatin, carboplatin and oxaliplatin accumulation.	Cisplatin	166-175	ATPase copper transporting alpha	Homo sapiens	119-124
27896900-3	2017	The P-type copper ATPases ATP7A and ATP7B provide an important system for acquisition, active transport, distribution and elimination of copper.	Copper	11-17	ATPase copper transporting alpha	Homo sapiens	26-31
28164426-1	2017	ATP7A and ATP7B are Cu+ -transporting ATPases of subclass IB and play a fundamental role in intracellular copper homeostasis.	Copper	106-112	ATPase copper transporting alpha	Homo sapiens	0-5
28164426-2	2017	ATP7A/B transfer Cu+ ions across the membrane from delivery to acceptor proteins without establishing a free Cu+ gradient.	Copper	17-20	ATPase copper transporting alpha	Homo sapiens	0-5
28164426-2	2017	ATP7A/B transfer Cu+ ions across the membrane from delivery to acceptor proteins without establishing a free Cu+ gradient.	Copper	109-112	ATPase copper transporting alpha	Homo sapiens	0-5
28164426-4	2017	Current measurements on solid supported membranes (SSM) were performed to investigate the mechanism of copper-related charge transfer across ATP7A and ATP7B.	Copper	103-109	ATPase copper transporting alpha	Homo sapiens	141-146
28164426-5	2017	SSM measurements demonstrated that electrogenic copper displacement occurs within ATP7A/B following addition of ATP and formation of the phosphorylated intermediate.	Copper	48-54	ATPase copper transporting alpha	Homo sapiens	82-87
28164426-7	2017	Moreover, 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.	Adenosine Triphosphate	10-13	ATPase copper transporting alpha	Homo sapiens	43-50
28164426-7	2017	Moreover, 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.	Copper	24-30	ATPase copper transporting alpha	Homo sapiens	43-50
28164426-8	2017	Platinum anticancer drugs activate ATP7A/B and are subjected to ATP-dependent vectorial displacement with a mechanism analogous to that of copper.	Platinum	0-8	ATPase copper transporting alpha	Homo sapiens	35-40
28164426-8	2017	Platinum anticancer drugs activate ATP7A/B and are subjected to ATP-dependent vectorial displacement with a mechanism analogous to that of copper.	Copper	139-145	ATPase copper transporting alpha	Homo sapiens	35-40
27980217-1	2017	Copper transporter 1 (CTR1), copper transporter 2 (CTR2), copper-transporting p-type adenosine triphosphatase 1 and 2 (ATP7A and ATP7B) are key mediators of cellular cisplatin, carboplatin and oxaliplatin accumulation.	Carboplatin	177-188	ATPase copper transporting alpha	Homo sapiens	119-124
27980217-1	2017	Copper transporter 1 (CTR1), copper transporter 2 (CTR2), copper-transporting p-type adenosine triphosphatase 1 and 2 (ATP7A and ATP7B) are key mediators of cellular cisplatin, carboplatin and oxaliplatin accumulation.	Oxaliplatin	193-204	ATPase copper transporting alpha	Homo sapiens	119-124
27877224-0	2016	The role of copper transporter ATP7A in platinum-resistance of esophageal squamous cell cancer (ESCC).	Platinum	40-48	ATPase copper transporting alpha	Homo sapiens	31-36
28164761-8	2017	Lately, the first two clinical programs targeting MNKs in oncology have been revealed (eFT508 and BAY 1143269), although several other MNK programs are currently running at the preclinical stage.	benzonaphthyridone	87-93	ATPase copper transporting alpha	Homo sapiens	50-53
28164761-8	2017	Lately, the first two clinical programs targeting MNKs in oncology have been revealed (eFT508 and BAY 1143269), although several other MNK programs are currently running at the preclinical stage.	BAY 1143269	98-109	ATPase copper transporting alpha	Homo sapiens	50-53
29687769-2	2017	Deficient activity of the ATP7A protein results in decreased intestinal absorption of copper, low copper level in serum and defective distribution of copper in tissues.	Copper	86-92	ATPase copper transporting alpha	Homo sapiens	26-31
29687769-2	2017	Deficient activity of the ATP7A protein results in decreased intestinal absorption of copper, low copper level in serum and defective distribution of copper in tissues.	Copper	98-104	ATPase copper transporting alpha	Homo sapiens	26-31
29687769-2	2017	Deficient activity of the ATP7A protein results in decreased intestinal absorption of copper, low copper level in serum and defective distribution of copper in tissues.	Copper	98-104	ATPase copper transporting alpha	Homo sapiens	26-31
27662474-2	2016	Here we investigated whether an antifungal agent, cercosporamide, which had been recently identified as a potent Mnk inhibitor, is active against HCC and angiogenesis.	cercosporamide	50-64	ATPase copper transporting alpha	Homo sapiens	113-116
27662474-6	2016	Cercosporamide blocked the phosphorylation of eIF4E but not Erk or p38 in a dose- and time-dependent manner in HCC and HCC-EC cells, suggesting that suppression of eIF4E phosphorylation was the result of inhibition of Mnk but not Mnk upstream pathways.	cercosporamide	0-14	ATPase copper transporting alpha	Homo sapiens	218-221
27662474-6	2016	Cercosporamide blocked the phosphorylation of eIF4E but not Erk or p38 in a dose- and time-dependent manner in HCC and HCC-EC cells, suggesting that suppression of eIF4E phosphorylation was the result of inhibition of Mnk but not Mnk upstream pathways.	cercosporamide	0-14	ATPase copper transporting alpha	Homo sapiens	230-233
27662474-8	2016	Altogether, our work demonstrates that cercosporamide acts as a Mnk inhibitor through blockage of eIF4E phosphorylation and selectively exhibits anti-HCC activities.	cercosporamide	39-53	ATPase copper transporting alpha	Homo sapiens	64-67
27806319-0	2016	Ammonium tetrathiomolybdate treatment targets the copper transporter ATP7A and enhances sensitivity of breast cancer to cisplatin.	tetrathiomolybdate	0-27	ATPase copper transporting alpha	Homo sapiens	69-74
27806319-4	2016	ATP7A is a copper ATPase transporter responsible for intercellular movement and sequestering of cisplatin.	Cisplatin	96-105	ATPase copper transporting alpha	Homo sapiens	0-5
27806319-5	2016	Pharmaceutical replacement for ATP7A by ammonium tetrathiomolybdate (TM) enhanced cisplatin treatment in breast cancer cells.	Cisplatin	82-91	ATPase copper transporting alpha	Homo sapiens	31-36
27806319-7	2016	Cisplatin/TM treatment of cisplatin-resistant tumors reduced ATP7A protein levels, attenuated cisplatin sequestering by ATP7A, increased nuclear availability of cisplatin, and subsequently enhanced DNA damage and apoptosis.	Cisplatin	0-9	ATPase copper transporting alpha	Homo sapiens	61-66
27806319-7	2016	Cisplatin/TM treatment of cisplatin-resistant tumors reduced ATP7A protein levels, attenuated cisplatin sequestering by ATP7A, increased nuclear availability of cisplatin, and subsequently enhanced DNA damage and apoptosis.	Cisplatin	0-9	ATPase copper transporting alpha	Homo sapiens	120-125
27806319-7	2016	Cisplatin/TM treatment of cisplatin-resistant tumors reduced ATP7A protein levels, attenuated cisplatin sequestering by ATP7A, increased nuclear availability of cisplatin, and subsequently enhanced DNA damage and apoptosis.	tetrathiomolybdate	10-12	ATPase copper transporting alpha	Homo sapiens	61-66
27806319-7	2016	Cisplatin/TM treatment of cisplatin-resistant tumors reduced ATP7A protein levels, attenuated cisplatin sequestering by ATP7A, increased nuclear availability of cisplatin, and subsequently enhanced DNA damage and apoptosis.	tetrathiomolybdate	10-12	ATPase copper transporting alpha	Homo sapiens	120-125
27806319-7	2016	Cisplatin/TM treatment of cisplatin-resistant tumors reduced ATP7A protein levels, attenuated cisplatin sequestering by ATP7A, increased nuclear availability of cisplatin, and subsequently enhanced DNA damage and apoptosis.	Cisplatin	26-35	ATPase copper transporting alpha	Homo sapiens	61-66
27806319-7	2016	Cisplatin/TM treatment of cisplatin-resistant tumors reduced ATP7A protein levels, attenuated cisplatin sequestering by ATP7A, increased nuclear availability of cisplatin, and subsequently enhanced DNA damage and apoptosis.	Cisplatin	26-35	ATPase copper transporting alpha	Homo sapiens	120-125
27878136-2	2016	Other ATP7A mutations have been linked to juvenile occipital horn syndrome and adult-onset hereditary motor neuropathy.1,2 About 5%-10% of the patients present with "atypical Menkes disease" characterized by longer survival, cerebellar ataxia, and developmental delay.2 The intracellular copper transport is regulated by 2 P type ATPase copper transporters ATP7A and ATP7B.	Copper	288-294	ATPase copper transporting alpha	Homo sapiens	6-11
27877224-3	2016	Recent studies have shown that the mammalian copper transporters CTR1, ATP7A and ATP7B are involved in cisplatin-resistance to some cancers.	Cisplatin	103-112	ATPase copper transporting alpha	Homo sapiens	71-76
27877224-5	2016	To determine whether knockdown the expression of ATP7A could reverse the platinum-resistance of EC109/DDP cells or not, we used RNA interference system to explore the role of ATP7A in platinum resistance.	Platinum	73-81	ATPase copper transporting alpha	Homo sapiens	49-54
27462781-0	2016	Inhibition of Mnk enhances apoptotic activity of cytarabine in acute myeloid leukemia cells.	Cytarabine	49-59	ATPase copper transporting alpha	Homo sapiens	14-17
27629586-3	2016	ATP7A, a main Cu(2+) transporting-ATPase, is necessary to efflux Cu across the plasma membrane and synthesize cuproenzymes.	Copper	14-16	ATPase copper transporting alpha	Homo sapiens	0-5
27714044-7	2016	This led us to postulate that Atp7a may influence intestinal iron flux.	Iron	61-65	ATPase copper transporting alpha	Homo sapiens	30-35
27714044-10	2016	Interestingly, 59Fe uptake and efflux were impaired in both cell lines by Atp7a silencing.	Iron-59	15-19	ATPase copper transporting alpha	Homo sapiens	74-79
27714044-12	2016	Expression of Dmt1 (the iron importer), Dcytb (an apical membrane ferrireductase) and Fpn1 (the iron exporter) was decreased in Atp7a knockdown (KD) cells.	Iron	24-28	ATPase copper transporting alpha	Homo sapiens	128-133
27714044-16	2016	In summary, in these reductionist models of the mammalian intestinal epithelium, Atp7a KD altered expression of iron transporters and impaired iron flux.	Iron	112-116	ATPase copper transporting alpha	Homo sapiens	81-86
27714044-17	2016	Since Atp7a is a copper transporter, it is a logical supposition that perturbations in intracellular copper homeostasis underlie the noted biologic changes in these cell lines.	Copper	17-23	ATPase copper transporting alpha	Homo sapiens	6-11
27462781-4	2016	In this study, we showed a strong synergistic effect of Ara-C with either our Mnk inhibitor (MNKI-8e) or short hairpin RNA (shRNA) mediated knockdown of Mnks in MV4-11 AML cells.	Cytarabine	56-61	ATPase copper transporting alpha	Homo sapiens	78-81
27462781-6	2016	We showed that both MNKI-8e and Mnk shRNAs enhanced the ability of Ara-C to induce apoptosis.	Cytarabine	67-72	ATPase copper transporting alpha	Homo sapiens	32-35
27462781-8	2016	Inhibition of Mnk activity suppressed the Ara-C-induced MAPK activity, and thus enhanced apoptosis in MV4-11 cells.	Cytarabine	42-47	ATPase copper transporting alpha	Homo sapiens	14-17
27462781-9	2016	Taken together, our study suggests that MAPK-Mnk-eIF4E pathway plays a critical role in Ara-C-treated MV4-11 cells and targeting Mnk may be a promising therapeutic strategy for sensitizing leukemic cells to Ara-C therapy.	Cytarabine	88-93	ATPase copper transporting alpha	Homo sapiens	45-48
27462781-9	2016	Taken together, our study suggests that MAPK-Mnk-eIF4E pathway plays a critical role in Ara-C-treated MV4-11 cells and targeting Mnk may be a promising therapeutic strategy for sensitizing leukemic cells to Ara-C therapy.	Cytarabine	207-212	ATPase copper transporting alpha	Homo sapiens	129-132
27587995-5	2016	In contrast, the addition of copper led to an increased expression of ATP7A, but a decreased expression of ATP7B.	Copper	29-35	ATPase copper transporting alpha	Homo sapiens	70-75
27587995-8	2016	Cells that express the normal ATP7A allele had a selective growth advantage at high copper concentrations, whereas more surprisingly, cells that express the mutant ATP7A allele had a selective growth advantage at low copper concentrations.	Copper	84-90	ATPase copper transporting alpha	Homo sapiens	30-35
27587995-0	2016	Metal-Dependent Regulation of ATP7A and ATP7B in Fibroblast Cultures.	Metals	0-5	ATPase copper transporting alpha	Homo sapiens	30-35
27587995-8	2016	Cells that express the normal ATP7A allele had a selective growth advantage at high copper concentrations, whereas more surprisingly, cells that express the mutant ATP7A allele had a selective growth advantage at low copper concentrations.	Copper	217-223	ATPase copper transporting alpha	Homo sapiens	164-169
27587995-2	2016	In order to investigate whether the ATP7A and the ATP7B genes may be transcriptionally regulated, we measured the expression level of the two genes at various concentrations of iron, copper, and insulin.	Copper	183-189	ATPase copper transporting alpha	Homo sapiens	36-41
27587995-9	2016	Thus, although the transcription of ATP7A is regulated by copper, clonal growth selection in mosaic cell cultures is affected by the level of copper.	Copper	58-64	ATPase copper transporting alpha	Homo sapiens	36-41
27587995-3	2016	Treating fibroblasts from controls or from individuals with MD or WD for 3 and 10 days with iron chelators revealed that iron deficiency led to increased transcript levels of both ATP7A and ATP7B.	Iron	92-96	ATPase copper transporting alpha	Homo sapiens	180-185
27587995-4	2016	Copper deficiency obtained by treatment with the copper chelator led to a downregulation of ATP7A in the control fibroblasts, but surprisingly not in the WD fibroblasts.	Copper	49-55	ATPase copper transporting alpha	Homo sapiens	92-97
27242196-0	2016	pH-regulated metal-ligand switching in the HM loop of ATP7A: a new paradigm for metal transfer chemistry.	Metals	13-18	ATPase copper transporting alpha	Homo sapiens	54-59
27226607-1	2016	Copper-transporting ATPase ATP7A is essential for mammalian copper homeostasis.	Copper	60-66	ATPase copper transporting alpha	Homo sapiens	27-32
27226607-3	2016	In cells, ATP7A inactivation disrupts copper transport from the cytosol into the secretory pathway.	Copper	38-44	ATPase copper transporting alpha	Homo sapiens	10-15
27226607-9	2016	Thus, ATP7A activity protects mitochondria from excessive copper entry, which is deleterious to redox buffers.	Copper	58-64	ATPase copper transporting alpha	Homo sapiens	6-11
27226607-10	2016	Mitochondrial redox misbalance could significantly contribute to pathologies associated with ATP7A inactivation in tissues with paradoxical accumulation of copper (i.e. renal epithelia).	Copper	156-162	ATPase copper transporting alpha	Homo sapiens	93-98
27242196-0	2016	pH-regulated metal-ligand switching in the HM loop of ATP7A: a new paradigm for metal transfer chemistry.	Metals	80-85	ATPase copper transporting alpha	Homo sapiens	54-59
27242196-2	2016	Colocation with the P1B-type ATPase ATP7A suggests that the latter is the source of copper and supports a mechanism where selectivity in metal transfer is achieved by spatial colocation of partner proteins in their specific organelles or vesicles.	Copper	84-90	ATPase copper transporting alpha	Homo sapiens	36-41
27242196-2	2016	Colocation with the P1B-type ATPase ATP7A suggests that the latter is the source of copper and supports a mechanism where selectivity in metal transfer is achieved by spatial colocation of partner proteins in their specific organelles or vesicles.	Metals	137-142	ATPase copper transporting alpha	Homo sapiens	36-41
27159396-6	2016	We also demonstrated that MNK kinases are important and direct targets of cabozantinib.	cabozantinib	74-86	ATPase copper transporting alpha	Homo sapiens	26-29
27307295-0	2016	Merestinib blocks Mnk kinase activity in acute myeloid leukemia progenitors and exhibits antileukemic effects in vitro and in vivo.	merestinib	0-10	ATPase copper transporting alpha	Homo sapiens	18-21
27307295-3	2016	We provide evidence for antileukemic effects of merestinib, an orally bioavailable multikinase inhibitor with suppressive effects on Mnk activity.	merestinib	48-58	ATPase copper transporting alpha	Homo sapiens	133-136
27112899-3	2016	Here we illustrate that cisplatin resistance in human ovarian cancer cells (A2780) correlates with a reduced expression of LRRC8A and copper transporter receptor 1 (CTR1), as well as a concomitant increased expression of copper-transporting P-type ATPases (ATP7A/ATP7B).	Cisplatin	24-33	ATPase copper transporting alpha	Homo sapiens	257-262
26675528-8	2016	However, the levels of ATP7A and ATP7B, copper efflux pumps that help eliminate cisplatin from cells, were increased when HClpP was overexpressed.	Copper	40-46	ATPase copper transporting alpha	Homo sapiens	23-28
27050281-3	2016	Rapamycin induces eIF4E phosphorylation by activating MAPK-interacting kinases (Mnks), and therefore targeting Mnk/eIF4E pathway represents a potential therapeutic strategy for the treatment of NSCLC.	Sirolimus	0-9	ATPase copper transporting alpha	Homo sapiens	80-83
27050281-5	2016	Meanwhile, inhibiting Mnk1 expression by Mnk inhibitor (CGP57380) could abrogate rapalogs (RAD001)-induced eIF4E phosphorylation and Akt activation.	CGP 57380	56-64	ATPase copper transporting alpha	Homo sapiens	22-25
27014726-2	2016	This data article describes the possible circumvention of resistance to specifically platinum (Pt)-based anticancer drugs by vatalanib via inhibition of two other efflux transporters ABCC2 and ATP7A.	Platinum	85-93	ATPase copper transporting alpha	Homo sapiens	193-198
27014726-2	2016	This data article describes the possible circumvention of resistance to specifically platinum (Pt)-based anticancer drugs by vatalanib via inhibition of two other efflux transporters ABCC2 and ATP7A.	Platinum	95-97	ATPase copper transporting alpha	Homo sapiens	193-198
27014726-2	2016	This data article describes the possible circumvention of resistance to specifically platinum (Pt)-based anticancer drugs by vatalanib via inhibition of two other efflux transporters ABCC2 and ATP7A.	vatalanib	125-134	ATPase copper transporting alpha	Homo sapiens	193-198
27014726-6	2016	Vatalanib was shown to suppress this upregulated ATP7A expression.	vatalanib	0-9	ATPase copper transporting alpha	Homo sapiens	49-54
26675528-8	2016	However, the levels of ATP7A and ATP7B, copper efflux pumps that help eliminate cisplatin from cells, were increased when HClpP was overexpressed.	Cisplatin	80-89	ATPase copper transporting alpha	Homo sapiens	23-28
26165234-6	2016	Through a structure-based drug-design approach, we have discovered a selective and potent BTK/MNK dual kinase inhibitor (QL-X-138), which exhibits covalent binding to BTK and noncovalent binding to MNK.	QL-X-138	121-129	ATPase copper transporting alpha	Homo sapiens	94-97
26609108-7	2016	Significantly, MNK inhibitors increase E-cadherin mRNA levels and decrease vimentin mRNA levels in human PDAC organoids without affecting ZEB1 mRNA levels.	pdac organoids	105-119	ATPase copper transporting alpha	Homo sapiens	15-18
26609108-8	2016	Importantly, MNK inhibitors also decrease growth of human PDAC organoids.	pdac organoids	58-72	ATPase copper transporting alpha	Homo sapiens	13-16
26910782-5	2016	Screened against a panel of cancer cells, Mnk inhibitors were most potent against MV4-11 acute myeloid leukemia cells.	mv4-	82-86	ATPase copper transporting alpha	Homo sapiens	42-45
26165234-6	2016	Through a structure-based drug-design approach, we have discovered a selective and potent BTK/MNK dual kinase inhibitor (QL-X-138), which exhibits covalent binding to BTK and noncovalent binding to MNK.	QL-X-138	121-129	ATPase copper transporting alpha	Homo sapiens	198-201
26165234-7	2016	Compared with the BTK kinase inhibitor (PCI-32765) and the MNK kinase inhibitor (cercosporamide), QL-X-138 enhanced the antiproliferative efficacies in vitro against a variety of B-cell cancer cell lines, as well as AML and CLL primary patient cells, which respond moderately to BTK inhibitor in vitro.	QL-X-138	98-106	ATPase copper transporting alpha	Homo sapiens	59-62
26603002-1	2015	Menkes disease is a congenital disorder caused by changes in copper metabolism derived from mutations in the ATP7A gene.	Copper	61-67	ATPase copper transporting alpha	Homo sapiens	109-114
26537407-3	2015	Most Cu-dependent enzymes obtain the metal from the membrane-bound Cu pumps ATP7A/B in the Golgi network.	Copper	5-7	ATPase copper transporting alpha	Homo sapiens	76-83
26537407-3	2015	Most Cu-dependent enzymes obtain the metal from the membrane-bound Cu pumps ATP7A/B in the Golgi network.	Metals	37-42	ATPase copper transporting alpha	Homo sapiens	76-83
26537407-3	2015	Most Cu-dependent enzymes obtain the metal from the membrane-bound Cu pumps ATP7A/B in the Golgi network.	Copper	67-69	ATPase copper transporting alpha	Homo sapiens	76-83
26537407-4	2015	ATP7A/B receives Cu from the cytoplasmic Cu chaperone Atox1 that acts as the cytoplasmic shuttle between the cell membrane Cu importer, Ctr1 and ATP7A/B.	Copper	17-19	ATPase copper transporting alpha	Homo sapiens	0-5
26537407-4	2015	ATP7A/B receives Cu from the cytoplasmic Cu chaperone Atox1 that acts as the cytoplasmic shuttle between the cell membrane Cu importer, Ctr1 and ATP7A/B.	Copper	17-19	ATPase copper transporting alpha	Homo sapiens	145-150
26537407-4	2015	ATP7A/B receives Cu from the cytoplasmic Cu chaperone Atox1 that acts as the cytoplasmic shuttle between the cell membrane Cu importer, Ctr1 and ATP7A/B.	Copper	41-43	ATPase copper transporting alpha	Homo sapiens	0-5
26537407-4	2015	ATP7A/B receives Cu from the cytoplasmic Cu chaperone Atox1 that acts as the cytoplasmic shuttle between the cell membrane Cu importer, Ctr1 and ATP7A/B.	Copper	41-43	ATPase copper transporting alpha	Homo sapiens	145-150
26537407-6	2015	Nonetheless, basic mechanistic-biophysical questions (such as how and where ATP7A/B receives Cu, how ATP7A/B conformational changes and domain-domain interactions facilitate Cu movement through the membrane, and, finally, how target polypeptides are loaded with Cu in the Golgi) remain elusive.	Copper	93-95	ATPase copper transporting alpha	Homo sapiens	76-81
26033426-1	2015	INTRODUCTION: This study is to evaluate the association of polymorphisms of glutathione S-transferase P1 (GSTP1), copper-transporting P-type adenosine triphosphatase A (ATP7A) and X-ray repair cross-complementing group 1 (XRCC1) with the efficacy and toxicity of cisplatin-based treatment in advanced non-small cell lung cancer (NSCLC) patients.	Cisplatin	263-272	ATPase copper transporting alpha	Homo sapiens	169-174
26732058-2	2015	The ATP7A protein is a copper (Cu)-transporting ATPase expressed in all tissues and plays a critical role in the maintenance of copper homeostasis in cells of the whole body.	Copper	23-29	ATPase copper transporting alpha	Homo sapiens	4-9
26732058-2	2015	The ATP7A protein is a copper (Cu)-transporting ATPase expressed in all tissues and plays a critical role in the maintenance of copper homeostasis in cells of the whole body.	Copper	128-134	ATPase copper transporting alpha	Homo sapiens	4-9
26732058-3	2015	ATP7A participates in copper absorption in the small intestine and in copper transport to the central nervous system (CNS) across the blood-brain-barrier (BBB) and blood-cerebrospinal fluid barrier (BCSFB).	Copper	22-28	ATPase copper transporting alpha	Homo sapiens	0-5
26732058-3	2015	ATP7A participates in copper absorption in the small intestine and in copper transport to the central nervous system (CNS) across the blood-brain-barrier (BBB) and blood-cerebrospinal fluid barrier (BCSFB).	Copper	70-76	ATPase copper transporting alpha	Homo sapiens	0-5
26732058-5	2015	In cells, ATP7A participates in the incorporation of copper into Cu-dependent enzymes during the course of its maturation in the secretory pathway.	Copper	53-59	ATPase copper transporting alpha	Homo sapiens	10-15
26732058-5	2015	In cells, ATP7A participates in the incorporation of copper into Cu-dependent enzymes during the course of its maturation in the secretory pathway.	Copper	65-67	ATPase copper transporting alpha	Homo sapiens	10-15
25583185-1	2015	ATP7A mutations impair copper metabolism resulting in three distinct genetic disorders in humans.	Copper	23-29	ATPase copper transporting alpha	Homo sapiens	0-5
25800647-0	2015	Discovery of 4-(dihydropyridinon-3-yl)amino-5-methylthieno[2,3-d]pyrimidine derivatives as potent Mnk inhibitors: synthesis, structure-activity relationship analysis and biological evaluation.	4-(dihydropyridinon-3-yl)amino-5-methylthieno[2,3-d]pyrimidine	13-75	ATPase copper transporting alpha	Homo sapiens	98-101
25639447-6	2015	Taken together, these data reveal autonomous requirements for ATP7A that reveal essential roles for copper in the maintenance and function of the motor neuron, and suggest that SMAX3 is caused by a loss of ATP7A function that specifically impacts the spinal motor neuron.	Copper	100-106	ATPase copper transporting alpha	Homo sapiens	62-67
25800647-3	2015	Herein, we report the discovery of 4-(dihydropyridinon-3-yl)amino-5-methylthieno[2,3-d]pyrimidine derivatives as potent Mnk inhibitors.	4-(dihydropyridinon-3-yl)amino-5-methylthieno[2,3-d]pyrimidine	35-97	ATPase copper transporting alpha	Homo sapiens	120-123
25801007-11	2015	Taken together, this study provides insight into that the co-manipulation of hCtrl and ATP7A by D-penicillamine could increase the therapeutic efficacy of platinum drugs in oxaliplatin resistant tumors, especially in resistant phenotype with downexpression of hCtrl and overexpression of ATP7A.	Penicillamine	96-111	ATPase copper transporting alpha	Homo sapiens	87-92
25801007-11	2015	Taken together, this study provides insight into that the co-manipulation of hCtrl and ATP7A by D-penicillamine could increase the therapeutic efficacy of platinum drugs in oxaliplatin resistant tumors, especially in resistant phenotype with downexpression of hCtrl and overexpression of ATP7A.	Penicillamine	96-111	ATPase copper transporting alpha	Homo sapiens	288-293
25801007-11	2015	Taken together, this study provides insight into that the co-manipulation of hCtrl and ATP7A by D-penicillamine could increase the therapeutic efficacy of platinum drugs in oxaliplatin resistant tumors, especially in resistant phenotype with downexpression of hCtrl and overexpression of ATP7A.	Oxaliplatin	173-184	ATPase copper transporting alpha	Homo sapiens	87-92
25337692-0	2015	Omeprazole, a gastric proton pump inhibitor, inhibits melanogenesis by blocking ATP7A trafficking.	Omeprazole	0-10	ATPase copper transporting alpha	Homo sapiens	80-85
25574028-6	2015	We show that adaptor protein (AP) complexes 1 and 2 physically interact with ATP7A and that binding is mediated in part by a carboxyl-terminal di-leucine motif.	di-leucine	143-153	ATPase copper transporting alpha	Homo sapiens	77-82
25574028-7	2015	In contrast to other ATP7A missense mutations, ATP7A(P1386S) partially disturbs interactions with both APs, leading to abnormal axonal localization in transfected NSC-34 motor neurons and altered calcium-signaling following glutamate stimulation.	Adenosine Phosphosulfate	103-106	ATPase copper transporting alpha	Homo sapiens	47-52
25574028-7	2015	In contrast to other ATP7A missense mutations, ATP7A(P1386S) partially disturbs interactions with both APs, leading to abnormal axonal localization in transfected NSC-34 motor neurons and altered calcium-signaling following glutamate stimulation.	Calcium	196-203	ATPase copper transporting alpha	Homo sapiens	47-52
25574028-7	2015	In contrast to other ATP7A missense mutations, ATP7A(P1386S) partially disturbs interactions with both APs, leading to abnormal axonal localization in transfected NSC-34 motor neurons and altered calcium-signaling following glutamate stimulation.	Glutamic Acid	224-233	ATPase copper transporting alpha	Homo sapiens	47-52
25337692-5	2015	Although melanocytes do not express ATP4A, they do express ATP7A, a copper transporting P-type ATPase in the trans-Golgi network that is required for copper acquisition by tyrosinase.	Copper	68-74	ATPase copper transporting alpha	Homo sapiens	59-64
25337692-6	2015	ATP7A relocalization from the trans-Golgi network to the plasma membrane in response to elevated copper concentrations in melanocytes was inhibited by omeprazole.	Copper	97-103	ATPase copper transporting alpha	Homo sapiens	0-5
25337692-6	2015	ATP7A relocalization from the trans-Golgi network to the plasma membrane in response to elevated copper concentrations in melanocytes was inhibited by omeprazole.	Omeprazole	151-161	ATPase copper transporting alpha	Homo sapiens	0-5
25337692-9	2015	Our findings are consistent with the hypothesis that omeprazole reduces melanogenesis by inhibiting ATP7A and by enhancing degradation of tyrosinase.	Omeprazole	53-63	ATPase copper transporting alpha	Homo sapiens	100-105
25634130-0	2015	Novel C-4 heteroaryl 13-cis-retinamide Mnk/AR degrading agents inhibit cell proliferation and migration and induce apoptosis in human breast and prostate cancer cells and suppress growth of MDA-MB-231 human breast and CWR22Rv1 human prostate tumor xenografts in mice.	13-cis-retinamide	21-38	ATPase copper transporting alpha	Homo sapiens	39-42
25527453-7	2015	In KYO-1 cells where Akt is not constitutively active, Mnk inhibitors increase the sensitivity of cells to rapamycin, resulting in a more pronounced anti-proliferative activity.	Sirolimus	107-116	ATPase copper transporting alpha	Homo sapiens	55-58
25634130-1	2015	The synthesis and in vitro and in vivo antibreast and antiprostate cancers activities of novel C-4 heteroaryl 13-cis-retinamides that modulate Mnk-eIF4E and AR signaling are discussed.	13-cis-retinamides	110-128	ATPase copper transporting alpha	Homo sapiens	143-146
25228517-7	2014	In turn, mutations of the ATP7A and PAH genes, regulating intracellular copper concentration and activity of phenylalanine hydroxylase, lead to Menkes syndrome and phenylketonuria.	Copper	72-78	ATPase copper transporting alpha	Homo sapiens	26-31
26598820-10	2015	Specifically, TRPM6 channels in Mg absorption, ZIP4 and ZnT1 transporters for Zn absorption, and CTR1 and ATP7A for Cu absorption are overviewed.	Copper	116-118	ATPase copper transporting alpha	Homo sapiens	106-111
25962064-1	2015	After Ctr1-mediated cell uptake, copper (Cu) is transported by the cytoplasmic Cu chaperone Atox1 to P1B type ATPases ATP7A and ATP7B in the Golgi network, for incorporation into Cudependent enzymes.	Copper	33-39	ATPase copper transporting alpha	Homo sapiens	118-123
25962064-1	2015	After Ctr1-mediated cell uptake, copper (Cu) is transported by the cytoplasmic Cu chaperone Atox1 to P1B type ATPases ATP7A and ATP7B in the Golgi network, for incorporation into Cudependent enzymes.	Copper	41-43	ATPase copper transporting alpha	Homo sapiens	118-123
25759057-2	2015	It is caused by defective intestinal absorption of copper resulting from a deficiency of a copper-transporting ATPase, ATP7A.	Copper	51-57	ATPase copper transporting alpha	Homo sapiens	119-124
25257349-1	2014	GNE myopathy is an autosomal recessive muscular disorder caused by mutations in the gene encoding the key enzyme in sialic acid biosynthesis, UDP-N-acetylglucosamine 2-epimerase/N-acetylmannosamine kinase (GNE/MNK).	N-Acetylneuraminic Acid	116-127	ATPase copper transporting alpha	Homo sapiens	210-213
25257349-6	2014	Alternatively, it is possible that the decreased activity of GNE/MNK itself, which would lead to decreased sialic content in platelets, is associated with thrombocytopenia in these patients.	sialic	107-113	ATPase copper transporting alpha	Homo sapiens	65-68
25187541-6	2014	Rather, MNK catalytic activity enabled viral IRES-mediated translation/host cell cytotoxicity through negative regulation of the Ser/Arg (SR)-rich protein kinase (SRPK).	Serine	129-132	ATPase copper transporting alpha	Homo sapiens	8-11
25187541-6	2014	Rather, MNK catalytic activity enabled viral IRES-mediated translation/host cell cytotoxicity through negative regulation of the Ser/Arg (SR)-rich protein kinase (SRPK).	Arginine	133-136	ATPase copper transporting alpha	Homo sapiens	8-11
25242165-4	2014	A specific component of copper ATPases is the NMBD (N-terminal metal-binding domain), containing up to six copper-binding sites in mammalian (ATP7A and ATP7B) enzymes.	Metals	63-68	ATPase copper transporting alpha	Homo sapiens	142-147
25242165-4	2014	A specific component of copper ATPases is the NMBD (N-terminal metal-binding domain), containing up to six copper-binding sites in mammalian (ATP7A and ATP7B) enzymes.	Copper	24-30	ATPase copper transporting alpha	Homo sapiens	142-147
25242165-8	2014	Cisplatin, a platinum-containing anti-cancer drug, binds to copper sites of ATP7A and ATP7B, and undergoes vectorial displacement in analogy with copper.	Cisplatin	0-9	ATPase copper transporting alpha	Homo sapiens	76-81
25242165-8	2014	Cisplatin, a platinum-containing anti-cancer drug, binds to copper sites of ATP7A and ATP7B, and undergoes vectorial displacement in analogy with copper.	Platinum	13-21	ATPase copper transporting alpha	Homo sapiens	76-81
25242165-8	2014	Cisplatin, a platinum-containing anti-cancer drug, binds to copper sites of ATP7A and ATP7B, and undergoes vectorial displacement in analogy with copper.	Copper	60-66	ATPase copper transporting alpha	Homo sapiens	76-81
25070243-8	2014	Importantly, we demonstrated for the first time that PDTC downregulated the expression of ATP7A, known to be responsible for Cu efflux, but did not affect the expression of CTR1, known as a copper uptake transporter.	Copper	125-127	ATPase copper transporting alpha	Homo sapiens	90-95
25070243-10	2014	Given that ATP7A plays a critical role in the resistance of platinum-drug (such as cisplatin) representing a first-line treatment for SCLC, PDTC could be a promising candidate of adjunct therapeutic reagent for the patients requiring treatment with platinum-based regimens.	Cisplatin	83-92	ATPase copper transporting alpha	Homo sapiens	11-16
25070243-10	2014	Given that ATP7A plays a critical role in the resistance of platinum-drug (such as cisplatin) representing a first-line treatment for SCLC, PDTC could be a promising candidate of adjunct therapeutic reagent for the patients requiring treatment with platinum-based regimens.	Platinum	60-68	ATPase copper transporting alpha	Homo sapiens	11-16
25281031-10	2014	We conclude that early copper histidine for Menkes disease is safe and efficacious, with treatment outcomes influenced by the timing of intervention, and ATP7A mutation.	copper histidine	23-39	ATPase copper transporting alpha	Homo sapiens	154-159
25685999-6	2015	Then we propose the binding mode of CGP57380 to active Mnk2, and evaluate key interactions that could be critical for future Mnk-targeted inhibitors.	CGP 57380	36-44	ATPase copper transporting alpha	Homo sapiens	55-58
25172213-11	2015	At low copper levels, ATP7A locates to the Trans-Golgi Network (TGN) to load cuproenzymes with copper, whereas at higher concentrations, ATP7A shifts to the post-Golgi compartments or to the plasma membrane to export copper out of the cell.	Copper	7-13	ATPase copper transporting alpha	Homo sapiens	22-27
25172213-11	2015	At low copper levels, ATP7A locates to the Trans-Golgi Network (TGN) to load cuproenzymes with copper, whereas at higher concentrations, ATP7A shifts to the post-Golgi compartments or to the plasma membrane to export copper out of the cell.	Copper	95-101	ATPase copper transporting alpha	Homo sapiens	22-27
25172213-11	2015	At low copper levels, ATP7A locates to the Trans-Golgi Network (TGN) to load cuproenzymes with copper, whereas at higher concentrations, ATP7A shifts to the post-Golgi compartments or to the plasma membrane to export copper out of the cell.	Copper	95-101	ATPase copper transporting alpha	Homo sapiens	22-27
25172213-12	2015	Impaired copper-regulation trafficking has been observed for ATP7A mutants, but its impact on the clinical outcome is not clear.	Copper	9-15	ATPase copper transporting alpha	Homo sapiens	61-66
25355947-5	2015	We show that 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 mutations.	Copper	66-72	ATPase copper transporting alpha	Homo sapiens	118-123
25355947-5	2015	We show that 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 mutations.	Copper	99-105	ATPase copper transporting alpha	Homo sapiens	118-123
25355947-5	2015	We show that 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 mutations.	Copper	99-105	ATPase copper transporting alpha	Homo sapiens	118-123
25962064-2	2015	Atox1 is a small 68-residue protein that binds Cu in a conserved CXXC motif; it delivers Cu to target domains in ATP7A/B via direct protein-protein interactions.	Copper	89-91	ATPase copper transporting alpha	Homo sapiens	113-120
25150085-1	2014	OBJECTIVE: To explore the changes in the body weight and height of Menkes disease (MNK) patients treated with long-term copper-histidine.	copper histidine	120-136	ATPase copper transporting alpha	Homo sapiens	83-86
25150085-8	2014	We suggest that the establishment of sufficient nutritional support is necessary along with early parenteral copper treatment to improve whole body condition in MNK patients.	Copper	109-115	ATPase copper transporting alpha	Homo sapiens	161-164
25156967-1	2014	The Menkes copper-transporting ATPase (Atp7a) has dual roles in mammalian enterocytes: pumping copper into the trans-Golgi network (to support cuproenzyme synthesis) and across the basolateral membrane (to deliver dietary copper to the blood).	Copper	11-17	ATPase copper transporting alpha	Homo sapiens	39-44
25156967-1	2014	The Menkes copper-transporting ATPase (Atp7a) has dual roles in mammalian enterocytes: pumping copper into the trans-Golgi network (to support cuproenzyme synthesis) and across the basolateral membrane (to deliver dietary copper to the blood).	Copper	95-101	ATPase copper transporting alpha	Homo sapiens	39-44
24816595-7	2014	These effects are consistent with a role for GRX1 in regulating ATP7A-mediated copper export, and further support a new function for GRX1 in neuronal copper homeostasis and in protection from copper-mediated oxidative injury.	Copper	79-85	ATPase copper transporting alpha	Homo sapiens	64-69
24983998-2	2014	This is related to the drug binding to proteins such as the copper influx transporter Ctr1, the copper chaperone Atox1, and the copper pumps ATP7A and ATP7B.	Copper	60-66	ATPase copper transporting alpha	Homo sapiens	141-146
24983998-2	2014	This is related to the drug binding to proteins such as the copper influx transporter Ctr1, the copper chaperone Atox1, and the copper pumps ATP7A and ATP7B.	Copper	96-102	ATPase copper transporting alpha	Homo sapiens	141-146
24983998-4	2014	Here we investigate the interaction of cisplatin with the first soluble domain of ATP7A.	Cisplatin	39-48	ATPase copper transporting alpha	Homo sapiens	82-87
24983998-7	2014	These calculations show quantitative agreement with CD spectra and (1)H, (13)C, and (15)N NMR chemical shifts, thus providing a quantitative molecular view of the 3D binding mode of cisplatin to ATP7A.	Cadmium	52-54	ATPase copper transporting alpha	Homo sapiens	195-200
24983998-7	2014	These calculations show quantitative agreement with CD spectra and (1)H, (13)C, and (15)N NMR chemical shifts, thus providing a quantitative molecular view of the 3D binding mode of cisplatin to ATP7A.	Cisplatin	182-191	ATPase copper transporting alpha	Homo sapiens	195-200
24983998-9	2014	Using this combined in silico-in vitro approach we provide here for the first time a quantitative 3D atomic view of the platinum binding to the first soluble domain of ATP7A.	Platinum	120-128	ATPase copper transporting alpha	Homo sapiens	168-173
25170252-1	2014	BACKGROUND: XARTEMIS  XR (formerly MNK-795) is a combination oxycodone (OC) and acetaminophen (APAP) analgesic with both immediate-release and extended-release (ER) components (ER OC/APAP).	Oxycodone	61-70	ATPase copper transporting alpha	Homo sapiens	35-38
25170252-1	2014	BACKGROUND: XARTEMIS  XR (formerly MNK-795) is a combination oxycodone (OC) and acetaminophen (APAP) analgesic with both immediate-release and extended-release (ER) components (ER OC/APAP).	Oxycodone	72-74	ATPase copper transporting alpha	Homo sapiens	35-38
25170252-1	2014	BACKGROUND: XARTEMIS  XR (formerly MNK-795) is a combination oxycodone (OC) and acetaminophen (APAP) analgesic with both immediate-release and extended-release (ER) components (ER OC/APAP).	Acetaminophen	80-93	ATPase copper transporting alpha	Homo sapiens	35-38
25170252-1	2014	BACKGROUND: XARTEMIS  XR (formerly MNK-795) is a combination oxycodone (OC) and acetaminophen (APAP) analgesic with both immediate-release and extended-release (ER) components (ER OC/APAP).	Acetaminophen	95-99	ATPase copper transporting alpha	Homo sapiens	35-38
24816595-3	2014	Previously we demonstrated that GRX1/GSH regulates the activity of the essential copper-transporting P1B-Type ATPases (ATP7A, ATP7B) in a copper-responsive manner.	Glutathione	37-40	ATPase copper transporting alpha	Homo sapiens	119-124
24816595-3	2014	Previously we demonstrated that GRX1/GSH regulates the activity of the essential copper-transporting P1B-Type ATPases (ATP7A, ATP7B) in a copper-responsive manner.	Copper	81-87	ATPase copper transporting alpha	Homo sapiens	119-124
24816595-7	2014	These effects are consistent with a role for GRX1 in regulating ATP7A-mediated copper export, and further support a new function for GRX1 in neuronal copper homeostasis and in protection from copper-mediated oxidative injury.	Copper	150-156	ATPase copper transporting alpha	Homo sapiens	64-69
24824562-2	2014	In humans, the cytoplasmic Cu chaperone Atox1 delivers Cu to metal-binding domains of ATP7A/B in the Golgi, for incorporation into Cu-dependent proteins.	Metals	61-66	ATPase copper transporting alpha	Homo sapiens	86-93
24824562-2	2014	In humans, the cytoplasmic Cu chaperone Atox1 delivers Cu to metal-binding domains of ATP7A/B in the Golgi, for incorporation into Cu-dependent proteins.	Copper	55-57	ATPase copper transporting alpha	Homo sapiens	86-93
24824562-2	2014	In humans, the cytoplasmic Cu chaperone Atox1 delivers Cu to metal-binding domains of ATP7A/B in the Golgi, for incorporation into Cu-dependent proteins.	Copper	27-29	ATPase copper transporting alpha	Homo sapiens	86-93
24824562-3	2014	The Cu-binding motif in Atox1, as well as in target Cu-binding domains of ATP7A/B, consists of a MX1CXXC motif where X1 = T. The same motif, with X1 = D, is found in metal-binding domains of bacterial zinc transporters, such as ZntA.	Copper	4-6	ATPase copper transporting alpha	Homo sapiens	74-81
24824562-3	2014	The Cu-binding motif in Atox1, as well as in target Cu-binding domains of ATP7A/B, consists of a MX1CXXC motif where X1 = T. The same motif, with X1 = D, is found in metal-binding domains of bacterial zinc transporters, such as ZntA.	Copper	52-54	ATPase copper transporting alpha	Homo sapiens	74-81
24824562-3	2014	The Cu-binding motif in Atox1, as well as in target Cu-binding domains of ATP7A/B, consists of a MX1CXXC motif where X1 = T. The same motif, with X1 = D, is found in metal-binding domains of bacterial zinc transporters, such as ZntA.	Metals	166-171	ATPase copper transporting alpha	Homo sapiens	74-81
24038379-0	2014	miR-495 enhances the sensitivity of non-small cell lung cancer cells to platinum by modulation of copper-transporting P-type adenosine triphosphatase A (ATP7A).	Platinum	72-80	ATPase copper transporting alpha	Homo sapiens	153-158
24038379-1	2014	Copper-transporting P-type adenosine triphosphatase A (ATP7A) is associated with platinum drug resistance in non-small cell lung cancer (NSCLC).	Platinum	81-89	ATPase copper transporting alpha	Homo sapiens	55-60
24038379-3	2014	In this study, the aim is to explore which miRNAs might participate in the platinum resistance by targeting ATP7A in NSCLC.	Platinum	75-83	ATPase copper transporting alpha	Homo sapiens	108-113
24038379-9	2014	Finally, we discovered that there was a converse relationship between miR-495 and ATP7A levels in NSCLC tissues sensitive or resistant to CDDP.	cddp	138-142	ATPase copper transporting alpha	Homo sapiens	82-87
24316150-9	2014	Taken together, these data indicate that CTR1 and ATP7A play important roles in Cu transport in choroidal epithelial cells, and the Pb-induced intracellular Cu accumulation appears to be mediated, at least in part, via the alteration of CTR1 and ATP7A expression levels following Pb exposure.	Copper	80-82	ATPase copper transporting alpha	Homo sapiens	50-55
24789146-2	2014	ATP7A and ATP7B (the Menkes and Wilson disease proteins, respectively) appear to be implicated in promoting tumor cell resistance to cisplatin.	Cisplatin	133-142	ATPase copper transporting alpha	Homo sapiens	0-5
24789146-4	2014	Here, we report the spectroscopic characterization of cisplatin binding to ATOX1 and MNK1, the first metal-binding domain of ATP7A, in the presence of the physiological reducing agent glutathione, a sulfur-containing molecule responsible for the majority of Pt detoxification in the cytosol.	Cisplatin	54-63	ATPase copper transporting alpha	Homo sapiens	125-130
24789146-4	2014	Here, we report the spectroscopic characterization of cisplatin binding to ATOX1 and MNK1, the first metal-binding domain of ATP7A, in the presence of the physiological reducing agent glutathione, a sulfur-containing molecule responsible for the majority of Pt detoxification in the cytosol.	Metals	101-106	ATPase copper transporting alpha	Homo sapiens	125-130
24789146-4	2014	Here, we report the spectroscopic characterization of cisplatin binding to ATOX1 and MNK1, the first metal-binding domain of ATP7A, in the presence of the physiological reducing agent glutathione, a sulfur-containing molecule responsible for the majority of Pt detoxification in the cytosol.	Glutathione	184-195	ATPase copper transporting alpha	Homo sapiens	125-130
24789146-4	2014	Here, we report the spectroscopic characterization of cisplatin binding to ATOX1 and MNK1, the first metal-binding domain of ATP7A, in the presence of the physiological reducing agent glutathione, a sulfur-containing molecule responsible for the majority of Pt detoxification in the cytosol.	Sulfur	199-205	ATPase copper transporting alpha	Homo sapiens	125-130
24754424-3	2014	MEDNIK syndrome is caused by mutation of the AP1S1 gene, which codes for the sigma1A subunit of adaptor protein complex 1, and directs intracellular trafficking of copper pumps ATP7A and ATP7B.	Copper	164-170	ATPase copper transporting alpha	Homo sapiens	177-182
24677692-4	2014	Herein, we report, for the first time, the discovery of a series of 5-(2-(phenylamino)pyrimidin-4-yl)thiazole-2(3H)-one derivatives as Mnk inhibitors.	5-(2-(phenylamino)pyrimidin-4-yl)thiazole-2(3h)-one	68-119	ATPase copper transporting alpha	Homo sapiens	135-138
24388330-1	2014	OBJECTIVE: To examine levels of lactate (LA) and pyruvate (PA) in both blood and cerebrospinal fluid (CSF) in patients with Menkes disease (MNK).	Lactic Acid	32-39	ATPase copper transporting alpha	Homo sapiens	140-143
24388330-1	2014	OBJECTIVE: To examine levels of lactate (LA) and pyruvate (PA) in both blood and cerebrospinal fluid (CSF) in patients with Menkes disease (MNK).	Pyruvic Acid	49-57	ATPase copper transporting alpha	Homo sapiens	140-143
24388330-1	2014	OBJECTIVE: To examine levels of lactate (LA) and pyruvate (PA) in both blood and cerebrospinal fluid (CSF) in patients with Menkes disease (MNK).	Pyruvic Acid	59-61	ATPase copper transporting alpha	Homo sapiens	140-143
24388330-8	2014	CONCLUSION: Our findings suggest that LA and PA levels, and in particular, the L/P ratio, and blood gas analysis can be used to guide the diagnosis and management of MNK.	Pyruvic Acid	45-47	ATPase copper transporting alpha	Homo sapiens	166-169
24614111-5	2014	In vitro experiments show that exposure to hypoxia or treatment with cobalt (CoCl2) also increased protein expression of CTR1, ATP7A, and LOX in pulmonary arterial smooth muscle cells (PASMC).	Cobalt	69-75	ATPase copper transporting alpha	Homo sapiens	127-132
24614111-5	2014	In vitro experiments show that exposure to hypoxia or treatment with cobalt (CoCl2) also increased protein expression of CTR1, ATP7A, and LOX in pulmonary arterial smooth muscle cells (PASMC).	cobaltous chloride	77-82	ATPase copper transporting alpha	Homo sapiens	127-132
24614111-9	2014	In summary, the data from this study indicate that increased Cu transportation due to upregulated CTR1 and ATP7A in pulmonary arteries and PASMC contributes to the development of hypoxia-induced pulmonary hypertension.	Copper	61-63	ATPase copper transporting alpha	Homo sapiens	107-112
25076894-4	2014	We propose increased copper levels as a direct effect of estrogen intake due to an augmented ATP7A-mRNA in the intestine.	Copper	21-27	ATPase copper transporting alpha	Homo sapiens	93-98
24316150-0	2014	Involvement of CTR1 and ATP7A in lead (Pb)-induced copper (Cu) accumulation in choroidal epithelial cells.	Lead	39-41	ATPase copper transporting alpha	Homo sapiens	24-29
24316150-6	2014	The expression level of ATP7A was down-regulated following the Pb exposure.	Lead	63-65	ATPase copper transporting alpha	Homo sapiens	24-29
24316150-7	2014	ATP7A siRNA knockdown, or PCMB treatment, inhibited the (64)Cu efflux from the cells, while the following additional incubation with Pb failed to further increase the intracellular (64)Cu retention.	Copper	60-62	ATPase copper transporting alpha	Homo sapiens	0-5
24316150-9	2014	Taken together, these data indicate that CTR1 and ATP7A play important roles in Cu transport in choroidal epithelial cells, and the Pb-induced intracellular Cu accumulation appears to be mediated, at least in part, via the alteration of CTR1 and ATP7A expression levels following Pb exposure.	Lead	132-134	ATPase copper transporting alpha	Homo sapiens	246-251
24041990-2	2014	It was reported to modulate active copper extrusion from cells, by affecting the function of the pumps ATP7A and B.	Copper	35-41	ATPase copper transporting alpha	Homo sapiens	103-114
24375922-6	2014	We then used NMR spectroscopy and ESI-MS to determine the binding mode of these drugs to the first N-terminal metal-binding domain of ATP7A (Mnk1).	Metals	110-115	ATPase copper transporting alpha	Homo sapiens	134-139
23988033-4	2014	The copper (Cu) transport proteins Ctr1 and ATP7A/B have been implicated in cellular resistance of CisPt, possibly exporting the drug out of the cell.	Copper	4-10	ATPase copper transporting alpha	Homo sapiens	44-51
24365357-3	2014	Copper disorders are divided into two classes: ATP7A- or ATP7B-related inherited copper transport disorders (Menkes disease, occipital horn syndrome, ATP7A-related distal motor neuropathy, and Wilson disease) and acquired diseases associated with copper deficiency or copper excess.	Copper	81-87	ATPase copper transporting alpha	Homo sapiens	47-52
24672633-7	2014	Some of the proteins involved in copper transport are the transporters CTR1, ATP7A, and ATP7B and the chaperone ATOX1.	Copper	33-39	ATPase copper transporting alpha	Homo sapiens	77-82
23988033-4	2014	The copper (Cu) transport proteins Ctr1 and ATP7A/B have been implicated in cellular resistance of CisPt, possibly exporting the drug out of the cell.	Cisplatin	99-104	ATPase copper transporting alpha	Homo sapiens	44-51
23963605-2	2013	It has been proposed that copper transporter 1 (CTR1) and the divalent metal transporter 1 (DMT1) translocate copper across the human intestinal epithelium, while Cu-ATPases: ATP7A and ATP7B serve as copper efflux pumps.	Copper	163-165	ATPase copper transporting alpha	Homo sapiens	175-180
23978201-4	2013	In this work, we investigated the electronic structure of the Cu(I)-S interactions during the copper transfer between Atox1 and a metal binding domain on the ATP7A or ATP7B protein.	Copper	94-100	ATPase copper transporting alpha	Homo sapiens	158-163
24056613-7	2013	In addition, Cu(i)-mediated hetero-protein interactions with ATP7A are present in the metal transfer of both Atox1 variants, although copper transfer is accompanied with smaller structural alteration in the K60A mutant.	cuprous ion	13-18	ATPase copper transporting alpha	Homo sapiens	61-66
24056613-7	2013	In addition, Cu(i)-mediated hetero-protein interactions with ATP7A are present in the metal transfer of both Atox1 variants, although copper transfer is accompanied with smaller structural alteration in the K60A mutant.	Metals	86-91	ATPase copper transporting alpha	Homo sapiens	61-66
24122981-3	2013	Several transporters are able to mediate the movement of cisplatin across the plasma membranes: Copper transporter-1 (Ctr1), copper transporter-2 (Ctr2), P-type copper-transporting ATPases ATP7A and ATP7B, organic cation transporter-2 (OCT2), and multidrug extrusion transporter-1 (MATE1).	Cisplatin	57-66	ATPase copper transporting alpha	Homo sapiens	189-194
23933386-2	2013	We previously demonstrated that increased DNA repair capacity and copper-transporting ATPase 1 (ATP7A) level contributed to oxaliplatin resistance in the human gastric carcinoma cell line TSGH-S3 (S3).	Oxaliplatin	124-135	ATPase copper transporting alpha	Homo sapiens	66-94
23933386-2	2013	We previously demonstrated that increased DNA repair capacity and copper-transporting ATPase 1 (ATP7A) level contributed to oxaliplatin resistance in the human gastric carcinoma cell line TSGH-S3 (S3).	Oxaliplatin	124-135	ATPase copper transporting alpha	Homo sapiens	96-101
23978201-4	2013	In this work, we investigated the electronic structure of the Cu(I)-S interactions during the copper transfer between Atox1 and a metal binding domain on the ATP7A or ATP7B protein.	Metals	130-135	ATPase copper transporting alpha	Homo sapiens	158-163
23751120-1	2013	Human copper transporters ATP7B (Wilson"s disease protein) and ATP7A (Menkes" disease protein) have been implicated in tumour resistance to cisplatin, a widely used anticancer drug.	Cisplatin	140-149	ATPase copper transporting alpha	Homo sapiens	63-68
23978201-9	2013	The transfer of Cu(I) from the Atox1 metallochaperone to a metal binding domain of the ATP7A or ATP7B protein was then modeled by using the CGGC Atox1 binding site for the donor model and the dithiotreitol ligand (DTT) for the acceptor model.	cuprous ion	16-21	ATPase copper transporting alpha	Homo sapiens	87-92
23978201-9	2013	The transfer of Cu(I) from the Atox1 metallochaperone to a metal binding domain of the ATP7A or ATP7B protein was then modeled by using the CGGC Atox1 binding site for the donor model and the dithiotreitol ligand (DTT) for the acceptor model.	Metals	37-42	ATPase copper transporting alpha	Homo sapiens	87-92
23978201-9	2013	The transfer of Cu(I) from the Atox1 metallochaperone to a metal binding domain of the ATP7A or ATP7B protein was then modeled by using the CGGC Atox1 binding site for the donor model and the dithiotreitol ligand (DTT) for the acceptor model.	Dithiothreitol	192-205	ATPase copper transporting alpha	Homo sapiens	87-92
23978201-9	2013	The transfer of Cu(I) from the Atox1 metallochaperone to a metal binding domain of the ATP7A or ATP7B protein was then modeled by using the CGGC Atox1 binding site for the donor model and the dithiotreitol ligand (DTT) for the acceptor model.	Dithiothreitol	214-217	ATPase copper transporting alpha	Homo sapiens	87-92
23846821-3	2013	The Golgi complex harbors copper-transporting ATPases, ATP7A and ATP7B that transfer copper from the cytosol into Golgi lumen for incorporation into copper-dependent enzymes.	Copper	85-91	ATPase copper transporting alpha	Homo sapiens	55-60
23751120-7	2013	Transfer of platinum along the copper-transport pathways in the cell may serve as a mechanism of drug delivery to its target in the cell nucleus, and explain tumour-cell resistance to cisplatin associated with the overexpression of copper transporters ATP7B and ATP7A.	Platinum	12-20	ATPase copper transporting alpha	Homo sapiens	262-267
23751120-7	2013	Transfer of platinum along the copper-transport pathways in the cell may serve as a mechanism of drug delivery to its target in the cell nucleus, and explain tumour-cell resistance to cisplatin associated with the overexpression of copper transporters ATP7B and ATP7A.	Copper	31-37	ATPase copper transporting alpha	Homo sapiens	262-267
23751120-7	2013	Transfer of platinum along the copper-transport pathways in the cell may serve as a mechanism of drug delivery to its target in the cell nucleus, and explain tumour-cell resistance to cisplatin associated with the overexpression of copper transporters ATP7B and ATP7A.	Cisplatin	184-193	ATPase copper transporting alpha	Homo sapiens	262-267
23596324-1	2013	The transporter ATP7A mediates systemic copper absorption and provides cuproenzymes in the trans-Golgi network (TGN) with copper.	Copper	40-46	ATPase copper transporting alpha	Homo sapiens	16-21
22797067-6	2013	Importantly, pharmacological inhibition of MNK activity synergistically enhanced the cytostatic effect of gemcitabine, by promoting apoptosis.	gemcitabine	106-117	ATPase copper transporting alpha	Homo sapiens	43-46
22797067-9	2013	Silencing of SRSF1 by RNAi abolished this splicing event and recapitulated the effects of MNK pharmacological or genetic inhibition on eIF4E phosphorylation and apoptosis in gemcitabine-treated cells.	gemcitabine	174-185	ATPase copper transporting alpha	Homo sapiens	90-93
22797067-10	2013	Our results highlight a novel pro-survival pathway triggered by gemcitabine in PDAC cells, which leads to MNK2-dependent phosphorylation of eIF4E, suggesting that the MNK/eIF4E pathway represents an escape route utilized by PDAC cells to withstand chemotherapeutic treatments.	gemcitabine	64-75	ATPase copper transporting alpha	Homo sapiens	106-109
23596324-1	2013	The transporter ATP7A mediates systemic copper absorption and provides cuproenzymes in the trans-Golgi network (TGN) with copper.	Copper	122-128	ATPase copper transporting alpha	Homo sapiens	16-21
23596324-2	2013	To regulate metal homeostasis, ATP7A constitutively cycles between the TGN and plasma membrane (PM).	Metals	12-17	ATPase copper transporting alpha	Homo sapiens	31-36
23596324-3	2013	ATP7A trafficking to the PM is elevated in response to increased copper load and is reversed when copper concentrations are lowered.	Copper	65-71	ATPase copper transporting alpha	Homo sapiens	0-5
23596324-3	2013	ATP7A trafficking to the PM is elevated in response to increased copper load and is reversed when copper concentrations are lowered.	Copper	98-104	ATPase copper transporting alpha	Homo sapiens	0-5
23596324-8	2013	Expression of the GTP-locked Rab22aQ64L mutant caused fragmentation of TGN membrane domains enriched for ATP7A.	Guanosine Triphosphate	18-21	ATPase copper transporting alpha	Homo sapiens	105-110
23596324-8	2013	Expression of the GTP-locked Rab22aQ64L mutant caused fragmentation of TGN membrane domains enriched for ATP7A.	rab22aq64l	29-39	ATPase copper transporting alpha	Homo sapiens	105-110
23596324-10	2013	Of importance, ATP7A remained in the Rab22aQ64L-generated structures after copper treatment and washout, suggesting that forward trafficking out of this compartment was blocked.	rab22aq64l	37-47	ATPase copper transporting alpha	Homo sapiens	15-20
23596324-10	2013	Of importance, ATP7A remained in the Rab22aQ64L-generated structures after copper treatment and washout, suggesting that forward trafficking out of this compartment was blocked.	Copper	75-81	ATPase copper transporting alpha	Homo sapiens	15-20
23345593-0	2013	COX19 mediates the transduction of a mitochondrial redox signal from SCO1 that regulates ATP7A-mediated cellular copper efflux.	Copper	113-119	ATPase copper transporting alpha	Homo sapiens	89-94
23437777-3	2013	The bifunctional enzyme UDP-GlcNAc 2-epimerase/ManNAc kinase (GNE/MNK), encoded by the GNE gene, catalyzes the first two committed, rate-limiting steps in the biosynthesis of N-acetylneunaminic acid (sialic acid).	Uridine Diphosphate N-Acetylglucosamine	24-34	ATPase copper transporting alpha	Homo sapiens	66-69
23437777-3	2013	The bifunctional enzyme UDP-GlcNAc 2-epimerase/ManNAc kinase (GNE/MNK), encoded by the GNE gene, catalyzes the first two committed, rate-limiting steps in the biosynthesis of N-acetylneunaminic acid (sialic acid).	n-acetylneunaminic acid	175-198	ATPase copper transporting alpha	Homo sapiens	66-69
23437777-3	2013	The bifunctional enzyme UDP-GlcNAc 2-epimerase/ManNAc kinase (GNE/MNK), encoded by the GNE gene, catalyzes the first two committed, rate-limiting steps in the biosynthesis of N-acetylneunaminic acid (sialic acid).	N-Acetylneuraminic Acid	200-211	ATPase copper transporting alpha	Homo sapiens	66-69
23281160-5	2013	ATP7A is an energy-dependent transmembrane protein, which is involved in the delivery of copper to the secreted copper enzymes and in the export of surplus copper from cells.	Copper	89-95	ATPase copper transporting alpha	Homo sapiens	0-5
23509154-0	2013	Inhibition of Mnk kinase activity by cercosporamide and suppressive effects on acute myeloid leukemia precursors.	cercosporamide	37-51	ATPase copper transporting alpha	Homo sapiens	14-17
23509154-3	2013	We determined whether cercosporamide, an antifungal agent that was recently shown to act as a unique Mnk inhibitor, exhibits antileukemic properties.	cercosporamide	22-36	ATPase copper transporting alpha	Homo sapiens	101-104
23509154-5	2013	Such suppression of Mnk kinase activity and eIF4E phosphorylation by cercosporamide resulted in dose-dependent suppressive effects on primitive leukemic progenitors (CFU-L) from AML patients and enhanced the antileukemic properties of cytarabine (Ara-C) or mammalian target of rapamycin (mTOR) complex 1 inhibition.	cercosporamide	69-83	ATPase copper transporting alpha	Homo sapiens	20-23
23509154-5	2013	Such suppression of Mnk kinase activity and eIF4E phosphorylation by cercosporamide resulted in dose-dependent suppressive effects on primitive leukemic progenitors (CFU-L) from AML patients and enhanced the antileukemic properties of cytarabine (Ara-C) or mammalian target of rapamycin (mTOR) complex 1 inhibition.	Cytarabine	235-245	ATPase copper transporting alpha	Homo sapiens	20-23
23509154-5	2013	Such suppression of Mnk kinase activity and eIF4E phosphorylation by cercosporamide resulted in dose-dependent suppressive effects on primitive leukemic progenitors (CFU-L) from AML patients and enhanced the antileukemic properties of cytarabine (Ara-C) or mammalian target of rapamycin (mTOR) complex 1 inhibition.	Cytarabine	247-252	ATPase copper transporting alpha	Homo sapiens	20-23
23509154-7	2013	Altogether, this work demonstrates that the unique Mnk inhibitor cercosporamide suppresses phosphorylation of eIF4E and exhibits antileukemic effects, in support of future clinical-translational efforts involving combinations of Mnk inhibitors with cytarabine and/or mTOR inhibitors for the treatment of AML.	cercosporamide	65-79	ATPase copper transporting alpha	Homo sapiens	51-54
23509154-7	2013	Altogether, this work demonstrates that the unique Mnk inhibitor cercosporamide suppresses phosphorylation of eIF4E and exhibits antileukemic effects, in support of future clinical-translational efforts involving combinations of Mnk inhibitors with cytarabine and/or mTOR inhibitors for the treatment of AML.	cercosporamide	65-79	ATPase copper transporting alpha	Homo sapiens	229-232
23509154-7	2013	Altogether, this work demonstrates that the unique Mnk inhibitor cercosporamide suppresses phosphorylation of eIF4E and exhibits antileukemic effects, in support of future clinical-translational efforts involving combinations of Mnk inhibitors with cytarabine and/or mTOR inhibitors for the treatment of AML.	Cytarabine	249-259	ATPase copper transporting alpha	Homo sapiens	51-54
23281160-5	2013	ATP7A is an energy-dependent transmembrane protein, which is involved in the delivery of copper to the secreted copper enzymes and in the export of surplus copper from cells.	Copper	112-118	ATPase copper transporting alpha	Homo sapiens	0-5
23281160-5	2013	ATP7A is an energy-dependent transmembrane protein, which is involved in the delivery of copper to the secreted copper enzymes and in the export of surplus copper from cells.	Copper	112-118	ATPase copper transporting alpha	Homo sapiens	0-5
23345593-4	2013	The copper deficiency in SCO patient fibroblasts is rescued by knockdown of ATP7A, a trans-Golgi, copper-transporting ATPase that traffics to the plasma membrane during copper overload to promote efflux.	Copper	4-10	ATPase copper transporting alpha	Homo sapiens	76-81
23345593-7	2013	These results demonstrate that COX19 is necessary for the transduction of a SCO1-dependent mitochondrial redox signal that regulates ATP7A-mediated cellular copper efflux.	Copper	157-163	ATPase copper transporting alpha	Homo sapiens	133-138
23174565-5	2013	The current study was thus designed to decipher mechanistic aspects of Atp7a regulation during iron deprivation using an established in vitro model of the mammalian intestine, rat intestinal epithelial (IEC-6) cells.	Iron	95-99	ATPase copper transporting alpha	Homo sapiens	71-76
23432957-5	2013	METHODS: Methylation of klotho gene promoter in GC-7901, MNK-45 and AGS gastric cancer cells as well as GES-1 normal gastric epithelial cells was detected by bisulfate-based PCR.	hydrogen sulfate	158-167	ATPase copper transporting alpha	Homo sapiens	57-60
23622398-1	2013	Two copper-transporting ATPases are essential for mammalian copper homeostasis: ATP7A, which mediates copper uptake in the gastrointestinal tract and copper delivery to the brain, and ATP7B, which mediates copper excretion by the liver into bile.	Copper	4-10	ATPase copper transporting alpha	Homo sapiens	80-85
24054147-0	2013	Catecholamine metabolites affected by the copper-dependent enzyme dopamine-beta-hydroxylase provide sensitive biomarkers for early diagnosis of menkes disease and viral-mediated ATP7A gene therapy.	Copper	42-48	ATPase copper transporting alpha	Homo sapiens	178-183
24054147-2	2013	Partial deficiency of dopamine-beta-hydroxylase is a biochemical hallmark of this illness due to the normal role of ATP7A in delivery of copper as an enzymatic cofactor.	Copper	137-143	ATPase copper transporting alpha	Homo sapiens	116-121
24054147-5	2013	In preclinical efforts to develop improved therapies for patients with non-copper-responsive ATP7A mutations, we used brain-directed adeno-associated viral gene therapy to rescue a murine model of the disease.	Copper	75-81	ATPase copper transporting alpha	Homo sapiens	93-98
24054147-0	2013	Catecholamine metabolites affected by the copper-dependent enzyme dopamine-beta-hydroxylase provide sensitive biomarkers for early diagnosis of menkes disease and viral-mediated ATP7A gene therapy.	Catecholamines	0-13	ATPase copper transporting alpha	Homo sapiens	178-183
23622398-1	2013	Two copper-transporting ATPases are essential for mammalian copper homeostasis: ATP7A, which mediates copper uptake in the gastrointestinal tract and copper delivery to the brain, and ATP7B, which mediates copper excretion by the liver into bile.	Copper	60-66	ATPase copper transporting alpha	Homo sapiens	80-85
23622398-1	2013	Two copper-transporting ATPases are essential for mammalian copper homeostasis: ATP7A, which mediates copper uptake in the gastrointestinal tract and copper delivery to the brain, and ATP7B, which mediates copper excretion by the liver into bile.	Copper	60-66	ATPase copper transporting alpha	Homo sapiens	80-85
23622398-1	2013	Two copper-transporting ATPases are essential for mammalian copper homeostasis: ATP7A, which mediates copper uptake in the gastrointestinal tract and copper delivery to the brain, and ATP7B, which mediates copper excretion by the liver into bile.	Copper	60-66	ATPase copper transporting alpha	Homo sapiens	80-85
23622398-1	2013	Two copper-transporting ATPases are essential for mammalian copper homeostasis: ATP7A, which mediates copper uptake in the gastrointestinal tract and copper delivery to the brain, and ATP7B, which mediates copper excretion by the liver into bile.	Copper	60-66	ATPase copper transporting alpha	Homo sapiens	80-85
23622398-11	2013	In the past 2 years (2012-2013), three new autosomal recessive copper metabolism conditions have been recognized: 1) Huppke-Brendel syndrome caused by mutations in an acetyl CoA transporter needed for acetylation of one or more copper proteins, 2) CCS deficiency caused by mutations in the copper chaperone to SODI, and 3) MEDNIK syndrome, which revealed that mutations in the sigma1A subunit of adaptor protein complex 1 (AP-1) have detrimental effects on trafficking of ATP7A and ATP7B.	Copper	63-69	ATPase copper transporting alpha	Homo sapiens	472-477
23064757-6	2012	Taken together, these data demonstrate unique and specific requirements for enterocyte Atp7a in neonatal and maternofetal copper acquisition that are dependent on dietary copper availability, thus providing new insights into the mechanisms of gene-nutrient interaction essential for early human development.	Copper	122-128	ATPase copper transporting alpha	Homo sapiens	87-92
23064757-6	2012	Taken together, these data demonstrate unique and specific requirements for enterocyte Atp7a in neonatal and maternofetal copper acquisition that are dependent on dietary copper availability, thus providing new insights into the mechanisms of gene-nutrient interaction essential for early human development.	Copper	171-177	ATPase copper transporting alpha	Homo sapiens	87-92
23075277-14	2012	Finally, we propose a model structure of ATP7A from Mnk6 (E561) to P1413 based on the crystal structure of LpCopA and docking simulations.	lpcopa	107-113	ATPase copper transporting alpha	Homo sapiens	41-46
22361452-4	2012	Subjects comprised 35 Japanese male patients with classical MNK who received copper histidine treatment.	copper histidine	77-93	ATPase copper transporting alpha	Homo sapiens	60-63
23075277-1	2012	Human copper-ATPases ATP7A and ATP7B are essential for intracellular copper homeostasis.	Copper	6-12	ATPase copper transporting alpha	Homo sapiens	21-26
23075277-2	2012	The main roles of the Menkes protein, ATP7A, are the delivery of copper to the secretory pathway and the export of excess copper from the enterocytes.	Copper	65-71	ATPase copper transporting alpha	Homo sapiens	38-43
23075277-2	2012	The main roles of the Menkes protein, ATP7A, are the delivery of copper to the secretory pathway and the export of excess copper from the enterocytes.	Copper	122-128	ATPase copper transporting alpha	Homo sapiens	38-43
23075277-3	2012	The N-terminal domain of membrane protein ATP7A consists of six repetitive sequences of 60-70 amino acids (Mnk1-Mnk6) that fold into individual metal binding domains (MBDs) and bind a single copper ion in the reduced Cu(I) form via two cysteine residues.	Metals	144-149	ATPase copper transporting alpha	Homo sapiens	42-47
23075277-3	2012	The N-terminal domain of membrane protein ATP7A consists of six repetitive sequences of 60-70 amino acids (Mnk1-Mnk6) that fold into individual metal binding domains (MBDs) and bind a single copper ion in the reduced Cu(I) form via two cysteine residues.	Copper	191-197	ATPase copper transporting alpha	Homo sapiens	42-47
23075277-3	2012	The N-terminal domain of membrane protein ATP7A consists of six repetitive sequences of 60-70 amino acids (Mnk1-Mnk6) that fold into individual metal binding domains (MBDs) and bind a single copper ion in the reduced Cu(I) form via two cysteine residues.	Cysteine	236-244	ATPase copper transporting alpha	Homo sapiens	42-47
22361452-10	2012	Using Mann-Whitney U tests, age at death was also significantly lower in MNK patients with CMs (P<0.05), compared to those without CMs, even though there was no significant difference of age onset, age at diagnosis and age at start of treatment with copper histidine between both groups of patients.	copper histidine	253-269	ATPase copper transporting alpha	Homo sapiens	73-76
22992316-7	2012	The patient presented low levels of serum copper and ceruloplasmin, and was shown to be hemizygous for the p.T1048I mutation in ATP7A.	Copper	42-48	ATPase copper transporting alpha	Homo sapiens	128-133
22854969-6	2012	As compared with SERCA, initial utilization of ATP by ATP7A/B is much slower and highly sensitive to temperature-dependent activation energy, suggesting conformational constraints of the headpiece domains.	Adenosine Triphosphate	47-50	ATPase copper transporting alpha	Homo sapiens	54-59
22854969-8	2012	ATP-dependent charge transfer in ATP7A and -B is observed, with no variation of net charge upon pH changes and no evidence of Cu(+)/H(+) exchange.	Adenosine Triphosphate	0-3	ATPase copper transporting alpha	Homo sapiens	33-45
22992316-11	2012	However, the clinical course of the patient was mild, and he responded to Cu-His treatment, which suggests that this mutation leads to partial conservation of the activity of ATP7A.	copper histidine	74-80	ATPase copper transporting alpha	Homo sapiens	175-180
22695177-0	2012	In utero copper treatment for Menkes disease associated with a severe ATP7A mutation.	Copper	9-15	ATPase copper transporting alpha	Homo sapiens	70-75
22711717-3	2012	The low serum copper and ceruloplasmin suggests the diagnosis, which is confirmed by mutation analysis of the ATP7A gene.	Copper	14-20	ATPase copper transporting alpha	Homo sapiens	110-115
22710939-0	2012	Sec61beta controls sensitivity to platinum-containing chemotherapeutic agents through modulation of the copper-transporting ATPase ATP7A.	Platinum	34-42	ATPase copper transporting alpha	Homo sapiens	131-136
22710939-11	2012	This modulation occurs through effects of Sec61beta on the expression and distribution of ATP7A, which was shown previously to control platinum drug sequestration and cytotoxicity.	Platinum	135-143	ATPase copper transporting alpha	Homo sapiens	90-95
23029640-1	2012	The human copper exporters ATP7A and ATP7B contain domains common to all P-type ATPases as well as class-specific features such as six sequential heavy-metal binding domains (HMBD1-HMBD6) and a type-specific constellation of transmembrane helices.	Copper	10-16	ATPase copper transporting alpha	Homo sapiens	27-32
22210628-1	2012	ATP7A is a P-type ATPase that regulates cellular copper homeostasis by activity at the trans-Golgi network (TGN) and plasma membrane (PM), with the location normally governed by intracellular copper concentration.	Copper	49-55	ATPase copper transporting alpha	Homo sapiens	0-5
22210628-1	2012	ATP7A is a P-type ATPase that regulates cellular copper homeostasis by activity at the trans-Golgi network (TGN) and plasma membrane (PM), with the location normally governed by intracellular copper concentration.	Copper	192-198	ATPase copper transporting alpha	Homo sapiens	0-5
22210628-9	2012	Flow cytometry documented that non-permeabilized ATP7A(P1386S) fibroblasts bound a carboxyl-terminal ATP7A antibody, consistent with relocation of the ATP7A di-leucine endocytic retrieval signal to the extracellular surface and partially destabilized insertion of the eighth transmembrane helix.	Leucine	160-167	ATPase copper transporting alpha	Homo sapiens	49-54
22577880-0	2012	Lumenal loop M672-P707 of the Menkes protein (ATP7A) transfers copper to peptidylglycine monooxygenase.	Copper	63-69	ATPase copper transporting alpha	Homo sapiens	46-51
22577880-1	2012	Copper transfer to cuproproteins located in vesicular compartments of the secretory pathway depends on activity of the copper-translocating ATPase (ATP7A), but the mechanism of transfer is largely unexplored.	Copper	0-6	ATPase copper transporting alpha	Homo sapiens	148-153
22577880-2	2012	Copper-ATPase ATP7A is unique in having a sequence rich in histidine and methionine residues located on the lumenal side of the membrane.	Histidine	59-68	ATPase copper transporting alpha	Homo sapiens	14-19
22577880-2	2012	Copper-ATPase ATP7A is unique in having a sequence rich in histidine and methionine residues located on the lumenal side of the membrane.	Methionine	73-83	ATPase copper transporting alpha	Homo sapiens	14-19
22577880-4	2012	Here we present evidence for a potential role of this lumenal region of ATP7A in copper transfer to cuproenzymes.	Copper	81-87	ATPase copper transporting alpha	Homo sapiens	72-77
23029640-1	2012	The human copper exporters ATP7A and ATP7B contain domains common to all P-type ATPases as well as class-specific features such as six sequential heavy-metal binding domains (HMBD1-HMBD6) and a type-specific constellation of transmembrane helices.	Metals	152-157	ATPase copper transporting alpha	Homo sapiens	27-32
22304828-0	2012	Copper-transporting P-type adenosine triphosphatase (ATP7A) is associated with platinum-resistance in non-small cell lung cancer (NSCLC).	Platinum	79-87	ATPase copper transporting alpha	Homo sapiens	53-58
22134099-2	2012	Mutations in ATP7A cause Menkes disease and occipital horn syndrome (OHS), allelic X-linked recessive conditions that feature vascular abnormalities ascribed to low activity of lysyl oxidase, a copper-dependent enzyme.	Copper	194-200	ATPase copper transporting alpha	Homo sapiens	13-18
22304828-1	2012	BACKGROUND: Copper export protein ATP7A is important for maintaining copper homeostasis.	Copper	12-18	ATPase copper transporting alpha	Homo sapiens	34-39
22304828-1	2012	BACKGROUND: Copper export protein ATP7A is important for maintaining copper homeostasis.	Copper	69-75	ATPase copper transporting alpha	Homo sapiens	34-39
22304828-3	2012	The goal of this study was to determine the role of ATP7A in the platinum-resistance of non-small cell lung cancer (NSCLC).	Platinum	65-73	ATPase copper transporting alpha	Homo sapiens	52-57
22304828-5	2012	ATP7A expression was evaluated by immunohistochemistry in tumor tissues of unresectable NSCLC patients who received cisplatin-basing chemotherapy.	Cisplatin	116-125	ATPase copper transporting alpha	Homo sapiens	0-5
22304828-9	2012	ATP7A-positive patients had a significantly poorer histological grade (p = 0.039) and poorer response to platinum-basing chemotherapy (p = 0.001) compared with ATP7A-negative patients.	Platinum	105-113	ATPase copper transporting alpha	Homo sapiens	0-5
22304828-11	2012	CONCLUSIONS: ATP7A overexpression played an important role in platinum-resistance of NSCLC, and was a negative prognostic factor of NSCLC patients treated with platinum-based chemotherapy.	Platinum	62-70	ATPase copper transporting alpha	Homo sapiens	13-18
22304828-11	2012	CONCLUSIONS: ATP7A overexpression played an important role in platinum-resistance of NSCLC, and was a negative prognostic factor of NSCLC patients treated with platinum-based chemotherapy.	Platinum	160-168	ATPase copper transporting alpha	Homo sapiens	13-18
21336677-0	2012	Human macrophage ATP7A is localized in the trans-Golgi apparatus, controls intracellular copper levels, and mediates macrophage responses to dermal wounds.	Copper	89-95	ATPase copper transporting alpha	Homo sapiens	17-22
21336677-10	2012	In summary, alongside our previous studies, these findings indicate that human macrophage ATP7A is localized in the trans-Golgi apparatus, regulates intracellular copper levels, and mediates macrophage responses to a dermal wound.	Copper	163-169	ATPase copper transporting alpha	Homo sapiens	90-95
21667063-0	2012	The copper-transporting capacity of ATP7A mutants associated with Menkes disease is ameliorated by COMMD1 as a result of improved protein expression.	Copper	4-10	ATPase copper transporting alpha	Homo sapiens	36-41
22226844-7	2012	Copper export is most likely mediated by the copper ATPase ATP7A, since this transporter is expressed in astrocyte cultures and its cellular location is strongly affected by the absence or the presence of extracellular copper.	Copper	0-6	ATPase copper transporting alpha	Homo sapiens	59-64
22226844-7	2012	Copper export is most likely mediated by the copper ATPase ATP7A, since this transporter is expressed in astrocyte cultures and its cellular location is strongly affected by the absence or the presence of extracellular copper.	Copper	45-51	ATPase copper transporting alpha	Homo sapiens	59-64
22130675-0	2012	Clusterin and COMMD1 independently regulate degradation of the mammalian copper ATPases ATP7A and ATP7B.	Copper	73-79	ATPase copper transporting alpha	Homo sapiens	88-93
22130675-1	2012	ATP7A and ATP7B are copper-transporting P(1B)-type ATPases (Cu-ATPases) that are critical for regulating intracellular copper homeostasis.	Copper	20-26	ATPase copper transporting alpha	Homo sapiens	0-5
22130675-1	2012	ATP7A and ATP7B are copper-transporting P(1B)-type ATPases (Cu-ATPases) that are critical for regulating intracellular copper homeostasis.	Copper	119-125	ATPase copper transporting alpha	Homo sapiens	0-5
22130675-5	2012	Overexpression and knockdown of clusterin/COMMD1 decreased and increased, respectively, endogenous levels of ATP7A and ATP7B, consistent with a role in facilitating Cu-ATPase degradation.	Copper	165-167	ATPase copper transporting alpha	Homo sapiens	109-114
21667063-3	2012	A diversity of mutations in the gene encoding of the Golgi-resident copper-transporting P(1B)-type ATPase ATP7A underlies MD.	Copper	68-74	ATPase copper transporting alpha	Homo sapiens	106-111
21667063-8	2012	Interestingly, in addition to adjusted growth temperature, binding of COMMD1 partially restored the expression, subcellular localization, and copper-exporting activities of the ATP7A mutants.	Copper	142-148	ATPase copper transporting alpha	Homo sapiens	177-182
21981264-5	2011	Evidence also suggests that ATP7A and ATP7B mediate cisplatin sequestration and efflux from cells, thus influencing drug resistance.	Cisplatin	52-61	ATPase copper transporting alpha	Homo sapiens	28-33
24278698-4	2012	Several transporters, which are expressed on the cell membranes, have been associated with cisplatin transport across the plasma membrane and across the cell: the copper transporter 1 (Ctr1), the copper transporter 2 (Ctr2), the P-type copper-transporting ATPases ATP7A and ATP7B, the organic cation transporter 2 (OCT2), and the multidrug extrusion transporter 1 (MATE1).	Cisplatin	91-100	ATPase copper transporting alpha	Homo sapiens	264-269
21981264-6	2011	The copper-chaperone Atox1, which normally binds Cu(I) via two cysteines and delivers the metal to ATP7A/B, has also been reported to interact with cisplatin in in vitro experiments.	Copper	4-10	ATPase copper transporting alpha	Homo sapiens	99-106
21390185-8	2011	Axitinib and SN-38 combined treatment greatly inhibited the expression of the ATP7A and ABCG2 genes in endothelial and cancer cells, increasing the SN-38 intracellular concentration.	Axitinib	0-8	ATPase copper transporting alpha	Homo sapiens	78-83
21981264-6	2011	The copper-chaperone Atox1, which normally binds Cu(I) via two cysteines and delivers the metal to ATP7A/B, has also been reported to interact with cisplatin in in vitro experiments.	cuprous ion	49-54	ATPase copper transporting alpha	Homo sapiens	99-106
21981264-6	2011	The copper-chaperone Atox1, which normally binds Cu(I) via two cysteines and delivers the metal to ATP7A/B, has also been reported to interact with cisplatin in in vitro experiments.	Metals	90-95	ATPase copper transporting alpha	Homo sapiens	99-106
21981264-6	2011	The copper-chaperone Atox1, which normally binds Cu(I) via two cysteines and delivers the metal to ATP7A/B, has also been reported to interact with cisplatin in in vitro experiments.	Cisplatin	148-157	ATPase copper transporting alpha	Homo sapiens	99-106
22074552-1	2011	BACKGROUND: Menkes disease (MD) is an X-linked, fatal neurodegenerative disorder of copper metabolism, caused by mutations in the ATP7A gene.	Copper	84-90	ATPase copper transporting alpha	Homo sapiens	130-135
21762080-0	2011	Targeting ATP7A to increase the sensitivity of neuroblastoma cells to retinoid therapy.	Retinoids	70-78	ATPase copper transporting alpha	Homo sapiens	10-15
21762080-3	2011	Recent evidence suggests that the copper metabolism gene, ATP7A, is retinoid-regulated and an important component of the retinoic acid receptor beta (RARbeta) anticancer effect in neuroblastoma cells.	Copper	34-40	ATPase copper transporting alpha	Homo sapiens	58-63
21762080-3	2011	Recent evidence suggests that the copper metabolism gene, ATP7A, is retinoid-regulated and an important component of the retinoic acid receptor beta (RARbeta) anticancer effect in neuroblastoma cells.	Retinoids	68-76	ATPase copper transporting alpha	Homo sapiens	58-63
21762080-4	2011	To highlight and further develop the concept of using ATP7A as a target in retinoid therapy, and combination therapy with copper chelators in neuroblastoma, the current literature and abstracts related to the clinical application of retinoids, the function of ATP7A and the clinical application of copper chelators are summarized.	Retinoids	75-83	ATPase copper transporting alpha	Homo sapiens	54-59
21762080-5	2011	We propose that strategies targeting the copper export protein, ATP7A, in combination therapy with retinoids and copper depletion therapy, may have great therapeutic potential in the clinical treatment of neuroblastoma and other malignancies.	Copper	41-47	ATPase copper transporting alpha	Homo sapiens	64-69
21762080-5	2011	We propose that strategies targeting the copper export protein, ATP7A, in combination therapy with retinoids and copper depletion therapy, may have great therapeutic potential in the clinical treatment of neuroblastoma and other malignancies.	Retinoids	99-108	ATPase copper transporting alpha	Homo sapiens	64-69
21762080-5	2011	We propose that strategies targeting the copper export protein, ATP7A, in combination therapy with retinoids and copper depletion therapy, may have great therapeutic potential in the clinical treatment of neuroblastoma and other malignancies.	Copper	113-119	ATPase copper transporting alpha	Homo sapiens	64-69
21454443-1	2011	ATP7A and ATP7B are copper-transporting P-type ATPases that are essential to eukaryotic copper homeostasis and must traffic between intracellular compartments to carry out their functions.	Copper	20-26	ATPase copper transporting alpha	Homo sapiens	0-5
21454443-1	2011	ATP7A and ATP7B are copper-transporting P-type ATPases that are essential to eukaryotic copper homeostasis and must traffic between intracellular compartments to carry out their functions.	Copper	88-94	ATPase copper transporting alpha	Homo sapiens	0-5
21454443-6	2011	L1373 at the end of transmembrane domain 8 is required for protein stability and Golgi retention in low copper, the trileucine motif (L1454-L1456) is required for retrograde trafficking, and the COOH terminus of ATP7B exhibits a higher sensitivity to copper than does ATP7A.	Carbonic Acid	195-199	ATPase copper transporting alpha	Homo sapiens	268-273
22332042-3	2011	Cu transporters CTR1, ATP7A, and ATP7B play key roles in ensuring that adequate Cu is available for Cu-requiring processes and the prevention of excess Cu accumulation within cells.	Copper	0-2	ATPase copper transporting alpha	Homo sapiens	22-27
22332042-3	2011	Cu transporters CTR1, ATP7A, and ATP7B play key roles in ensuring that adequate Cu is available for Cu-requiring processes and the prevention of excess Cu accumulation within cells.	Copper	80-82	ATPase copper transporting alpha	Homo sapiens	22-27
21924848-9	2011	Molecular consequences of the pathogenic ATP7A gene mutation lead to impairment in copper transport, which in turn causes deficiencies of key copper containing enzymes (dopamine beta hydroxylase and cytochrome c oxidase).	Copper	83-89	ATPase copper transporting alpha	Homo sapiens	41-46
21924848-9	2011	Molecular consequences of the pathogenic ATP7A gene mutation lead to impairment in copper transport, which in turn causes deficiencies of key copper containing enzymes (dopamine beta hydroxylase and cytochrome c oxidase).	Copper	142-148	ATPase copper transporting alpha	Homo sapiens	41-46
21924848-13	2011	Early diagnosis and institution of copper supplementation has been shown to be beneficial particularly in patients with residual ATP7A activity.	Copper	35-41	ATPase copper transporting alpha	Homo sapiens	129-134
21646353-0	2011	The lumenal loop Met672-Pro707 of copper-transporting ATPase ATP7A binds metals and facilitates copper release from the intramembrane sites.	Copper	34-40	ATPase copper transporting alpha	Homo sapiens	61-66
21646353-2	2011	ATP7A transfers the copper cofactor to metalloenzymes within the secretory pathway; inactivation of ATP7A results in an untreatable neurodegenerative disorder, Menkes disease.	Copper	20-26	ATPase copper transporting alpha	Homo sapiens	0-5
21646353-2	2011	ATP7A transfers the copper cofactor to metalloenzymes within the secretory pathway; inactivation of ATP7A results in an untreatable neurodegenerative disorder, Menkes disease.	Copper	20-26	ATPase copper transporting alpha	Homo sapiens	100-105
21646353-3	2011	Presently, the mechanism of ATP7A-mediated copper release into the secretory pathway is not understood.	Copper	43-49	ATPase copper transporting alpha	Homo sapiens	28-33
21646353-4	2011	We demonstrate that the characteristic His/Met-rich segment Met(672)-Pro(707) (HM-loop) that connects the first two transmembrane segments of ATP7A is important for copper release.	Histidine	39-42	ATPase copper transporting alpha	Homo sapiens	142-147
21646353-4	2011	We demonstrate that the characteristic His/Met-rich segment Met(672)-Pro(707) (HM-loop) that connects the first two transmembrane segments of ATP7A is important for copper release.	Proline	69-72	ATPase copper transporting alpha	Homo sapiens	142-147
21646353-4	2011	We demonstrate that the characteristic His/Met-rich segment Met(672)-Pro(707) (HM-loop) that connects the first two transmembrane segments of ATP7A is important for copper release.	Copper	165-171	ATPase copper transporting alpha	Homo sapiens	142-147
21646353-10	2011	We also show that copper binding within the HM-loop stabilizes Cu(I) and protects it from oxidation, which may further aid the transfer of copper from ATP7A to acceptor proteins.	Copper	18-24	ATPase copper transporting alpha	Homo sapiens	151-156
21646353-10	2011	We also show that copper binding within the HM-loop stabilizes Cu(I) and protects it from oxidation, which may further aid the transfer of copper from ATP7A to acceptor proteins.	cuprous ion	63-68	ATPase copper transporting alpha	Homo sapiens	151-156
21646353-10	2011	We also show that copper binding within the HM-loop stabilizes Cu(I) and protects it from oxidation, which may further aid the transfer of copper from ATP7A to acceptor proteins.	Copper	139-145	ATPase copper transporting alpha	Homo sapiens	151-156
21242307-0	2011	Clusterin (apolipoprotein J), a molecular chaperone that facilitates degradation of the copper-ATPases ATP7A and ATP7B.	Copper	88-94	ATPase copper transporting alpha	Homo sapiens	103-108
21242307-1	2011	The copper-transporting P(1B)-type ATPases (Cu-ATPases) ATP7A and ATP7B are key regulators of physiological copper levels.	Copper	4-10	ATPase copper transporting alpha	Homo sapiens	56-61
21242307-1	2011	The copper-transporting P(1B)-type ATPases (Cu-ATPases) ATP7A and ATP7B are key regulators of physiological copper levels.	Copper	108-114	ATPase copper transporting alpha	Homo sapiens	56-61
22332042-3	2011	Cu transporters CTR1, ATP7A, and ATP7B play key roles in ensuring that adequate Cu is available for Cu-requiring processes and the prevention of excess Cu accumulation within cells.	Copper	80-82	ATPase copper transporting alpha	Homo sapiens	22-27
22332042-4	2011	Two diseases of Cu metabolism, Menkes disease and Wilson disease, which are caused by mutations in ATP7A and ATP7B, respectively, exemplify the critical importance of regulating Cu balance in humans.	Copper	16-18	ATPase copper transporting alpha	Homo sapiens	99-104
21390185-8	2011	Axitinib and SN-38 combined treatment greatly inhibited the expression of the ATP7A and ABCG2 genes in endothelial and cancer cells, increasing the SN-38 intracellular concentration.	Irinotecan	13-18	ATPase copper transporting alpha	Homo sapiens	78-83
21390185-8	2011	Axitinib and SN-38 combined treatment greatly inhibited the expression of the ATP7A and ABCG2 genes in endothelial and cancer cells, increasing the SN-38 intracellular concentration.	Irinotecan	148-153	ATPase copper transporting alpha	Homo sapiens	78-83
21143467-2	2011	The recent observation of ATP7A mutations in dHMN provides insight for a common disease mechanism that may involve copper homeostasis.	Copper	115-121	ATPase copper transporting alpha	Homo sapiens	26-31
21167140-3	2011	The Human ATP7A copper transport ATPase modulates intracellular copper distribution, which is critical for copper-dependent enzymes such as superoxide dismutase (SOD1).	Copper	16-22	ATPase copper transporting alpha	Homo sapiens	10-15
21167140-3	2011	The Human ATP7A copper transport ATPase modulates intracellular copper distribution, which is critical for copper-dependent enzymes such as superoxide dismutase (SOD1).	Copper	64-70	ATPase copper transporting alpha	Homo sapiens	10-15
21034850-2	2011	When intracellular copper levels are elevated, the Menkes (ATP7A) P-Type ATPase traffics from the trans-Golgi network (TGN) towards the plasma membrane to facilitate copper efflux.	Copper	19-25	ATPase copper transporting alpha	Homo sapiens	59-64
20831904-4	2011	Disturbances in copper metabolism caused by mutations in the ATP7A/Atp7a gene lead to severe metabolic syndromes Menkes disease in humans and the lethal mottled phenotype in mice.	Copper	16-22	ATPase copper transporting alpha	Homo sapiens	61-66
20831904-4	2011	Disturbances in copper metabolism caused by mutations in the ATP7A/Atp7a gene lead to severe metabolic syndromes Menkes disease in humans and the lethal mottled phenotype in mice.	Copper	16-22	ATPase copper transporting alpha	Homo sapiens	67-72
20831904-7	2011	The aim of this study was to analyse the expression of the Atp7a gene in mosaic mutants in early postnatal development, a critical period for starting copper supplementation therapy in both Menkes patients and mutant mice.	Copper	151-157	ATPase copper transporting alpha	Homo sapiens	59-64
21034850-2	2011	When intracellular copper levels are elevated, the Menkes (ATP7A) P-Type ATPase traffics from the trans-Golgi network (TGN) towards the plasma membrane to facilitate copper efflux.	Copper	166-172	ATPase copper transporting alpha	Homo sapiens	59-64
21034850-3	2011	The ADP-ribosylation factor 1 (Arf1) is required for maintenance of Golgi architecture and for vesicular trafficking, including the copper-responsive trafficking of ATP7A.	Copper	132-138	ATPase copper transporting alpha	Homo sapiens	165-170
21034850-4	2011	Here we report an ATP7A-independent role of Arf1 in copper homeostasis.	Copper	52-58	ATPase copper transporting alpha	Homo sapiens	18-23
21034850-6	2011	Arf1 therefore affected copper levels independently of ATP7A mediated copper efflux.	Copper	70-76	ATPase copper transporting alpha	Homo sapiens	55-60
21115196-3	2011	Two copper transporting ATPases, Menkes (ATP7A; MNK) and Wilson (ATP7B; WND) are known to be expressed in the placenta and are thought to have a role in copper transport to the fetus.	Copper	4-10	ATPase copper transporting alpha	Homo sapiens	41-46
21275100-6	2011	Typical intracellular copper-binding proteins, such as the Cu-transporting P-type ATPases ATP7B (Wilson ATPase) and ATP7A (Menkes ATPase), bind copper as Cu(I).	Copper	22-28	ATPase copper transporting alpha	Homo sapiens	116-121
21275100-6	2011	Typical intracellular copper-binding proteins, such as the Cu-transporting P-type ATPases ATP7B (Wilson ATPase) and ATP7A (Menkes ATPase), bind copper as Cu(I).	Copper	144-150	ATPase copper transporting alpha	Homo sapiens	116-121
21221114-2	2011	Involvement of ATP7A in axonal outgrowth, synapse integrity and neuronal activation underscores the fundamental importance of copper metabolism to neurological function.	Copper	126-132	ATPase copper transporting alpha	Homo sapiens	15-20
21221114-4	2011	Neonatal diagnosis and early treatment with copper injections enhance survival in patients with this disease, and can normalize clinical outcomes if mutant ATP7A molecules retain small amounts of residual activity.	Copper	44-50	ATPase copper transporting alpha	Homo sapiens	156-161
21115196-3	2011	Two copper transporting ATPases, Menkes (ATP7A; MNK) and Wilson (ATP7B; WND) are known to be expressed in the placenta and are thought to have a role in copper transport to the fetus.	Copper	4-10	ATPase copper transporting alpha	Homo sapiens	48-51
20664001-2	2010	We determined the effects of chemotherapy (cytarabine) on the activation status of Mnk in AML cells and its role in the generation of antileukemic responses.	Cytarabine	43-53	ATPase copper transporting alpha	Homo sapiens	83-86
21949767-12	2011	MNK kinase mediated the eIF4E phosphorylation and inhibition or depletion of MNK markedly suppressed proliferation of the CTCL cells when combined with the rapamycin-mediated inhibition of mTORC1.	Sirolimus	156-165	ATPase copper transporting alpha	Homo sapiens	0-3
20799318-1	2010	The primary mechanism of copper transport to the brain is unknown, although this process is drastically impaired in Menkes disease, an X-linked neurodevelopmental disorder caused by mutations in an evolutionarily conserved copper transporter, ATP7A.	Copper	25-31	ATPase copper transporting alpha	Homo sapiens	243-248
20799318-3	2010	We exploited a rare (and first reported) example of somatic mosaicism for an ATP7A mutation to shed light on questions about copper transport into the developing brain.	Copper	125-131	ATPase copper transporting alpha	Homo sapiens	77-82
20664001-4	2010	Cytarabine induced phosphorylation/activation of Mnk and Mnk-mediated phosphorylation of eIF4E on Ser209, as evidenced by studies involving pharmacological inhibition of Mnk or experiments using cells with targeted disruption of Mnk1 and Mnk2 genes.	Cytarabine	0-10	ATPase copper transporting alpha	Homo sapiens	57-60
20664001-5	2010	To assess the functional relevance of cytarabine-inducible engagement of Mnk/eIF4E pathway, the effects of pharmacological inhibition of Mnk on cytarabine-mediated suppression of primitive leukemic progenitors [leukemic colony forming unit (CFU-L)] were examined.	Cytarabine	38-48	ATPase copper transporting alpha	Homo sapiens	73-76
20664001-4	2010	Cytarabine induced phosphorylation/activation of Mnk and Mnk-mediated phosphorylation of eIF4E on Ser209, as evidenced by studies involving pharmacological inhibition of Mnk or experiments using cells with targeted disruption of Mnk1 and Mnk2 genes.	Cytarabine	0-10	ATPase copper transporting alpha	Homo sapiens	49-52
20664001-5	2010	To assess the functional relevance of cytarabine-inducible engagement of Mnk/eIF4E pathway, the effects of pharmacological inhibition of Mnk on cytarabine-mediated suppression of primitive leukemic progenitors [leukemic colony forming unit (CFU-L)] were examined.	Cytarabine	144-154	ATPase copper transporting alpha	Homo sapiens	137-140
20664001-4	2010	Cytarabine induced phosphorylation/activation of Mnk and Mnk-mediated phosphorylation of eIF4E on Ser209, as evidenced by studies involving pharmacological inhibition of Mnk or experiments using cells with targeted disruption of Mnk1 and Mnk2 genes.	Cytarabine	0-10	ATPase copper transporting alpha	Homo sapiens	57-60
20664001-6	2010	Concomitant treatment of cells with a pharmacological inhibitor of Mnk or siRNA-mediated knockdown of Mnk1/2 strongly enhanced the suppressive effects of low cytarabine concentrations on CFU-L.	Cytarabine	158-168	ATPase copper transporting alpha	Homo sapiens	67-70
22966390-0	2010	Association of ATP7A expression and in vitro sensitivity to cisplatin in non-small cell lung cancer.	Cisplatin	60-69	ATPase copper transporting alpha	Homo sapiens	15-20
20664001-7	2010	It is noteworthy that the mammalian target of rapamycin (mTOR) inhibitor rapamycin also induced phosphorylation of eIF4E in a Mnk-dependent manner, whereas inhibition strongly enhanced its antileukemic effects.	Sirolimus	46-55	ATPase copper transporting alpha	Homo sapiens	126-129
20927323-6	2010	Inhibition of PP2A using either okadaic acid or PP2A small interfering RNA (siRNA) increased eIF4E phosphorylation, which could be abolished by the presence of the Mnk inhibitor CGP57380 or deficiency of Mnk genes.	Okadaic Acid	32-44	ATPase copper transporting alpha	Homo sapiens	164-167
20927323-6	2010	Inhibition of PP2A using either okadaic acid or PP2A small interfering RNA (siRNA) increased eIF4E phosphorylation, which could be abolished by the presence of the Mnk inhibitor CGP57380 or deficiency of Mnk genes.	Okadaic Acid	32-44	ATPase copper transporting alpha	Homo sapiens	204-207
20671235-2	2010	Bioavailability of intracellular copper is regulated not only by the copper importer CTR1 (copper transporter 1) but also by the copper exporter ATP7A (Menkes ATPase), whose function is achieved through copper-dependent translocation from trans-Golgi network (TGN).	Copper	33-39	ATPase copper transporting alpha	Homo sapiens	145-150
20671235-5	2010	METHODS AND RESULTS: Depletion of ATP7A inhibited VSMC migration in response to PDGF or wound scratch in a CTR1/copper-dependent manner.	Copper	112-118	ATPase copper transporting alpha	Homo sapiens	34-39
20671235-8	2010	In addition, ATP7A depletion prevented a PDGF-induced decrease in copper level and secretory copper enzyme precursor prolysyl oxidase (Pro-LOX) in lipid raft fraction, as well as PDGF-induced increase in LOX activity.	Copper	66-72	ATPase copper transporting alpha	Homo sapiens	13-18
20671235-8	2010	In addition, ATP7A depletion prevented a PDGF-induced decrease in copper level and secretory copper enzyme precursor prolysyl oxidase (Pro-LOX) in lipid raft fraction, as well as PDGF-induced increase in LOX activity.	Copper	93-99	ATPase copper transporting alpha	Homo sapiens	13-18
20671235-10	2010	CONCLUSIONS: These findings suggest that ATP7A plays an important role in copper-dependent PDGF-stimulated VSMC migration via recruiting Rac1 to lipid rafts at the leading edge, as well as regulating LOX activity.	Copper	74-80	ATPase copper transporting alpha	Homo sapiens	41-46
20713646-1	2010	Hypopigmentation is a feature of copper deficiency in humans, as caused by mutation of the copper (Cu(2+)) transporter ATP7A in Menkes disease, or an inability to absorb copper after gastric surgery.	Copper	33-39	ATPase copper transporting alpha	Homo sapiens	119-124
20713646-1	2010	Hypopigmentation is a feature of copper deficiency in humans, as caused by mutation of the copper (Cu(2+)) transporter ATP7A in Menkes disease, or an inability to absorb copper after gastric surgery.	Copper	91-97	ATPase copper transporting alpha	Homo sapiens	119-124
22966390-1	2010	Expression of copper-transporting P-type adenosine triphosphatase A (ATP7A) is reportedly associated with platinum drug resistance in various types of solid tumors.	Platinum	106-114	ATPase copper transporting alpha	Homo sapiens	69-74
22966390-2	2010	However, the impact of ATP7A expression on platinum drug resistance in non-small cell lung cancer (NSCLC) has yet to be adequately elucidated.	Platinum	43-51	ATPase copper transporting alpha	Homo sapiens	23-28
22966390-4	2010	The relationship between the ATP7A expression levels and the in vitro CDDP sensitivity was then evaluated.	cddp	70-74	ATPase copper transporting alpha	Homo sapiens	29-34
22966390-5	2010	The ATP7A mRNA expression levels in the CDDP-resistant tumors were significantly higher than those in the CDDP-sensitive tumors (p=0.0167, Mann-Whitney U test).	cddp	40-44	ATPase copper transporting alpha	Homo sapiens	4-9
22966390-6	2010	In conclusion, the results suggest that evaluation of ATP7A expression is useful as a marker for cisplatin chemoresistance.	Cisplatin	97-106	ATPase copper transporting alpha	Homo sapiens	54-59
20566629-0	2010	Role of glutaredoxin1 and glutathione in regulating the activity of the copper-transporting P-type ATPases, ATP7A and ATP7B.	Glutathione	26-37	ATPase copper transporting alpha	Homo sapiens	108-113
20566629-1	2010	The copper-transporting P-type ATPases (Cu-ATPases), ATP7A and ATP7B, are essential for the regulation of intracellular copper homeostasis.	Copper	4-10	ATPase copper transporting alpha	Homo sapiens	53-58
19965596-1	2010	ATP7A primarily functions to egress copper from cells, thereby supplying this cofactor to secreted copper-accepting enzymes.	Copper	36-42	ATPase copper transporting alpha	Homo sapiens	0-5
19830392-1	2010	Menkes disease is an effect of ATP7A gene mutation in humans, coding the Cu-ATP-ase which is essential in intestinal copper absorption and its subsequent transfer to circulation.	Copper	117-123	ATPase copper transporting alpha	Homo sapiens	31-36
20333435-2	2010	Cellular copper homeostasis in mammals is predominantly maintained by regulating copper transport through the copper import CTR proteins and the copper exporters ATP7A and ATP7B.	Copper	9-15	ATPase copper transporting alpha	Homo sapiens	162-167
20333435-2	2010	Cellular copper homeostasis in mammals is predominantly maintained by regulating copper transport through the copper import CTR proteins and the copper exporters ATP7A and ATP7B.	Copper	81-87	ATPase copper transporting alpha	Homo sapiens	162-167
20333435-2	2010	Cellular copper homeostasis in mammals is predominantly maintained by regulating copper transport through the copper import CTR proteins and the copper exporters ATP7A and ATP7B.	Copper	81-87	ATPase copper transporting alpha	Homo sapiens	162-167
20363758-5	2010	Although CtpA shares significant sequence homologies with the homeostasis copper efflux P1B-type ATPases including the bacterial CopA and the human ATP7A and ATP7B, disruption of ctpA did not result in any sensitivity to excess copper.	Copper	74-80	ATPase copper transporting alpha	Homo sapiens	148-153
20372979-2	2010	Copper-induced trafficking of mammalian ATP7A and ATP7B from the trans-Golgi Network towards the plasma membrane is critical for their role in copper homeostasis.	Copper	0-6	ATPase copper transporting alpha	Homo sapiens	40-45
20372979-2	2010	Copper-induced trafficking of mammalian ATP7A and ATP7B from the trans-Golgi Network towards the plasma membrane is critical for their role in copper homeostasis.	Copper	143-149	ATPase copper transporting alpha	Homo sapiens	40-45
19965596-1	2010	ATP7A primarily functions to egress copper from cells, thereby supplying this cofactor to secreted copper-accepting enzymes.	Copper	99-105	ATPase copper transporting alpha	Homo sapiens	0-5
19965596-11	2010	Finally, cPLA(2)alpha overexpression increased LDL oxidation, which was blocked by coadministration of ATP7A siRNA oligonucleotides.	Oligonucleotides	115-131	ATPase copper transporting alpha	Homo sapiens	103-108
19917666-1	2010	The bifunctional enzyme UDP-GlcNAc 2-epimerase/ ManNAc kinase (GNE/MNK), encoded by the GNE gene, catalyzes the first two committed, rate-limiting steps in the biosynthesis of N-acetylneuraminic acid (sialic acid).	Uridine Diphosphate N-Acetylglucosamine	24-34	ATPase copper transporting alpha	Homo sapiens	67-70
20170900-0	2010	Missense mutations in the copper transporter gene ATP7A cause X-linked distal hereditary motor neuropathy.	Copper	26-32	ATPase copper transporting alpha	Homo sapiens	50-55
20170900-3	2010	The region of genetic linkage included ATP7A, which encodes a copper-transporting P-type ATPase mutated in patients with Menkes disease, a severe infantile-onset neurodegenerative condition.	Copper	62-68	ATPase copper transporting alpha	Homo sapiens	39-44
20170900-8	2010	This previously unrecognized genotype-phenotype correlation suggests an important role of the ATP7A copper transporter in motor-neuron maintenance and function.	Copper	100-106	ATPase copper transporting alpha	Homo sapiens	94-99
19888294-5	2010	ATP7A is an energy dependent transmembrane protein, which is involved in the delivery of copper to the secreted copper enzymes and in the export of surplus copper from cells.	Copper	89-95	ATPase copper transporting alpha	Homo sapiens	0-5
19888294-5	2010	ATP7A is an energy dependent transmembrane protein, which is involved in the delivery of copper to the secreted copper enzymes and in the export of surplus copper from cells.	Copper	112-118	ATPase copper transporting alpha	Homo sapiens	0-5
19888294-5	2010	ATP7A is an energy dependent transmembrane protein, which is involved in the delivery of copper to the secreted copper enzymes and in the export of surplus copper from cells.	Copper	112-118	ATPase copper transporting alpha	Homo sapiens	0-5
19917666-1	2010	The bifunctional enzyme UDP-GlcNAc 2-epimerase/ ManNAc kinase (GNE/MNK), encoded by the GNE gene, catalyzes the first two committed, rate-limiting steps in the biosynthesis of N-acetylneuraminic acid (sialic acid).	N-Acetylneuraminic Acid	176-199	ATPase copper transporting alpha	Homo sapiens	67-70
19917666-1	2010	The bifunctional enzyme UDP-GlcNAc 2-epimerase/ ManNAc kinase (GNE/MNK), encoded by the GNE gene, catalyzes the first two committed, rate-limiting steps in the biosynthesis of N-acetylneuraminic acid (sialic acid).	N-Acetylneuraminic Acid	201-212	ATPase copper transporting alpha	Homo sapiens	67-70
19917666-2	2010	GNE/MNK is feedback inhibited by binding of the downstream product, CMP-sialic acid in its allosteric site.	Cytidine Monophosphate	68-71	ATPase copper transporting alpha	Homo sapiens	4-7
19917666-2	2010	GNE/MNK is feedback inhibited by binding of the downstream product, CMP-sialic acid in its allosteric site.	N-Acetylneuraminic Acid	72-83	ATPase copper transporting alpha	Homo sapiens	4-7
20470945-6	2010	Second, through inhibiting MNK, a P-type ATPase with steady-state localization at the trans-Golgi network, PPIs can hamper copper transport and consequently curb lysyl oxidase activity.	Copper	123-129	ATPase copper transporting alpha	Homo sapiens	27-30
19917612-0	2010	The binding mode of ATP revealed by the solution structure of the N-domain of human ATP7A.	Adenosine Triphosphate	20-23	ATPase copper transporting alpha	Homo sapiens	84-89
19917612-1	2010	We report the solution NMR structures of the N-domain of the Menkes protein (ATP7A) in the ATP-free and ATP-bound forms.	Adenosine Triphosphate	91-94	ATPase copper transporting alpha	Homo sapiens	77-82
19576997-10	2009	These studies demonstrate that phosphorylation of specific serine residues in ATP7A regulates its sub-cellular localization and hence function and will facilitate identification of the kinases and signaling pathways involved in regulating this pivotal copper transporter.	Serine	59-65	ATPase copper transporting alpha	Homo sapiens	78-83
19813030-2	2010	Cellular copper homeostasis in mammals is predominantly maintained by posttranslational regulation of copper import and export through the copper import proteins hCTR1 and hCTR2 and the copper exporters ATP7A and ATP7B.	Copper	9-15	ATPase copper transporting alpha	Homo sapiens	203-208
19813030-2	2010	Cellular copper homeostasis in mammals is predominantly maintained by posttranslational regulation of copper import and export through the copper import proteins hCTR1 and hCTR2 and the copper exporters ATP7A and ATP7B.	Copper	102-108	ATPase copper transporting alpha	Homo sapiens	203-208
19813030-2	2010	Cellular copper homeostasis in mammals is predominantly maintained by posttranslational regulation of copper import and export through the copper import proteins hCTR1 and hCTR2 and the copper exporters ATP7A and ATP7B.	Copper	102-108	ATPase copper transporting alpha	Homo sapiens	203-208
19813030-2	2010	Cellular copper homeostasis in mammals is predominantly maintained by posttranslational regulation of copper import and export through the copper import proteins hCTR1 and hCTR2 and the copper exporters ATP7A and ATP7B.	Copper	102-108	ATPase copper transporting alpha	Homo sapiens	203-208
20038716-1	2010	Human Menkes disease is a lethal neurodegenerative disorder of copper metabolism that is caused by mutations in the ATP7A copper-transporting gene.	Copper	63-69	ATPase copper transporting alpha	Homo sapiens	116-121
21117320-2	2010	ATP7A and ATP7B proteins play the key role in copper homeostasis in the organism.	Copper	46-52	ATPase copper transporting alpha	Homo sapiens	0-5
19576997-1	2009	The Menkes copper-translocating P-type ATPase (ATP7A) is a critical copper transport protein functioning in systemic copper absorption and supply of copper to cuproenzymes in the secretory pathway.	Copper	11-17	ATPase copper transporting alpha	Homo sapiens	47-52
19576997-1	2009	The Menkes copper-translocating P-type ATPase (ATP7A) is a critical copper transport protein functioning in systemic copper absorption and supply of copper to cuproenzymes in the secretory pathway.	Copper	68-74	ATPase copper transporting alpha	Homo sapiens	47-52
19576997-1	2009	The Menkes copper-translocating P-type ATPase (ATP7A) is a critical copper transport protein functioning in systemic copper absorption and supply of copper to cuproenzymes in the secretory pathway.	Copper	68-74	ATPase copper transporting alpha	Homo sapiens	47-52
19576997-3	2009	ATP7A function is regulated by copper-responsive trafficking between the trans-Golgi Network and the plasma membrane.	Copper	31-37	ATPase copper transporting alpha	Homo sapiens	0-5
19576997-5	2009	As copper stimulates both trafficking and phosphorylation of ATP7A we aimed to identify all the specific phosphosites and to determine whether trafficking and phosphorylation are linked.	Copper	3-9	ATPase copper transporting alpha	Homo sapiens	61-66
19650764-9	2009	We also identified a conserved phenylalanine residue in an Mnk-specific insert as playing a key role in governing the ease with which Mnk1a can be phosphorylated.	Phenylalanine	31-44	ATPase copper transporting alpha	Homo sapiens	59-62
19501626-1	2009	Menkes syndrome is an X-linked, fatal neurodegenerative disorder of copper metabolism, caused by mutations in the ATP7A gene, encoding a copper-transporting P1B-type ATPase.	Copper	68-74	ATPase copper transporting alpha	Homo sapiens	114-119
19596068-4	2009	In affected individuals distinct mutations have been identified in the GNE gene, which encodes the bifunctional enzyme uridine diphospho-N-acetylglucosamine (UDP-GlcNAc) 2-epimerase/N-acetyl-mannosamine (ManNAc) kinase (GNE/MNK).	Uridine Diphosphate N-Acetylglucosamine	119-156	ATPase copper transporting alpha	Homo sapiens	224-227
19596068-4	2009	In affected individuals distinct mutations have been identified in the GNE gene, which encodes the bifunctional enzyme uridine diphospho-N-acetylglucosamine (UDP-GlcNAc) 2-epimerase/N-acetyl-mannosamine (ManNAc) kinase (GNE/MNK).	Uridine Diphosphate N-Acetylglucosamine	158-168	ATPase copper transporting alpha	Homo sapiens	224-227
19596068-5	2009	GNE/MNK catalyzes the first two committed steps in the biosynthesis of acetylneuraminic acid (Neu5Ac), an abundant and functionally important sugar.	N-Acetylneuraminic Acid	71-92	ATPase copper transporting alpha	Homo sapiens	4-7
19596068-5	2009	GNE/MNK catalyzes the first two committed steps in the biosynthesis of acetylneuraminic acid (Neu5Ac), an abundant and functionally important sugar.	N-Acetylneuraminic Acid	94-100	ATPase copper transporting alpha	Homo sapiens	4-7
19596068-5	2009	GNE/MNK catalyzes the first two committed steps in the biosynthesis of acetylneuraminic acid (Neu5Ac), an abundant and functionally important sugar.	Sugars	142-147	ATPase copper transporting alpha	Homo sapiens	4-7
20454597-5	2009	This review summarizes current information on the molecular characteristics of copper transporters CTR1, CTR2, ATP7A and ATP7B, their roles in mammalian copper homeostasis and the physiological consequences of their inactivation.	Copper	79-85	ATPase copper transporting alpha	Homo sapiens	111-116
19645496-1	2009	ATP7A and ATP7B are two human P(1B)-type ATPases that have a crucial role in maintaining copper(I) homeostasis.	Copper	89-95	ATPase copper transporting alpha	Homo sapiens	0-5
19645496-7	2009	In particular, it can be concluded that mutations occurring in the A-domain either destabilize the fold of the domain (such as Gly860Val in ATP7A) or affect the network of communication within the domain (such as Leu873Arg in ATP7A) or with the other domains of the enzyme (such as Gly853Arg in ATP7A).	leu873arg	213-222	ATPase copper transporting alpha	Homo sapiens	140-145
19645496-7	2009	In particular, it can be concluded that mutations occurring in the A-domain either destabilize the fold of the domain (such as Gly860Val in ATP7A) or affect the network of communication within the domain (such as Leu873Arg in ATP7A) or with the other domains of the enzyme (such as Gly853Arg in ATP7A).	leu873arg	213-222	ATPase copper transporting alpha	Homo sapiens	226-231
19645496-7	2009	In particular, it can be concluded that mutations occurring in the A-domain either destabilize the fold of the domain (such as Gly860Val in ATP7A) or affect the network of communication within the domain (such as Leu873Arg in ATP7A) or with the other domains of the enzyme (such as Gly853Arg in ATP7A).	leu873arg	213-222	ATPase copper transporting alpha	Homo sapiens	226-231
19296535-1	2009	Recently, the copper efflux transporters ATP7B and ATP7A have been implicated in the transport of and resistance to platinum drugs in breast and ovarian cancers.	Platinum	116-124	ATPase copper transporting alpha	Homo sapiens	51-56
19509135-2	2009	Several other Cu transporters, including the influx transporter CTR1 and the two efflux transporters ATP7A and ATP7B, also regulate sensitivity to the platinum-containing drugs.	Platinum	151-159	ATPase copper transporting alpha	Homo sapiens	101-106
19449859-1	2009	ATP7A/B are human P(1B)-type ATPases involved in cellular Cu homeostasis.	Copper	58-60	ATPase copper transporting alpha	Homo sapiens	0-7
19205902-1	2009	Copper egress is an essential regulator of the kinetics of cellular copper and is primarily regulated by ATP7A, a copper-transporting P-type ATPase.	Copper	0-6	ATPase copper transporting alpha	Homo sapiens	105-110
19205902-1	2009	Copper egress is an essential regulator of the kinetics of cellular copper and is primarily regulated by ATP7A, a copper-transporting P-type ATPase.	Copper	68-74	ATPase copper transporting alpha	Homo sapiens	105-110
19205902-8	2009	Collectively, we demonstrate that PMA induces copper egress in THP-1 cells, which is regulated by ATP7A, and ATP7A regulates VEGFR1 expression.	Copper	46-52	ATPase copper transporting alpha	Homo sapiens	98-103
19205902-3	2009	In current manuscript, using THP-1 cells, a human monocytic cell line, we found that ATP7A expression was increased in cells exposed to phorbol-12-myristate-13-acetate (PMA), a potent inducer of neovascularization and cancer.	Tetradecanoylphorbol Acetate	136-167	ATPase copper transporting alpha	Homo sapiens	85-90
19205902-3	2009	In current manuscript, using THP-1 cells, a human monocytic cell line, we found that ATP7A expression was increased in cells exposed to phorbol-12-myristate-13-acetate (PMA), a potent inducer of neovascularization and cancer.	Tetradecanoylphorbol Acetate	169-172	ATPase copper transporting alpha	Homo sapiens	85-90
19205902-8	2009	Collectively, we demonstrate that PMA induces copper egress in THP-1 cells, which is regulated by ATP7A, and ATP7A regulates VEGFR1 expression.	Tetradecanoylphorbol Acetate	34-37	ATPase copper transporting alpha	Homo sapiens	98-103
18998134-2	2009	Expression of the human copper transporter 1 (hCtr1) is thought to result in increased sensitivity to cisplatin, whereas expression of ATP7A and ATP7B are thought to be involved in resistance to cisplatin either by sequestering drug away from its targets (ATP7A) or by exporting the drug from the cell (ATP7B).	Cisplatin	195-204	ATPase copper transporting alpha	Homo sapiens	135-140
18998134-6	2009	In contrast, overexpression of ATP7A and ATP7B in Me32a fibroblasts resulted in increased resistance to cisplatin, but not to carboplatin or oxaliplatin.	Cisplatin	104-113	ATPase copper transporting alpha	Homo sapiens	31-36
18998134-7	2009	ATP7A-expressing cells (MeMNK) showed a significant enhancement of cisplatin cytotoxicity following O (6)-benzylguanine treatment, but ATP7B-expressing cells (MeWND) did not.	Cisplatin	67-76	ATPase copper transporting alpha	Homo sapiens	0-5
18761103-3	2009	ATOX1 plays an important role in the transfer of copper to the copper export P-type ATPases ATP7A and ATP7B to facilitate copper excretion.	Copper	49-55	ATPase copper transporting alpha	Homo sapiens	92-97
18998134-7	2009	ATP7A-expressing cells (MeMNK) showed a significant enhancement of cisplatin cytotoxicity following O (6)-benzylguanine treatment, but ATP7B-expressing cells (MeWND) did not.	O(6)-benzylguanine	100-119	ATPase copper transporting alpha	Homo sapiens	0-5
19482593-6	2009	Transfer of Cu to newly synthesized cuproenzymes and Cu disposal is performed by the individual or concerted actions of the P-type ATPases ATP7A and ATP7B expressed in tissues.	Copper	12-14	ATPase copper transporting alpha	Homo sapiens	139-144
19482593-6	2009	Transfer of Cu to newly synthesized cuproenzymes and Cu disposal is performed by the individual or concerted actions of the P-type ATPases ATP7A and ATP7B expressed in tissues.	Copper	53-55	ATPase copper transporting alpha	Homo sapiens	139-144
18761103-3	2009	ATOX1 plays an important role in the transfer of copper to the copper export P-type ATPases ATP7A and ATP7B to facilitate copper excretion.	Copper	63-69	ATPase copper transporting alpha	Homo sapiens	92-97
19046832-3	2009	Several severe hereditary human disorders of copper regulatory mechanisms have been identified; they are related to mutations in gene ATP7A and ATP7B coding for copper-transporting proteins.	Copper	45-51	ATPase copper transporting alpha	Homo sapiens	134-139
19416479-1	2009	Human Cu-ATPases ATP7A and ATP7B maintain copper homeostasis through regulated trafficking between intracellular compartments.	Copper	42-48	ATPase copper transporting alpha	Homo sapiens	17-22
19046832-3	2009	Several severe hereditary human disorders of copper regulatory mechanisms have been identified; they are related to mutations in gene ATP7A and ATP7B coding for copper-transporting proteins.	Copper	161-167	ATPase copper transporting alpha	Homo sapiens	134-139
19046832-4	2009	Those mutations result in copper deficiency for ATP7A (Menkes disease) and copper overload for ATP7B (Wilson disease).	Copper	26-32	ATPase copper transporting alpha	Homo sapiens	48-53
18545997-11	2009	The most CDDP-sensitive HSC-3 cells exhibited an increased intracellular cisplatin accumulation, high Na(+),K(+)-ATPase activity and over-expressed Na(+),K(+)-ATPase alpha and beta subunits, ATP7A and ATP7B, compared to the most CDDP-resistant BHY cells, but there were no such differences between the two in the CDDP efflux level or Cu(2+)-ATPase activity.	Cisplatin	9-13	ATPase copper transporting alpha	Homo sapiens	191-196
19130269-1	2009	The copper-translocating Menkes (ATP7A, MNK protein) and Wilson (ATP7B, WND protein) P-type ATPases are pivotal for copper (Cu) homeostasis, functioning in the biosynthetic incorporation of Cu into copper-dependent enzymes of the secretory pathway, Cu detoxification via Cu efflux, and specialized roles such as systemic Cu absorption (MNK) and Cu excretion (WND).	Copper	4-10	ATPase copper transporting alpha	Homo sapiens	33-38
19092723-2	2009	The MD gene, ATP7A (ATPase Cu++ transporting alpha polypeptide), encodes an ATP-dependent copper-binding membrane protein.	Copper	90-96	ATPase copper transporting alpha	Homo sapiens	13-62
19130269-1	2009	The copper-translocating Menkes (ATP7A, MNK protein) and Wilson (ATP7B, WND protein) P-type ATPases are pivotal for copper (Cu) homeostasis, functioning in the biosynthetic incorporation of Cu into copper-dependent enzymes of the secretory pathway, Cu detoxification via Cu efflux, and specialized roles such as systemic Cu absorption (MNK) and Cu excretion (WND).	Copper	116-122	ATPase copper transporting alpha	Homo sapiens	336-339
19130269-1	2009	The copper-translocating Menkes (ATP7A, MNK protein) and Wilson (ATP7B, WND protein) P-type ATPases are pivotal for copper (Cu) homeostasis, functioning in the biosynthetic incorporation of Cu into copper-dependent enzymes of the secretory pathway, Cu detoxification via Cu efflux, and specialized roles such as systemic Cu absorption (MNK) and Cu excretion (WND).	Copper	4-10	ATPase copper transporting alpha	Homo sapiens	40-43
19130269-1	2009	The copper-translocating Menkes (ATP7A, MNK protein) and Wilson (ATP7B, WND protein) P-type ATPases are pivotal for copper (Cu) homeostasis, functioning in the biosynthetic incorporation of Cu into copper-dependent enzymes of the secretory pathway, Cu detoxification via Cu efflux, and specialized roles such as systemic Cu absorption (MNK) and Cu excretion (WND).	Copper	190-192	ATPase copper transporting alpha	Homo sapiens	33-38
19130269-1	2009	The copper-translocating Menkes (ATP7A, MNK protein) and Wilson (ATP7B, WND protein) P-type ATPases are pivotal for copper (Cu) homeostasis, functioning in the biosynthetic incorporation of Cu into copper-dependent enzymes of the secretory pathway, Cu detoxification via Cu efflux, and specialized roles such as systemic Cu absorption (MNK) and Cu excretion (WND).	Copper	4-10	ATPase copper transporting alpha	Homo sapiens	336-339
19130269-1	2009	The copper-translocating Menkes (ATP7A, MNK protein) and Wilson (ATP7B, WND protein) P-type ATPases are pivotal for copper (Cu) homeostasis, functioning in the biosynthetic incorporation of Cu into copper-dependent enzymes of the secretory pathway, Cu detoxification via Cu efflux, and specialized roles such as systemic Cu absorption (MNK) and Cu excretion (WND).	Copper	190-192	ATPase copper transporting alpha	Homo sapiens	40-43
19130269-1	2009	The copper-translocating Menkes (ATP7A, MNK protein) and Wilson (ATP7B, WND protein) P-type ATPases are pivotal for copper (Cu) homeostasis, functioning in the biosynthetic incorporation of Cu into copper-dependent enzymes of the secretory pathway, Cu detoxification via Cu efflux, and specialized roles such as systemic Cu absorption (MNK) and Cu excretion (WND).	Copper	116-122	ATPase copper transporting alpha	Homo sapiens	33-38
19130269-1	2009	The copper-translocating Menkes (ATP7A, MNK protein) and Wilson (ATP7B, WND protein) P-type ATPases are pivotal for copper (Cu) homeostasis, functioning in the biosynthetic incorporation of Cu into copper-dependent enzymes of the secretory pathway, Cu detoxification via Cu efflux, and specialized roles such as systemic Cu absorption (MNK) and Cu excretion (WND).	Copper	190-192	ATPase copper transporting alpha	Homo sapiens	336-339
19130269-1	2009	The copper-translocating Menkes (ATP7A, MNK protein) and Wilson (ATP7B, WND protein) P-type ATPases are pivotal for copper (Cu) homeostasis, functioning in the biosynthetic incorporation of Cu into copper-dependent enzymes of the secretory pathway, Cu detoxification via Cu efflux, and specialized roles such as systemic Cu absorption (MNK) and Cu excretion (WND).	Copper	190-192	ATPase copper transporting alpha	Homo sapiens	33-38
19130269-1	2009	The copper-translocating Menkes (ATP7A, MNK protein) and Wilson (ATP7B, WND protein) P-type ATPases are pivotal for copper (Cu) homeostasis, functioning in the biosynthetic incorporation of Cu into copper-dependent enzymes of the secretory pathway, Cu detoxification via Cu efflux, and specialized roles such as systemic Cu absorption (MNK) and Cu excretion (WND).	Copper	116-122	ATPase copper transporting alpha	Homo sapiens	40-43
19130269-1	2009	The copper-translocating Menkes (ATP7A, MNK protein) and Wilson (ATP7B, WND protein) P-type ATPases are pivotal for copper (Cu) homeostasis, functioning in the biosynthetic incorporation of Cu into copper-dependent enzymes of the secretory pathway, Cu detoxification via Cu efflux, and specialized roles such as systemic Cu absorption (MNK) and Cu excretion (WND).	Copper	190-192	ATPase copper transporting alpha	Homo sapiens	40-43
19130269-1	2009	The copper-translocating Menkes (ATP7A, MNK protein) and Wilson (ATP7B, WND protein) P-type ATPases are pivotal for copper (Cu) homeostasis, functioning in the biosynthetic incorporation of Cu into copper-dependent enzymes of the secretory pathway, Cu detoxification via Cu efflux, and specialized roles such as systemic Cu absorption (MNK) and Cu excretion (WND).	Copper	190-192	ATPase copper transporting alpha	Homo sapiens	336-339
19130269-1	2009	The copper-translocating Menkes (ATP7A, MNK protein) and Wilson (ATP7B, WND protein) P-type ATPases are pivotal for copper (Cu) homeostasis, functioning in the biosynthetic incorporation of Cu into copper-dependent enzymes of the secretory pathway, Cu detoxification via Cu efflux, and specialized roles such as systemic Cu absorption (MNK) and Cu excretion (WND).	Copper	116-122	ATPase copper transporting alpha	Homo sapiens	336-339
19130269-1	2009	The copper-translocating Menkes (ATP7A, MNK protein) and Wilson (ATP7B, WND protein) P-type ATPases are pivotal for copper (Cu) homeostasis, functioning in the biosynthetic incorporation of Cu into copper-dependent enzymes of the secretory pathway, Cu detoxification via Cu efflux, and specialized roles such as systemic Cu absorption (MNK) and Cu excretion (WND).	Copper	190-192	ATPase copper transporting alpha	Homo sapiens	33-38
19130269-1	2009	The copper-translocating Menkes (ATP7A, MNK protein) and Wilson (ATP7B, WND protein) P-type ATPases are pivotal for copper (Cu) homeostasis, functioning in the biosynthetic incorporation of Cu into copper-dependent enzymes of the secretory pathway, Cu detoxification via Cu efflux, and specialized roles such as systemic Cu absorption (MNK) and Cu excretion (WND).	Copper	124-126	ATPase copper transporting alpha	Homo sapiens	33-38
19130269-1	2009	The copper-translocating Menkes (ATP7A, MNK protein) and Wilson (ATP7B, WND protein) P-type ATPases are pivotal for copper (Cu) homeostasis, functioning in the biosynthetic incorporation of Cu into copper-dependent enzymes of the secretory pathway, Cu detoxification via Cu efflux, and specialized roles such as systemic Cu absorption (MNK) and Cu excretion (WND).	Copper	190-192	ATPase copper transporting alpha	Homo sapiens	40-43
19130269-1	2009	The copper-translocating Menkes (ATP7A, MNK protein) and Wilson (ATP7B, WND protein) P-type ATPases are pivotal for copper (Cu) homeostasis, functioning in the biosynthetic incorporation of Cu into copper-dependent enzymes of the secretory pathway, Cu detoxification via Cu efflux, and specialized roles such as systemic Cu absorption (MNK) and Cu excretion (WND).	Copper	190-192	ATPase copper transporting alpha	Homo sapiens	336-339
19130269-1	2009	The copper-translocating Menkes (ATP7A, MNK protein) and Wilson (ATP7B, WND protein) P-type ATPases are pivotal for copper (Cu) homeostasis, functioning in the biosynthetic incorporation of Cu into copper-dependent enzymes of the secretory pathway, Cu detoxification via Cu efflux, and specialized roles such as systemic Cu absorption (MNK) and Cu excretion (WND).	Copper	190-192	ATPase copper transporting alpha	Homo sapiens	33-38
19130269-1	2009	The copper-translocating Menkes (ATP7A, MNK protein) and Wilson (ATP7B, WND protein) P-type ATPases are pivotal for copper (Cu) homeostasis, functioning in the biosynthetic incorporation of Cu into copper-dependent enzymes of the secretory pathway, Cu detoxification via Cu efflux, and specialized roles such as systemic Cu absorption (MNK) and Cu excretion (WND).	Copper	190-192	ATPase copper transporting alpha	Homo sapiens	40-43
19130269-1	2009	The copper-translocating Menkes (ATP7A, MNK protein) and Wilson (ATP7B, WND protein) P-type ATPases are pivotal for copper (Cu) homeostasis, functioning in the biosynthetic incorporation of Cu into copper-dependent enzymes of the secretory pathway, Cu detoxification via Cu efflux, and specialized roles such as systemic Cu absorption (MNK) and Cu excretion (WND).	Copper	190-192	ATPase copper transporting alpha	Homo sapiens	336-339
19130269-2	2009	Essential to these functions is their Cu and hormone-responsive distribution between the trans-Golgi network (TGN) and exocytic vesicles located at or proximal to the apical (WND) or basolateral (MNK) cell surface.	Copper	38-40	ATPase copper transporting alpha	Homo sapiens	196-199
19130269-1	2009	The copper-translocating Menkes (ATP7A, MNK protein) and Wilson (ATP7B, WND protein) P-type ATPases are pivotal for copper (Cu) homeostasis, functioning in the biosynthetic incorporation of Cu into copper-dependent enzymes of the secretory pathway, Cu detoxification via Cu efflux, and specialized roles such as systemic Cu absorption (MNK) and Cu excretion (WND).	Copper	124-126	ATPase copper transporting alpha	Homo sapiens	40-43
19130269-1	2009	The copper-translocating Menkes (ATP7A, MNK protein) and Wilson (ATP7B, WND protein) P-type ATPases are pivotal for copper (Cu) homeostasis, functioning in the biosynthetic incorporation of Cu into copper-dependent enzymes of the secretory pathway, Cu detoxification via Cu efflux, and specialized roles such as systemic Cu absorption (MNK) and Cu excretion (WND).	Copper	124-126	ATPase copper transporting alpha	Homo sapiens	336-339
19130269-1	2009	The copper-translocating Menkes (ATP7A, MNK protein) and Wilson (ATP7B, WND protein) P-type ATPases are pivotal for copper (Cu) homeostasis, functioning in the biosynthetic incorporation of Cu into copper-dependent enzymes of the secretory pathway, Cu detoxification via Cu efflux, and specialized roles such as systemic Cu absorption (MNK) and Cu excretion (WND).	Copper	190-192	ATPase copper transporting alpha	Homo sapiens	33-38
19130269-1	2009	The copper-translocating Menkes (ATP7A, MNK protein) and Wilson (ATP7B, WND protein) P-type ATPases are pivotal for copper (Cu) homeostasis, functioning in the biosynthetic incorporation of Cu into copper-dependent enzymes of the secretory pathway, Cu detoxification via Cu efflux, and specialized roles such as systemic Cu absorption (MNK) and Cu excretion (WND).	Copper	190-192	ATPase copper transporting alpha	Homo sapiens	40-43
19130269-1	2009	The copper-translocating Menkes (ATP7A, MNK protein) and Wilson (ATP7B, WND protein) P-type ATPases are pivotal for copper (Cu) homeostasis, functioning in the biosynthetic incorporation of Cu into copper-dependent enzymes of the secretory pathway, Cu detoxification via Cu efflux, and specialized roles such as systemic Cu absorption (MNK) and Cu excretion (WND).	Copper	190-192	ATPase copper transporting alpha	Homo sapiens	336-339
19130269-1	2009	The copper-translocating Menkes (ATP7A, MNK protein) and Wilson (ATP7B, WND protein) P-type ATPases are pivotal for copper (Cu) homeostasis, functioning in the biosynthetic incorporation of Cu into copper-dependent enzymes of the secretory pathway, Cu detoxification via Cu efflux, and specialized roles such as systemic Cu absorption (MNK) and Cu excretion (WND).	Copper	116-122	ATPase copper transporting alpha	Homo sapiens	33-38
19130269-1	2009	The copper-translocating Menkes (ATP7A, MNK protein) and Wilson (ATP7B, WND protein) P-type ATPases are pivotal for copper (Cu) homeostasis, functioning in the biosynthetic incorporation of Cu into copper-dependent enzymes of the secretory pathway, Cu detoxification via Cu efflux, and specialized roles such as systemic Cu absorption (MNK) and Cu excretion (WND).	Copper	116-122	ATPase copper transporting alpha	Homo sapiens	40-43
18779306-11	2008	Thus, maturation of small intestine copper transport occurs through increased abundance and altered localization of Ctr1, Atp7A, and Atp7B.	Copper	36-42	ATPase copper transporting alpha	Homo sapiens	122-127
19127267-5	2009	ATP7A, the copper efflux pump, is a retinoid-responsive gene, was upregulated by ectopic overexpression of RARbeta(2).	Copper	11-17	ATPase copper transporting alpha	Homo sapiens	0-5
18990686-8	2009	To test the hypothesis, we utilized human fibroblasts that are deleted or overexpressing the Menkes protein (MNK), a major mammalian copper efflux protein.	Copper	133-139	ATPase copper transporting alpha	Homo sapiens	93-107
18990686-8	2009	To test the hypothesis, we utilized human fibroblasts that are deleted or overexpressing the Menkes protein (MNK), a major mammalian copper efflux protein.	Copper	133-139	ATPase copper transporting alpha	Homo sapiens	109-112
18990686-11	2009	Here we demonstrate that copper depletion in MNK overexpressed fibroblasts decreases cellular prion protein and PRNP gene levels.	Copper	25-31	ATPase copper transporting alpha	Homo sapiens	45-48
18990686-12	2009	Conversely, expression of transcription factors SP1 and/or MTF-1 significantly increases prion protein levels and up-regulates prion gene expression in copper-replete MNK deletion cells.	Copper	152-158	ATPase copper transporting alpha	Homo sapiens	167-170
19194885-4	2009	Here, we identify and characterize native read-through of a nonsense mutation (R201X) in the human copper transport gene, ATP7A.	Copper	99-105	ATPase copper transporting alpha	Homo sapiens	122-127
19194885-5	2009	Western blotting, in vitro expression analyses, immunohistochemistry, and yeast complementation assays using cultured fibroblasts from a classic Menkes disease patient all indicated small amounts of native ATP7A(R201X) read-through and were associated with a dramatic clinical response to early copper treatment.	Copper	295-301	ATPase copper transporting alpha	Homo sapiens	206-211
19153371-8	2009	Additional fine mapping in the family refined the DSMAX locus to a 1.44-cM interval between DXS8046 and DXS8114.	dxs8046	92-99	ATPase copper transporting alpha	Homo sapiens	50-55
19153371-8	2009	Additional fine mapping in the family refined the DSMAX locus to a 1.44-cM interval between DXS8046 and DXS8114.	dxs8114	104-111	ATPase copper transporting alpha	Homo sapiens	50-55
19127267-5	2009	ATP7A, the copper efflux pump, is a retinoid-responsive gene, was upregulated by ectopic overexpression of RARbeta(2).	Retinoids	36-44	ATPase copper transporting alpha	Homo sapiens	0-5
19127267-6	2009	The ectopic overexpression of the RARbeta(2) ABC domain was sufficient to induce ATP7A expression, whereas, RARbeta(2) siRNA blocked the induction of ATP7A expression in retinoid-treated neuroblastoma cells.	Retinoids	170-178	ATPase copper transporting alpha	Homo sapiens	150-155
19127267-7	2009	Forced downregulation of ATP7A reduced copper efflux and increased viability of retinoid-treated neuroblastoma cells.	Copper	39-45	ATPase copper transporting alpha	Homo sapiens	25-30
19127267-7	2009	Forced downregulation of ATP7A reduced copper efflux and increased viability of retinoid-treated neuroblastoma cells.	Retinoids	80-88	ATPase copper transporting alpha	Homo sapiens	25-30
19127267-9	2009	Taken together, our data demonstrates ATP7A expression is regulated by retinoic acid receptor beta and it has effects on intracellular copper levels, revealing a link between the anticancer action of retinoids and copper metabolism.	Copper	135-141	ATPase copper transporting alpha	Homo sapiens	38-43
19127267-9	2009	Taken together, our data demonstrates ATP7A expression is regulated by retinoic acid receptor beta and it has effects on intracellular copper levels, revealing a link between the anticancer action of retinoids and copper metabolism.	Retinoids	200-209	ATPase copper transporting alpha	Homo sapiens	38-43
19127267-9	2009	Taken together, our data demonstrates ATP7A expression is regulated by retinoic acid receptor beta and it has effects on intracellular copper levels, revealing a link between the anticancer action of retinoids and copper metabolism.	Copper	214-220	ATPase copper transporting alpha	Homo sapiens	38-43
20045993-0	2009	Genetic polymorphisms of copper- and platinum drug-efflux transporters ATP7A and ATP7B in Japanese cancer patients.	Copper	25-31	ATPase copper transporting alpha	Homo sapiens	71-76
20045993-1	2009	ATP7A and ATP7B are involved in cellular resistance to platinum compounds such as cisplatin.	Platinum	55-63	ATPase copper transporting alpha	Homo sapiens	0-5
20045993-1	2009	ATP7A and ATP7B are involved in cellular resistance to platinum compounds such as cisplatin.	Cisplatin	82-91	ATPase copper transporting alpha	Homo sapiens	0-5
19114980-6	2009	In this review, we summarize current progress on the copper transport system, the structural and functional properties of the Cu-ATPases, ATP7A and ATP7B, in copper homeostasis, and their roles in anti-tumor drug resistance and cancer metastasis.	Copper	158-164	ATPase copper transporting alpha	Homo sapiens	138-143
18752978-0	2008	Clinical outcomes in Menkes disease patients with a copper-responsive ATP7A mutation, G727R.	Copper	52-58	ATPase copper transporting alpha	Homo sapiens	70-75
18752978-3	2008	In three unrelated infants, we identified the same mutation, G727R, in the second transmembrane segment of ATP7A that complemented a Saccharomyces cerevisiae copper transport mutant, consistent with partial copper transport activity.	Copper	158-164	ATPase copper transporting alpha	Homo sapiens	107-112
18752978-3	2008	In three unrelated infants, we identified the same mutation, G727R, in the second transmembrane segment of ATP7A that complemented a Saccharomyces cerevisiae copper transport mutant, consistent with partial copper transport activity.	Copper	207-213	ATPase copper transporting alpha	Homo sapiens	107-112
18752978-5	2008	We confirmed the latter by comparing degradation rates of mutant and wild-type ATP7A via cyclohexamide treatment of cultured fibroblasts; half-life of the G727R mutant was 2.9h and for the wild-type, 11.4h.	4-[2-(3,5-dimethyl-2-oxocyclohexyl)-2-hydroxyethyl]piperidine-2,6-dione	89-102	ATPase copper transporting alpha	Homo sapiens	79-84
18694961-8	2008	We also identified multiple substrates of the mTOR, Rsk, and Mnk kinases as targets of CGP57380.	CGP 57380	87-95	ATPase copper transporting alpha	Homo sapiens	61-64
18694961-9	2008	Finally, we found a novel negative-feedback loop to the mitogen-activated protein kinase/Mnk pathway that is triggered by CGP57380 and demonstrated that an interruption of the loop further increased the activity of the combination against imatinib-sensitive and -resistant CML cells.	Imatinib Mesylate	239-247	ATPase copper transporting alpha	Homo sapiens	89-92
18779306-3	2008	Copper is subsequently absorbed by Ctr1 and then transferred in the enterocyte by the chaperone Atox1 to reach ATP7A for export from the cell.	Copper	0-6	ATPase copper transporting alpha	Homo sapiens	111-116
18779306-5	2008	In situations of high copper exposure, Ctr1 is endocytosed, metallothionein is induced, and ATP7A moves to a more basolateral localization.	Copper	22-28	ATPase copper transporting alpha	Homo sapiens	92-97
18030470-10	2008	In addition, the cellular accumulation of platinum and level of ATP7A mRNA may be factors affecting the cytotoxicity of cisplatin, while the cytotoxicity of oxaliplatin was suggested to be affected by the levels of ATP7A and hOCT1 mRNAs.	Cisplatin	120-129	ATPase copper transporting alpha	Homo sapiens	64-69
18030470-10	2008	In addition, the cellular accumulation of platinum and level of ATP7A mRNA may be factors affecting the cytotoxicity of cisplatin, while the cytotoxicity of oxaliplatin was suggested to be affected by the levels of ATP7A and hOCT1 mRNAs.	Oxaliplatin	157-168	ATPase copper transporting alpha	Homo sapiens	215-220
18565219-0	2008	Altered localisation of the copper efflux transporters ATP7A and ATP7B associated with cisplatin resistance in human ovarian carcinoma cells.	Cisplatin	87-96	ATPase copper transporting alpha	Homo sapiens	55-60
18515074-0	2008	Copper transport during lactation in transgenic mice expressing the human ATP7A protein.	Copper	0-6	ATPase copper transporting alpha	Homo sapiens	74-79
18508032-15	2008	Oxaliplatin accumulation was related to hCTR1 and, at low concentration, ATP7A to DNA adducts formation while the retention was related to hCTR1, OCT2 and ATP7B.	Oxaliplatin	0-11	ATPase copper transporting alpha	Homo sapiens	73-78
19787087-3	2008	Development of this disease is related to expression in family members of an autosomal recessive mutation of the GNE gene, which encodes the bifunctional enzyme UDP-GlcNAc 2-epimerase/ManNAc kinase (GNE/MNK).	Uridine Diphosphate N-Acetylglucosamine	161-171	ATPase copper transporting alpha	Homo sapiens	203-206
18565219-1	2008	BACKGROUND: Copper homeostasis proteins ATP7A and ATP7B are assumed to be involved in the intracellular transport of cisplatin.	Copper	12-18	ATPase copper transporting alpha	Homo sapiens	40-45
18565219-1	2008	BACKGROUND: Copper homeostasis proteins ATP7A and ATP7B are assumed to be involved in the intracellular transport of cisplatin.	Cisplatin	117-126	ATPase copper transporting alpha	Homo sapiens	40-45
18565219-10	2008	Changes in sub cellular localisation of ATP7A and ATP7B may facilitate sequestration of cisplatin in the vesicular structures of A2780cis cells, which may prevent drug binding to genomic DNA and thereby contribute to cisplatin resistance.	Cisplatin	88-97	ATPase copper transporting alpha	Homo sapiens	40-45
18565219-10	2008	Changes in sub cellular localisation of ATP7A and ATP7B may facilitate sequestration of cisplatin in the vesicular structures of A2780cis cells, which may prevent drug binding to genomic DNA and thereby contribute to cisplatin resistance.	Cisplatin	217-226	ATPase copper transporting alpha	Homo sapiens	40-45
17987273-1	2008	Both Atp7b (Wilson disease gene) and Atp7a (Menkes disease gene) have been reported to be trafficked by copper.	Copper	104-110	ATPase copper transporting alpha	Homo sapiens	37-42
18299328-6	2008	Consistent with this, pharmacological inhibition of Mnk activity enhances the suppressive effects of arsenic trioxide on primary leukemic progenitors from patients with acute leukemias.	Arsenic Trioxide	101-117	ATPase copper transporting alpha	Homo sapiens	52-55
18299328-7	2008	Taken together, these findings indicate an important role for Mnk kinases, acting as negative regulators for signals that control generation of arsenic trioxide-dependent apoptosis and antileukemic responses.	Arsenic Trioxide	144-160	ATPase copper transporting alpha	Homo sapiens	62-65
18508592-8	2008	Other Mnk substrates bind to AU-rich elements that modulate the stability/translation of specific mRNAs.	Gold	29-31	ATPase copper transporting alpha	Homo sapiens	6-9
18688737-1	2008	Copper-transporting ATPase 1 and 2 (ATP7A and ATP7B) are two highly homologous P-type copper ATPase exporters.	Copper	86-92	ATPase copper transporting alpha	Homo sapiens	0-34
18688737-1	2008	Copper-transporting ATPase 1 and 2 (ATP7A and ATP7B) are two highly homologous P-type copper ATPase exporters.	Copper	86-92	ATPase copper transporting alpha	Homo sapiens	36-41
18081851-5	2008	Furthermore, we show that the Mnk inhibitor CGP57380 is capable of inhibiting the phosphorylation of eIF4E in keratinocytes, and that the abolishment of eIF4E phosphorylation dramatically decreases the anisomycin-induced protein release of the pro-inflammatory cytokines tumor necrosis factor-alpha (TNF-alpha), IL-1beta and IL-6 as well as the IL-1beta-induced protein release of TNF-alpha.	CGP 57380	44-52	ATPase copper transporting alpha	Homo sapiens	30-33
18081851-5	2008	Furthermore, we show that the Mnk inhibitor CGP57380 is capable of inhibiting the phosphorylation of eIF4E in keratinocytes, and that the abolishment of eIF4E phosphorylation dramatically decreases the anisomycin-induced protein release of the pro-inflammatory cytokines tumor necrosis factor-alpha (TNF-alpha), IL-1beta and IL-6 as well as the IL-1beta-induced protein release of TNF-alpha.	Anisomycin	202-212	ATPase copper transporting alpha	Homo sapiens	30-33
18384105-0	2008	Investigating copper-regulated protein expression in Menkes fibroblasts using antibody microarrays.	Copper	14-20	ATPase copper transporting alpha	Homo sapiens	53-59
18004558-7	2008	Of significance are internal copper transporters, ATP7A and ATP7B, notable for their role in disorders of copper deficiency and toxicity, Menkes and Wilson"s disease, respectively.	Copper	29-35	ATPase copper transporting alpha	Homo sapiens	50-55
18180385-5	2008	Trafficking of ATP7B was copper dependent, suggesting that the hormone-induced redistribution of ATP7A was mediated through an increase in intracellular copper.	Copper	25-31	ATPase copper transporting alpha	Homo sapiens	97-102
18180385-5	2008	Trafficking of ATP7B was copper dependent, suggesting that the hormone-induced redistribution of ATP7A was mediated through an increase in intracellular copper.	Copper	153-159	ATPase copper transporting alpha	Homo sapiens	97-102
17913844-9	2007	Importantly, preventing Arf activation inhibits copper-responsive trafficking of MNK to the PM.	Copper	48-54	ATPase copper transporting alpha	Homo sapiens	81-84
18164262-5	2008	The addition of CGP57380, a specific inhibitor of the eIF-4E kinase Mnk, not only inhibited eIF-4E phosphorylation but also resulted in reduced interaction between eIF-4E and eIF-4G.	CGP 57380	16-24	ATPase copper transporting alpha	Homo sapiens	68-71
18256395-1	2008	BACKGROUND: Menkes disease is a fatal neurodegenerative disorder of infancy caused by diverse mutations in a copper-transport gene, ATP7A.	Copper	109-115	ATPase copper transporting alpha	Homo sapiens	132-137
18256395-12	2008	Affected newborns who have mutations that do not completely abrogate ATP7A function may be especially responsive to early copper treatment.	Copper	122-128	ATPase copper transporting alpha	Homo sapiens	69-74
17989919-1	2008	Menkes disease is caused by mutations in the copper-transporting P(1B)-type ATPase ATP7A.	Copper	45-51	ATPase copper transporting alpha	Homo sapiens	83-88
17989919-2	2008	ATP7A has a dual function: it serves to incorporate copper into copper-dependent enzymes, and it maintains intracellular copper levels by removing excess copper from the cytosol.	Copper	52-58	ATPase copper transporting alpha	Homo sapiens	0-5
17989919-2	2008	ATP7A has a dual function: it serves to incorporate copper into copper-dependent enzymes, and it maintains intracellular copper levels by removing excess copper from the cytosol.	Copper	64-70	ATPase copper transporting alpha	Homo sapiens	0-5
17989919-2	2008	ATP7A has a dual function: it serves to incorporate copper into copper-dependent enzymes, and it maintains intracellular copper levels by removing excess copper from the cytosol.	Copper	64-70	ATPase copper transporting alpha	Homo sapiens	0-5
17989919-2	2008	ATP7A has a dual function: it serves to incorporate copper into copper-dependent enzymes, and it maintains intracellular copper levels by removing excess copper from the cytosol.	Copper	64-70	ATPase copper transporting alpha	Homo sapiens	0-5
19075668-9	2008	We, and others, found that ATP7A and ATP7B are involved in drug resistance against the anti-tumor drug cis-diamminedichloroplatinum (II) (CDDP).	Cisplatin	103-131	ATPase copper transporting alpha	Homo sapiens	27-32
19075668-9	2008	We, and others, found that ATP7A and ATP7B are involved in drug resistance against the anti-tumor drug cis-diamminedichloroplatinum (II) (CDDP).	Cisplatin	138-142	ATPase copper transporting alpha	Homo sapiens	27-32
19075668-10	2008	A relationship between the expression of ATP7A or ATP7B in tumors and CDDP resistance is supported by clinical studies.	Cisplatin	70-74	ATPase copper transporting alpha	Homo sapiens	41-46
19075668-12	2008	Furthermore, we have recently found that the effect of ATP7A on drug resistance is not limited to CDDP.	Cisplatin	98-102	ATPase copper transporting alpha	Homo sapiens	55-60
19075668-13	2008	Using an ex vivo drug sensitivity assay, the histoculture drug response assay (HDRA), the expression of ATP7A in human surgically resected colon cancer cells correlated with sensitivity to 7-ethyl-10-hydroxy-camptothecin (SN-38).	Irinotecan	222-227	ATPase copper transporting alpha	Homo sapiens	104-109
19075668-14	2008	ATP7A-overexpressing cells are resistant to many anticancer drugs including SN-38, 7-ethyl-10-[4-(1-piperidino)-1-piperidino] carbonyloxycamptothecin (CPT-11), vincristine, paclitaxel, etoposide, doxorubicin (Dox), and mitoxantron.	Irinotecan	76-81	ATPase copper transporting alpha	Homo sapiens	0-5
19075668-14	2008	ATP7A-overexpressing cells are resistant to many anticancer drugs including SN-38, 7-ethyl-10-[4-(1-piperidino)-1-piperidino] carbonyloxycamptothecin (CPT-11), vincristine, paclitaxel, etoposide, doxorubicin (Dox), and mitoxantron.	Irinotecan	83-149	ATPase copper transporting alpha	Homo sapiens	0-5
19075668-14	2008	ATP7A-overexpressing cells are resistant to many anticancer drugs including SN-38, 7-ethyl-10-[4-(1-piperidino)-1-piperidino] carbonyloxycamptothecin (CPT-11), vincristine, paclitaxel, etoposide, doxorubicin (Dox), and mitoxantron.	Irinotecan	151-157	ATPase copper transporting alpha	Homo sapiens	0-5
19075668-14	2008	ATP7A-overexpressing cells are resistant to many anticancer drugs including SN-38, 7-ethyl-10-[4-(1-piperidino)-1-piperidino] carbonyloxycamptothecin (CPT-11), vincristine, paclitaxel, etoposide, doxorubicin (Dox), and mitoxantron.	Vincristine	160-171	ATPase copper transporting alpha	Homo sapiens	0-5
19075668-14	2008	ATP7A-overexpressing cells are resistant to many anticancer drugs including SN-38, 7-ethyl-10-[4-(1-piperidino)-1-piperidino] carbonyloxycamptothecin (CPT-11), vincristine, paclitaxel, etoposide, doxorubicin (Dox), and mitoxantron.	Paclitaxel	173-183	ATPase copper transporting alpha	Homo sapiens	0-5
19075668-14	2008	ATP7A-overexpressing cells are resistant to many anticancer drugs including SN-38, 7-ethyl-10-[4-(1-piperidino)-1-piperidino] carbonyloxycamptothecin (CPT-11), vincristine, paclitaxel, etoposide, doxorubicin (Dox), and mitoxantron.	Etoposide	185-194	ATPase copper transporting alpha	Homo sapiens	0-5
19075668-14	2008	ATP7A-overexpressing cells are resistant to many anticancer drugs including SN-38, 7-ethyl-10-[4-(1-piperidino)-1-piperidino] carbonyloxycamptothecin (CPT-11), vincristine, paclitaxel, etoposide, doxorubicin (Dox), and mitoxantron.	Doxorubicin	196-207	ATPase copper transporting alpha	Homo sapiens	0-5
19075668-14	2008	ATP7A-overexpressing cells are resistant to many anticancer drugs including SN-38, 7-ethyl-10-[4-(1-piperidino)-1-piperidino] carbonyloxycamptothecin (CPT-11), vincristine, paclitaxel, etoposide, doxorubicin (Dox), and mitoxantron.	Doxorubicin	209-212	ATPase copper transporting alpha	Homo sapiens	0-5
19075668-14	2008	ATP7A-overexpressing cells are resistant to many anticancer drugs including SN-38, 7-ethyl-10-[4-(1-piperidino)-1-piperidino] carbonyloxycamptothecin (CPT-11), vincristine, paclitaxel, etoposide, doxorubicin (Dox), and mitoxantron.	Mitoxantrone	219-230	ATPase copper transporting alpha	Homo sapiens	0-5
19075668-16	2008	In ATP7A overexpressing cells, Dox accumulates in the Golgi apparatus.	Doxorubicin	31-34	ATPase copper transporting alpha	Homo sapiens	3-8
19075668-18	2008	Disruption of the intracellular vesicle transport system with monensin, a Na+/H+ ionophore, induced the relocalization of Dox from the Golgi apparatus to the nuclei in the ATP7A overexpressing cells.	Doxorubicin	122-125	ATPase copper transporting alpha	Homo sapiens	172-177
17913844-1	2007	ATP7A (MNK) regulates copper homeostasis by translocating from a compartment localized within the trans-Golgi network to the plasma membrane (PM) in response to increased copper load.	Copper	22-28	ATPase copper transporting alpha	Homo sapiens	0-5
17913844-1	2007	ATP7A (MNK) regulates copper homeostasis by translocating from a compartment localized within the trans-Golgi network to the plasma membrane (PM) in response to increased copper load.	Copper	22-28	ATPase copper transporting alpha	Homo sapiens	7-10
17913844-1	2007	ATP7A (MNK) regulates copper homeostasis by translocating from a compartment localized within the trans-Golgi network to the plasma membrane (PM) in response to increased copper load.	Copper	171-177	ATPase copper transporting alpha	Homo sapiens	0-5
17913844-1	2007	ATP7A (MNK) regulates copper homeostasis by translocating from a compartment localized within the trans-Golgi network to the plasma membrane (PM) in response to increased copper load.	Copper	171-177	ATPase copper transporting alpha	Homo sapiens	7-10
17913844-6	2007	Despite altered localization MNK trafficking still occurs, and MNK relocates from and returns to the fragmented compartment in response to copper.	Copper	139-145	ATPase copper transporting alpha	Homo sapiens	63-66
17913844-10	2007	Our findings support a model in which active Arf is essential for the generation of the MNK compartment and for copper-responsive trafficking of MNK from there to the PM.	Copper	112-118	ATPase copper transporting alpha	Homo sapiens	145-148
17609664-8	2007	Partial reversal of the resistance of S3 cells to oxaliplatin and CDDP was observed by treating cell with ATP7A-targeted siRNA oligonucleotides or P-type ATPase-inhibitor sodium orthovanadate.	Oxaliplatin	50-61	ATPase copper transporting alpha	Homo sapiens	106-111
18000748-3	2007	The biosynthetic incorporation of copper into these enzymes takes places within the secretory pathway and is critically dependent on the activity of copper-transporting ATPases ATP7A or ATP7B.	Copper	34-40	ATPase copper transporting alpha	Homo sapiens	177-182
18000748-4	2007	In addition, ATP7A and ATP7B regulate intracellular copper concentration by removing excess copper from the cell.	Copper	52-58	ATPase copper transporting alpha	Homo sapiens	13-18
18000748-4	2007	In addition, ATP7A and ATP7B regulate intracellular copper concentration by removing excess copper from the cell.	Copper	92-98	ATPase copper transporting alpha	Homo sapiens	13-18
17717039-3	2007	Central regulators of cellular copper metabolism are the copper-transporting P-type ATPases ATP7A and ATP7B.	Copper	31-37	ATPase copper transporting alpha	Homo sapiens	92-97
17717039-3	2007	Central regulators of cellular copper metabolism are the copper-transporting P-type ATPases ATP7A and ATP7B.	Copper	57-63	ATPase copper transporting alpha	Homo sapiens	92-97
17717039-4	2007	Mutations in ATP7A or ATP7B disrupt the homeostatic copper balance, resulting in copper deficiency (Menkes disease) or copper overload (Wilson disease), respectively.	Copper	52-58	ATPase copper transporting alpha	Homo sapiens	13-18
17717039-4	2007	Mutations in ATP7A or ATP7B disrupt the homeostatic copper balance, resulting in copper deficiency (Menkes disease) or copper overload (Wilson disease), respectively.	Copper	81-87	ATPase copper transporting alpha	Homo sapiens	13-18
17717039-5	2007	ATP7A and ATP7B exert their functions in copper transport through a variety of interdependent mechanisms and regulatory events, including their catalytic ATPase activity, copper-induced trafficking, post-translational modifications and protein-protein interactions.	Copper	41-47	ATPase copper transporting alpha	Homo sapiens	0-5
17717039-5	2007	ATP7A and ATP7B exert their functions in copper transport through a variety of interdependent mechanisms and regulatory events, including their catalytic ATPase activity, copper-induced trafficking, post-translational modifications and protein-protein interactions.	Copper	171-177	ATPase copper transporting alpha	Homo sapiens	0-5
17545667-0	2007	The different intermolecular interactions of the soluble copper-binding domains of the menkes protein, ATP7A.	Copper	57-63	ATPase copper transporting alpha	Homo sapiens	103-108
17545667-1	2007	ATP7A is a P-type ATPase involved in copper(I) homeostasis in humans.	Copper	37-43	ATPase copper transporting alpha	Homo sapiens	0-5
17545667-7	2007	The present data, together with available in vivo studies, suggest that the localization of ATP7A between the trans-Golgi network and the plasma membrane may be regulated by the accumulation of the adducts with HAH1, whereas the main role of domains 5 and 6 is to assist copper(I) translocation.	Copper	271-277	ATPase copper transporting alpha	Homo sapiens	92-97
17987894-2	2007	The ATP7A gene encodes for a copper transporting P-type ATPase (ATP7A), which is ubiquitously expressed.	Copper	29-35	ATPase copper transporting alpha	Homo sapiens	4-9
17987894-2	2007	The ATP7A gene encodes for a copper transporting P-type ATPase (ATP7A), which is ubiquitously expressed.	Copper	29-35	ATPase copper transporting alpha	Homo sapiens	64-69
17987894-3	2007	A defect of the ATP7A protein leads to both a reduced transport of copper from the intestine into the circulation and into the central nervous system, as well as reduced transport of copper into the Golgi apparatus for incorporation into various copper-dependent enzymes.	Copper	67-73	ATPase copper transporting alpha	Homo sapiens	16-21
17987894-3	2007	A defect of the ATP7A protein leads to both a reduced transport of copper from the intestine into the circulation and into the central nervous system, as well as reduced transport of copper into the Golgi apparatus for incorporation into various copper-dependent enzymes.	Copper	183-189	ATPase copper transporting alpha	Homo sapiens	16-21
17987894-3	2007	A defect of the ATP7A protein leads to both a reduced transport of copper from the intestine into the circulation and into the central nervous system, as well as reduced transport of copper into the Golgi apparatus for incorporation into various copper-dependent enzymes.	Copper	183-189	ATPase copper transporting alpha	Homo sapiens	16-21
17483305-1	2007	Owing to mutations in the copper-transporting P-type ATPase, ATP7A (or MNK), patients with Menkes disease (MD) have an inadequate supply of copper to various copper-dependent enzymes.	Copper	26-32	ATPase copper transporting alpha	Homo sapiens	61-66
17483305-1	2007	Owing to mutations in the copper-transporting P-type ATPase, ATP7A (or MNK), patients with Menkes disease (MD) have an inadequate supply of copper to various copper-dependent enzymes.	Copper	26-32	ATPase copper transporting alpha	Homo sapiens	71-74
17483305-1	2007	Owing to mutations in the copper-transporting P-type ATPase, ATP7A (or MNK), patients with Menkes disease (MD) have an inadequate supply of copper to various copper-dependent enzymes.	Copper	140-146	ATPase copper transporting alpha	Homo sapiens	61-66
17483305-1	2007	Owing to mutations in the copper-transporting P-type ATPase, ATP7A (or MNK), patients with Menkes disease (MD) have an inadequate supply of copper to various copper-dependent enzymes.	Copper	140-146	ATPase copper transporting alpha	Homo sapiens	71-74
17609664-8	2007	Partial reversal of the resistance of S3 cells to oxaliplatin and CDDP was observed by treating cell with ATP7A-targeted siRNA oligonucleotides or P-type ATPase-inhibitor sodium orthovanadate.	Cisplatin	66-70	ATPase copper transporting alpha	Homo sapiens	106-111
17609664-8	2007	Partial reversal of the resistance of S3 cells to oxaliplatin and CDDP was observed by treating cell with ATP7A-targeted siRNA oligonucleotides or P-type ATPase-inhibitor sodium orthovanadate.	Oligonucleotides	127-143	ATPase copper transporting alpha	Homo sapiens	106-111
17609664-10	2007	Together, our results show that the mechanism responsible for oxaliplatin and CDDP resistance in S3 cells is the combination of increased DNA repair and overexpression of ATP7A.	Oxaliplatin	62-73	ATPase copper transporting alpha	Homo sapiens	171-176
17609664-10	2007	Together, our results show that the mechanism responsible for oxaliplatin and CDDP resistance in S3 cells is the combination of increased DNA repair and overexpression of ATP7A.	Cisplatin	78-82	ATPase copper transporting alpha	Homo sapiens	171-176
17616150-1	2007	The human antioxidant protein, HAH1, is an important participant in a Cu(I) transport chain, delivering one Cu(I) ion to the Wilson"s (WND) or Menkes disease protein (MNK).	cuprous ion	70-75	ATPase copper transporting alpha	Homo sapiens	167-170
17496194-4	2007	RESULTS: In two brothers (family A) with A1362D, RNase protection and Western blot analyses revealed higher amounts of ATP7A transcript and protein in the older, mildly affected patient, who also had a higher plasma copper level and lower cerebrospinal fluid dihydroxyphenylalanine : dihydroxyphenylglycol ratio.	Copper	216-222	ATPase copper transporting alpha	Homo sapiens	119-124
17496194-4	2007	RESULTS: In two brothers (family A) with A1362D, RNase protection and Western blot analyses revealed higher amounts of ATP7A transcript and protein in the older, mildly affected patient, who also had a higher plasma copper level and lower cerebrospinal fluid dihydroxyphenylalanine : dihydroxyphenylglycol ratio.	Dihydroxyphenylalanine	259-281	ATPase copper transporting alpha	Homo sapiens	119-124
17496194-4	2007	RESULTS: In two brothers (family A) with A1362D, RNase protection and Western blot analyses revealed higher amounts of ATP7A transcript and protein in the older, mildly affected patient, who also had a higher plasma copper level and lower cerebrospinal fluid dihydroxyphenylalanine : dihydroxyphenylglycol ratio.	dihydroxyphenylglycol	284-305	ATPase copper transporting alpha	Homo sapiens	119-124
17616150-1	2007	The human antioxidant protein, HAH1, is an important participant in a Cu(I) transport chain, delivering one Cu(I) ion to the Wilson"s (WND) or Menkes disease protein (MNK).	cuprous ion	108-113	ATPase copper transporting alpha	Homo sapiens	167-170
17562324-2	2007	The biosynthetic incorporation of copper into secreted and plasma membrane-bound proteins requires activity of the copper-transporting ATPases (Cu-ATPases) ATP7A and ATP7B.	Copper	34-40	ATPase copper transporting alpha	Homo sapiens	156-161
17531189-0	2007	Trafficking of the copper-ATPases, ATP7A and ATP7B: role in copper homeostasis.	Copper	60-66	ATPase copper transporting alpha	Homo sapiens	35-40
17229731-3	2007	The MBDs interact with the copper chaperone Atox1 and are believed to play roles in catalysis and in copper-mediated cellular relocalization of WND and MNK.	Copper	27-33	ATPase copper transporting alpha	Homo sapiens	152-155
17531189-2	2007	The copper-transporting P-type ATPases, ATP7A and ATP7B are key molecules required for the regulation and maintenance of mammalian copper homeostasis.	Copper	4-10	ATPase copper transporting alpha	Homo sapiens	40-45
17531189-2	2007	The copper-transporting P-type ATPases, ATP7A and ATP7B are key molecules required for the regulation and maintenance of mammalian copper homeostasis.	Copper	131-137	ATPase copper transporting alpha	Homo sapiens	40-45
17531189-5	2007	A unique feature of ATP7A and ATP7B that is integral to these functions is their ability to sense and respond to intracellular copper levels, the latter manifested through their copper-regulated trafficking from the transGolgi network to the appropriate cellular membrane domain (basolateral or apical, respectively) to eliminate excess copper from the cell.	Copper	127-133	ATPase copper transporting alpha	Homo sapiens	20-25
17531189-5	2007	A unique feature of ATP7A and ATP7B that is integral to these functions is their ability to sense and respond to intracellular copper levels, the latter manifested through their copper-regulated trafficking from the transGolgi network to the appropriate cellular membrane domain (basolateral or apical, respectively) to eliminate excess copper from the cell.	Copper	178-184	ATPase copper transporting alpha	Homo sapiens	20-25
17531189-5	2007	A unique feature of ATP7A and ATP7B that is integral to these functions is their ability to sense and respond to intracellular copper levels, the latter manifested through their copper-regulated trafficking from the transGolgi network to the appropriate cellular membrane domain (basolateral or apical, respectively) to eliminate excess copper from the cell.	Copper	178-184	ATPase copper transporting alpha	Homo sapiens	20-25
17510416-0	2007	Copper-transporting P-type ATPase, ATP7A, confers multidrug resistance and its expression is related to resistance to SN-38 in clinical colon cancer.	Irinotecan	118-123	ATPase copper transporting alpha	Homo sapiens	35-40
17510416-1	2007	We and others have shown that the copper transporters ATP7A and ATP7B play a role in cellular resistance to cis-diaminedichloroplatinum (II) (CDDP).	cis-diaminedichloroplatinum (ii)	108-140	ATPase copper transporting alpha	Homo sapiens	54-59
17510416-1	2007	We and others have shown that the copper transporters ATP7A and ATP7B play a role in cellular resistance to cis-diaminedichloroplatinum (II) (CDDP).	cddp	142-146	ATPase copper transporting alpha	Homo sapiens	54-59
17510416-3	2007	ATP7A preferentially localized doxorubicin fluorescence to the Golgi apparatus in contrast to the more intense nuclear staining of doxorubicin in the parental cells.	Doxorubicin	31-42	ATPase copper transporting alpha	Homo sapiens	0-5
17510416-4	2007	Brefeldin A partially and monensin completely altered the distribution of doxorubicin to the nuclei in the ATP7A-expressing cells.	Brefeldin A	0-11	ATPase copper transporting alpha	Homo sapiens	107-112
17510416-4	2007	Brefeldin A partially and monensin completely altered the distribution of doxorubicin to the nuclei in the ATP7A-expressing cells.	Doxorubicin	74-85	ATPase copper transporting alpha	Homo sapiens	107-112
17510416-5	2007	ATP7A expression also enhanced the efflux rates of doxorubicin and SN-38 from cells and increased the uptake of SN-38 in membrane vesicles.	Doxorubicin	51-62	ATPase copper transporting alpha	Homo sapiens	0-5
17510416-5	2007	ATP7A expression also enhanced the efflux rates of doxorubicin and SN-38 from cells and increased the uptake of SN-38 in membrane vesicles.	Irinotecan	67-72	ATPase copper transporting alpha	Homo sapiens	0-5
17510416-5	2007	ATP7A expression also enhanced the efflux rates of doxorubicin and SN-38 from cells and increased the uptake of SN-38 in membrane vesicles.	Irinotecan	112-117	ATPase copper transporting alpha	Homo sapiens	0-5
17510416-8	2007	Using the histoculture drug response assay that is useful for the prediction of drug sensitivity of clinical cancers, ATP7A-expressing colon cancer cells were significantly more resistant to SN-38 than ATP7A-negative cells.	Irinotecan	191-196	ATPase copper transporting alpha	Homo sapiens	118-123
17336116-1	2007	Classical Menkes disease is an X-linked recessive neurodegenerative disorder caused by mutations in a P-type ATPase (ATP7A) that normally delivers copper to the developing central nervous system.	Copper	147-153	ATPase copper transporting alpha	Homo sapiens	117-122
17336116-2	2007	Infants with large deletions, or other mutations in ATP7A that incapacitate copper transport to the brain, show poor clinical outcomes and subnormal brain copper despite early subcutaneous copper histidine (CuHis) injections.	Copper	76-82	ATPase copper transporting alpha	Homo sapiens	52-57
17336116-2	2007	Infants with large deletions, or other mutations in ATP7A that incapacitate copper transport to the brain, show poor clinical outcomes and subnormal brain copper despite early subcutaneous copper histidine (CuHis) injections.	Copper	155-161	ATPase copper transporting alpha	Homo sapiens	52-57
17336116-2	2007	Infants with large deletions, or other mutations in ATP7A that incapacitate copper transport to the brain, show poor clinical outcomes and subnormal brain copper despite early subcutaneous copper histidine (CuHis) injections.	copper histidine	189-205	ATPase copper transporting alpha	Homo sapiens	52-57
17336116-2	2007	Infants with large deletions, or other mutations in ATP7A that incapacitate copper transport to the brain, show poor clinical outcomes and subnormal brain copper despite early subcutaneous copper histidine (CuHis) injections.	copper histidine	207-212	ATPase copper transporting alpha	Homo sapiens	52-57
17695505-0	2007	Effect of copper and role of the copper transporters ATP7A and CTR1 in intracellular accumulation of cisplatin.	Cisplatin	101-110	ATPase copper transporting alpha	Homo sapiens	53-58
17695505-5	2007	ATP7A expression was markedly increased by exposure to CDDP with or without copper in KB cells but not in KBR/1.2 cells.	cddp	55-59	ATPase copper transporting alpha	Homo sapiens	0-5
17695505-5	2007	ATP7A expression was markedly increased by exposure to CDDP with or without copper in KB cells but not in KBR/1.2 cells.	Copper	76-82	ATPase copper transporting alpha	Homo sapiens	0-5
17695505-7	2007	These results indicate that a high concentration of copper causes a significant increase in the cellular accumulation of CDDP and binding of platinum to DNA independently of CTR1 expression in KB cells and CDDP-resistant sublines thereof and that the acquisition of CDDP resistance is associated with a greatly reduced level of ATP7A and a marginally lower expression of CTR1.	Copper	52-58	ATPase copper transporting alpha	Homo sapiens	328-333
17158254-0	2007	Dynamics of endogenous ATP7A (Menkes protein) in intestinal epithelial cells: copper-dependent redistribution between two intracellular sites.	Copper	78-84	ATPase copper transporting alpha	Homo sapiens	23-28
17158254-2	2007	We used high-resolution, confocal immunofluorescence combined with quantitative cell surface biotinylation and found that the vast majority of endogenous ATP7A was localized intracellularly under all copper conditions.	Copper	200-206	ATPase copper transporting alpha	Homo sapiens	154-159
17158254-3	2007	In copper-depleted cells, virtually all of the ATP7A localized to a post-TGN compartment, with <3% of the total protein detectable at the basolateral cell surface.	Copper	3-9	ATPase copper transporting alpha	Homo sapiens	47-52
17158254-4	2007	When copper levels were elevated, ATP7A dispersed to the cell periphery in punctae whose pattern did not overlap with the steady-state distributions of post-Golgi, endosomal, or basolateral membrane markers; only approximately 8-10% of the recovered ATP7A was detected at the basolateral cell surface.	Copper	5-11	ATPase copper transporting alpha	Homo sapiens	34-39
17158254-4	2007	When copper levels were elevated, ATP7A dispersed to the cell periphery in punctae whose pattern did not overlap with the steady-state distributions of post-Golgi, endosomal, or basolateral membrane markers; only approximately 8-10% of the recovered ATP7A was detected at the basolateral cell surface.	Copper	5-11	ATPase copper transporting alpha	Homo sapiens	250-255
17229731-3	2007	The MBDs interact with the copper chaperone Atox1 and are believed to play roles in catalysis and in copper-mediated cellular relocalization of WND and MNK.	Copper	101-107	ATPase copper transporting alpha	Homo sapiens	152-155
17318448-5	2007	Evidence also suggests that the two copper efflux transporters ATP7A and ATP7B regulate the efflux of cisplatin.	Cisplatin	102-111	ATPase copper transporting alpha	Homo sapiens	63-68
17109627-3	2007	Two copper-transporting ATPases, Menkes (ATP7A; MNK) and Wilson (ATP7B; WND), are expressed in the placenta and both are involved in placental copper transport, as copper accumulates in the placenta in both Menkes and Wilson disease.	Copper	4-10	ATPase copper transporting alpha	Homo sapiens	41-46
17109627-3	2007	Two copper-transporting ATPases, Menkes (ATP7A; MNK) and Wilson (ATP7B; WND), are expressed in the placenta and both are involved in placental copper transport, as copper accumulates in the placenta in both Menkes and Wilson disease.	Copper	4-10	ATPase copper transporting alpha	Homo sapiens	48-51
17109627-7	2007	Insulin and oestrogen increased both MNK mRNA and protein levels, altered the localization of MNK towards the basolateral membrane in a copper-independent manner, and increased the transport of copper across this membrane.	Copper	136-142	ATPase copper transporting alpha	Homo sapiens	94-97
17109627-9	2007	These results are consistent with a model of copper transport in the placenta in which MNK delivers copper to the foetus and WND returns excess copper to the maternal circulation.	Copper	45-51	ATPase copper transporting alpha	Homo sapiens	87-90
17109627-9	2007	These results are consistent with a model of copper transport in the placenta in which MNK delivers copper to the foetus and WND returns excess copper to the maternal circulation.	Copper	100-106	ATPase copper transporting alpha	Homo sapiens	87-90
17109627-9	2007	These results are consistent with a model of copper transport in the placenta in which MNK delivers copper to the foetus and WND returns excess copper to the maternal circulation.	Copper	100-106	ATPase copper transporting alpha	Homo sapiens	87-90
17109627-10	2007	Insulin and oestrogen stimulate copper transport to the foetus by increasing the expression of MNK and reducing the expression of WND.	Copper	32-38	ATPase copper transporting alpha	Homo sapiens	95-98
17318448-8	2007	While the mechanisms by which hCtr1, ATP7A and ATP7B transport copper ions have been studied extensively, very little is known about the mechanisms by which these transporters shuffle platinum-based antitumor agents.	Copper	63-69	ATPase copper transporting alpha	Homo sapiens	37-42
17009961-5	2007	Formation of the classical vanadate-sensitive phosphoenzyme by purified MNK was activated by Cu(I) [EC50=0.7 microM; h (Hill coefficient) was 4.6].	cuprous ion	93-98	ATPase copper transporting alpha	Homo sapiens	72-75
17009961-7	2007	The purified MNK demonstrated active ATP-dependent vectorial 64Cu transport when reconstituted into soya-bean asolectin liposomes.	Adenosine Triphosphate	37-40	ATPase copper transporting alpha	Homo sapiens	13-16
17009961-1	2007	The MNK (Menkes disease protein; ATP7A) is a major copper- transporting P-type ATPase involved in the delivery of copper to cuproenzymes in the secretory pathway and the efflux of excess copper from extrahepatic tissues.	Copper	51-57	ATPase copper transporting alpha	Homo sapiens	4-7
17009961-8	2007	Together, these data demonstrated that Cu(I) interacts with MNK in a co-operative manner and with high affinity in the sub-micromolar range.	cuprous ion	39-44	ATPase copper transporting alpha	Homo sapiens	60-63
17009961-1	2007	The MNK (Menkes disease protein; ATP7A) is a major copper- transporting P-type ATPase involved in the delivery of copper to cuproenzymes in the secretory pathway and the efflux of excess copper from extrahepatic tissues.	Copper	51-57	ATPase copper transporting alpha	Homo sapiens	33-38
17009961-1	2007	The MNK (Menkes disease protein; ATP7A) is a major copper- transporting P-type ATPase involved in the delivery of copper to cuproenzymes in the secretory pathway and the efflux of excess copper from extrahepatic tissues.	Copper	114-120	ATPase copper transporting alpha	Homo sapiens	4-7
17975309-1	2007	BACKGROUND/AIMS: The copper transporting ATPases, Menkes (ATP7A; MNK) and Wilson (ATP7B; WND) are essential for normal copper transport in the human body.	Copper	21-27	ATPase copper transporting alpha	Homo sapiens	58-63
17009961-1	2007	The MNK (Menkes disease protein; ATP7A) is a major copper- transporting P-type ATPase involved in the delivery of copper to cuproenzymes in the secretory pathway and the efflux of excess copper from extrahepatic tissues.	Copper	114-120	ATPase copper transporting alpha	Homo sapiens	33-38
17009961-3	2007	Currently, detailed biochemical and biophysical analyses of MNK to better understand its mechanisms of copper transport are not possible due to the lack of purified MNK in an active form.	Copper	103-109	ATPase copper transporting alpha	Homo sapiens	60-63
17009961-4	2007	To address this issue, we expressed human MNK with an N-terminal Glu-Glu tag in Sf9 [Spodoptera frugiperda (fall armyworm) 9] insect cells and purified it by antibody affinity chromatography followed by size-exclusion chromatography in the presence of the non-ionic detergent DDM (n-dodecyl beta-D-maltopyranoside).	Glutamic Acid	65-68	ATPase copper transporting alpha	Homo sapiens	42-45
17009961-4	2007	To address this issue, we expressed human MNK with an N-terminal Glu-Glu tag in Sf9 [Spodoptera frugiperda (fall armyworm) 9] insect cells and purified it by antibody affinity chromatography followed by size-exclusion chromatography in the presence of the non-ionic detergent DDM (n-dodecyl beta-D-maltopyranoside).	Glutamic Acid	69-72	ATPase copper transporting alpha	Homo sapiens	42-45
17009961-4	2007	To address this issue, we expressed human MNK with an N-terminal Glu-Glu tag in Sf9 [Spodoptera frugiperda (fall armyworm) 9] insect cells and purified it by antibody affinity chromatography followed by size-exclusion chromatography in the presence of the non-ionic detergent DDM (n-dodecyl beta-D-maltopyranoside).	dodecyl maltopyranoside	276-279	ATPase copper transporting alpha	Homo sapiens	42-45
17009961-4	2007	To address this issue, we expressed human MNK with an N-terminal Glu-Glu tag in Sf9 [Spodoptera frugiperda (fall armyworm) 9] insect cells and purified it by antibody affinity chromatography followed by size-exclusion chromatography in the presence of the non-ionic detergent DDM (n-dodecyl beta-D-maltopyranoside).	dodecyl maltopyranoside	281-313	ATPase copper transporting alpha	Homo sapiens	42-45
17009961-5	2007	Formation of the classical vanadate-sensitive phosphoenzyme by purified MNK was activated by Cu(I) [EC50=0.7 microM; h (Hill coefficient) was 4.6].	Vanadates	27-35	ATPase copper transporting alpha	Homo sapiens	72-75
17506666-3	2007	For iron, this regulation is achieved by transferrin receptor, DMT1, and ferroportin, whereas mammary gland copper metabolism is regulated by Ctr1, ATP7A, and ATP7B.	Copper	108-114	ATPase copper transporting alpha	Homo sapiens	148-153
17975309-1	2007	BACKGROUND/AIMS: The copper transporting ATPases, Menkes (ATP7A; MNK) and Wilson (ATP7B; WND) are essential for normal copper transport in the human body.	Copper	21-27	ATPase copper transporting alpha	Homo sapiens	65-68
17975309-4	2007	METHODS/RESULTS: Using polarized placental Jeg-3 cells, siRNA technology and radio-labelled 64Cu transport assays, MNK and WND were shown to have distinct roles in the vectorial transport of copper.	Copper	191-197	ATPase copper transporting alpha	Homo sapiens	115-118
17975309-5	2007	MNK transported copper from the cell via the basolateral membrane and in contrast, WND transported copper from the apical membrane.	Copper	16-22	ATPase copper transporting alpha	Homo sapiens	0-3
17975309-7	2007	CONCLUSIONS: Overall, these results provide definitive evidence for distinct roles of MNK and WND in the human placenta, and are consistent with a role for MNK in the transport of copper into the fetal circulation, and through delivery of copper to placental cuproenzymes, whilst WND contributes to the maintenance of placental copper homeostasis by transporting copper to the maternal circulation.	Copper	180-186	ATPase copper transporting alpha	Homo sapiens	156-159
17975309-7	2007	CONCLUSIONS: Overall, these results provide definitive evidence for distinct roles of MNK and WND in the human placenta, and are consistent with a role for MNK in the transport of copper into the fetal circulation, and through delivery of copper to placental cuproenzymes, whilst WND contributes to the maintenance of placental copper homeostasis by transporting copper to the maternal circulation.	Copper	239-245	ATPase copper transporting alpha	Homo sapiens	156-159
17975309-7	2007	CONCLUSIONS: Overall, these results provide definitive evidence for distinct roles of MNK and WND in the human placenta, and are consistent with a role for MNK in the transport of copper into the fetal circulation, and through delivery of copper to placental cuproenzymes, whilst WND contributes to the maintenance of placental copper homeostasis by transporting copper to the maternal circulation.	Copper	239-245	ATPase copper transporting alpha	Homo sapiens	156-159
17975309-7	2007	CONCLUSIONS: Overall, these results provide definitive evidence for distinct roles of MNK and WND in the human placenta, and are consistent with a role for MNK in the transport of copper into the fetal circulation, and through delivery of copper to placental cuproenzymes, whilst WND contributes to the maintenance of placental copper homeostasis by transporting copper to the maternal circulation.	Copper	239-245	ATPase copper transporting alpha	Homo sapiens	156-159
16824500-5	2006	If the cell accumulates too much copper or copper is needed by other cells, then copper can be chaperoned to the trans-Golgi secretory compartment where it is transported into the Golgi by ATP-dependent pumps ATP7A/B.	Copper	33-39	ATPase copper transporting alpha	Homo sapiens	209-216
16824500-5	2006	If the cell accumulates too much copper or copper is needed by other cells, then copper can be chaperoned to the trans-Golgi secretory compartment where it is transported into the Golgi by ATP-dependent pumps ATP7A/B.	Copper	43-49	ATPase copper transporting alpha	Homo sapiens	209-216
16824500-5	2006	If the cell accumulates too much copper or copper is needed by other cells, then copper can be chaperoned to the trans-Golgi secretory compartment where it is transported into the Golgi by ATP-dependent pumps ATP7A/B.	Copper	43-49	ATPase copper transporting alpha	Homo sapiens	209-216
16824500-5	2006	If the cell accumulates too much copper or copper is needed by other cells, then copper can be chaperoned to the trans-Golgi secretory compartment where it is transported into the Golgi by ATP-dependent pumps ATP7A/B.	Adenosine Triphosphate	189-192	ATPase copper transporting alpha	Homo sapiens	209-216
16917500-3	2006	In a Mnk1 crystal structure, the activation segment is repositioned via a Mnk-specific sequence insertion at the N-terminal lobe with the following consequences: (i) the peptide substrate binding site is deconstructed, (ii) the interlobal cleft is narrowed, (iii) an essential Lys-Glu pair is disrupted and (iv) the magnesium-binding loop is locked into an ATP-competitive conformation.	Lysine	277-280	ATPase copper transporting alpha	Homo sapiens	5-8
16873374-0	2006	Solution structure and intermolecular interactions of the third metal-binding domain of ATP7A, the Menkes disease protein.	Metals	64-69	ATPase copper transporting alpha	Homo sapiens	88-93
16884690-0	2006	Copper-dependent interaction of glutaredoxin with the N termini of the copper-ATPases (ATP7A and ATP7B) defective in Menkes and Wilson diseases.	Copper	0-6	ATPase copper transporting alpha	Homo sapiens	87-92
16884690-1	2006	The P-type ATPases affected in Menkes and Wilson diseases, ATP7A and ATP7B, respectively, are key copper transporters that regulate copper homeostasis.	Copper	98-104	ATPase copper transporting alpha	Homo sapiens	59-64
16917500-3	2006	In a Mnk1 crystal structure, the activation segment is repositioned via a Mnk-specific sequence insertion at the N-terminal lobe with the following consequences: (i) the peptide substrate binding site is deconstructed, (ii) the interlobal cleft is narrowed, (iii) an essential Lys-Glu pair is disrupted and (iv) the magnesium-binding loop is locked into an ATP-competitive conformation.	Glutamic Acid	281-284	ATPase copper transporting alpha	Homo sapiens	5-8
16917500-3	2006	In a Mnk1 crystal structure, the activation segment is repositioned via a Mnk-specific sequence insertion at the N-terminal lobe with the following consequences: (i) the peptide substrate binding site is deconstructed, (ii) the interlobal cleft is narrowed, (iii) an essential Lys-Glu pair is disrupted and (iv) the magnesium-binding loop is locked into an ATP-competitive conformation.	Magnesium	316-325	ATPase copper transporting alpha	Homo sapiens	5-8
16917500-3	2006	In a Mnk1 crystal structure, the activation segment is repositioned via a Mnk-specific sequence insertion at the N-terminal lobe with the following consequences: (i) the peptide substrate binding site is deconstructed, (ii) the interlobal cleft is narrowed, (iii) an essential Lys-Glu pair is disrupted and (iv) the magnesium-binding loop is locked into an ATP-competitive conformation.	Adenosine Triphosphate	357-360	ATPase copper transporting alpha	Homo sapiens	5-8
16917500-4	2006	Consistently, deletion of the Mnk-specific insertion or removal of a conserved phenylalanine side chain, which induces a blockade of the ATP pocket, increase the ATP affinity of Mnk1.	Phenylalanine	79-92	ATPase copper transporting alpha	Homo sapiens	30-33
16917500-4	2006	Consistently, deletion of the Mnk-specific insertion or removal of a conserved phenylalanine side chain, which induces a blockade of the ATP pocket, increase the ATP affinity of Mnk1.	Adenosine Triphosphate	137-140	ATPase copper transporting alpha	Homo sapiens	30-33
16917500-4	2006	Consistently, deletion of the Mnk-specific insertion or removal of a conserved phenylalanine side chain, which induces a blockade of the ATP pocket, increase the ATP affinity of Mnk1.	Adenosine Triphosphate	162-165	ATPase copper transporting alpha	Homo sapiens	30-33
16826513-2	2006	It is caused by mutations in the ATP7A gene encoding a copper-translocating P-type ATPase, which contains six N-terminal copper-binding sites (CBS1-CBS6).	Copper	55-61	ATPase copper transporting alpha	Homo sapiens	33-38
16826513-10	2006	Cellular localization and copper-dependent trafficking of the major part of endogenous and recombinant ATP7A(Delta ex3+ex4) proteins were similar to the wild-type ATP7A protein.	Copper	26-32	ATPase copper transporting alpha	Homo sapiens	103-108
16773204-5	2006	Our data also confirmed that copper transporters and chaperones are involved in OXA resistance in colorectal cancer cells as evidenced by the overexpression of ATP7A and CCS in response to OXA exposure.	Oxaliplatin	80-83	ATPase copper transporting alpha	Homo sapiens	160-165
16890543-5	2006	Copper metabolism in calamity is restored by human ATP7A, and transplantation experiments reveal that atp7a functions cell autonomously, findings with important therapeutic implications.	Copper	0-6	ATPase copper transporting alpha	Homo sapiens	51-56
16890543-5	2006	Copper metabolism in calamity is restored by human ATP7A, and transplantation experiments reveal that atp7a functions cell autonomously, findings with important therapeutic implications.	Copper	0-6	ATPase copper transporting alpha	Homo sapiens	102-107
16515558-0	2006	Mnk is a negative regulator of cap-dependent translation in Aplysia neurons.	cap	31-34	ATPase copper transporting alpha	Homo sapiens	0-3
16397091-0	2006	Alteration of copper physiology in mice overexpressing the human Menkes protein ATP7A.	Copper	14-20	ATPase copper transporting alpha	Homo sapiens	80-85
16515558-3	2006	As expected, purified Aplysia Mnk phosphorylated Aplysia eIF4E at a conserved carboxy-terminal serine and over-expression of Aplysia Mnk in sensory neurons led to increased phosphorylation of endogenous eIF4E.	Serine	95-101	ATPase copper transporting alpha	Homo sapiens	30-33
16515558-3	2006	As expected, purified Aplysia Mnk phosphorylated Aplysia eIF4E at a conserved carboxy-terminal serine and over-expression of Aplysia Mnk in sensory neurons led to increased phosphorylation of endogenous eIF4E.	Serine	95-101	ATPase copper transporting alpha	Homo sapiens	133-136
16858971-1	2005	Menkes syndrome is caused by mutation of ATP7A gene that encode copper-binding membrane protein localized to the trans-Golgi membrane.	Copper	64-70	ATPase copper transporting alpha	Homo sapiens	41-46
16549268-1	2006	ATP7A is a P-type ATPase that transports copper from cytosol into the secretory pathway for loading onto cuproproteins or efflux.	Copper	41-47	ATPase copper transporting alpha	Homo sapiens	0-5
16172131-0	2005	A NMR study of the interaction of a three-domain construct of ATP7A with copper(I) and copper(I)-HAH1: the interplay of domains.	Copper	73-79	ATPase copper transporting alpha	Homo sapiens	62-67
16172131-0	2005	A NMR study of the interaction of a three-domain construct of ATP7A with copper(I) and copper(I)-HAH1: the interplay of domains.	Copper	87-93	ATPase copper transporting alpha	Homo sapiens	62-67
16172131-1	2005	ATP7A is a P-type ATPase involved in copper(I) homeostasis in humans.	Copper	37-43	ATPase copper transporting alpha	Homo sapiens	0-5
16172131-3	2005	ATP7A receives copper from a soluble protein, the metallochaperone HAH1.	Copper	15-21	ATPase copper transporting alpha	Homo sapiens	0-5
15987957-1	2005	Hereditary inclusion body myopathy (HIBM) is an autosomal recessive neuromuscular disorder associated with mutations in uridine diphosphate (UDP)-N-acetylglucosamine (GlcNAc) 2-epimerase (GNE)/N-acetylmannosamine (ManNAc) kinase (MNK), the bifunctional and rate-limiting enzyme of sialic acid biosynthesis.	Uridine Diphosphate	120-139	ATPase copper transporting alpha	Homo sapiens	230-233
15987957-1	2005	Hereditary inclusion body myopathy (HIBM) is an autosomal recessive neuromuscular disorder associated with mutations in uridine diphosphate (UDP)-N-acetylglucosamine (GlcNAc) 2-epimerase (GNE)/N-acetylmannosamine (ManNAc) kinase (MNK), the bifunctional and rate-limiting enzyme of sialic acid biosynthesis.	Uridine Diphosphate	141-144	ATPase copper transporting alpha	Homo sapiens	230-233
15987957-1	2005	Hereditary inclusion body myopathy (HIBM) is an autosomal recessive neuromuscular disorder associated with mutations in uridine diphosphate (UDP)-N-acetylglucosamine (GlcNAc) 2-epimerase (GNE)/N-acetylmannosamine (ManNAc) kinase (MNK), the bifunctional and rate-limiting enzyme of sialic acid biosynthesis.	Acetylglucosamine	167-173	ATPase copper transporting alpha	Homo sapiens	230-233
15981243-1	2005	ATP7A encodes a copper-translocating ATPase that belongs to the large family of P-type ATPases.	Copper	16-22	ATPase copper transporting alpha	Homo sapiens	0-5
16083905-1	2005	Menkes disease is a fatal disease that can be induced by various mutations in the ATP7A gene, leading to unpaired uptake of dietary copper.	Copper	132-138	ATPase copper transporting alpha	Homo sapiens	82-87
16083905-5	2005	The interaction in vitro with the physiological ATP7A copper(I)-donor (HAH1) was additionally studied.	cuprous ion	54-63	ATPase copper transporting alpha	Homo sapiens	48-53
16083905-6	2005	The A629P mutation makes the protein beta-sheet more solvent accessible, possibly resulting in an enhanced susceptibility of ATP7A to proteolytic cleavage and/or in reduced capability of copper(I)-translocation.	Copper	187-193	ATPase copper transporting alpha	Homo sapiens	125-130
16051599-5	2005	To identify other proteins important for copper homeostasis, while also elucidating the protein-protein interactions that are integral to the process, we have utilized a known copper protein, the copper ATPase ATP7A, as a bait in a yeast two-hybrid screen of a human cDNA library to search for interacting partners.	Copper	176-182	ATPase copper transporting alpha	Homo sapiens	210-215
16098018-1	2005	We describe a child with classical Menkes disease with a novel ATP7A mutation, intractable seizures, severe hypotonia and developmental delay, hypopigmentation of the skin and hair, and failure to thrive, who was treated with daily subcutaneous copper histidine injections for 2(1/2) years, beginning at 15 months of age.	copper histidine	245-261	ATPase copper transporting alpha	Homo sapiens	63-68
15981243-3	2005	We report here the identification of 21 novel missense mutations in the conserved part of ATP7A that encodes the residues p.V842-p.S1404.	v842-p	124-130	ATPase copper transporting alpha	Homo sapiens	90-95
15790412-6	2005	In contrast, many of these (including ATP7A, ATP7B, ceruloplasmin, and metallothionein) were significantly reduced in the DH group.	Dihydrotestosterone	122-124	ATPase copper transporting alpha	Homo sapiens	38-43
15923132-1	2005	Menkes disease (MD) is an X-linked recessive neurodegenerative disorder caused by mutations in a copper-transporting p-type ATPase (ATP7A) that normally delivers copper to the central nervous system.	Copper	97-103	ATPase copper transporting alpha	Homo sapiens	132-137
16076012-5	2005	To further address Cu transporter as a potential Pb target, a heavy metal-binding (HMB) domain of Cu-transporting ATPase (Atp7a) was overexpressed and purified.	Metals	68-73	ATPase copper transporting alpha	Homo sapiens	122-127
16076012-7	2005	These findings suggest that Pb-induced oxidative stress results from the impairment of Cu metabolism by Pb targeting of Atp7a.	Lead	28-30	ATPase copper transporting alpha	Homo sapiens	120-125
16076012-7	2005	These findings suggest that Pb-induced oxidative stress results from the impairment of Cu metabolism by Pb targeting of Atp7a.	Copper	87-89	ATPase copper transporting alpha	Homo sapiens	120-125
16076012-7	2005	These findings suggest that Pb-induced oxidative stress results from the impairment of Cu metabolism by Pb targeting of Atp7a.	Lead	104-106	ATPase copper transporting alpha	Homo sapiens	120-125
15670166-1	2005	The interaction between the human copper(I) chaperone, HAH1, and one of its two physiological partners, the Menkes disease protein (ATP7A), was investigated in solution using heteronuclear NMR.	Copper	34-40	ATPase copper transporting alpha	Homo sapiens	132-137
15634671-2	2005	The copper-transporting ATPases ATP7A and ATP7B play a central role in distribution of copper in the central nervous system; genetic mutations in ATP7A and ATP7B lead to severe neurodegenerative disorders, Menkes disease and Wilson disease, respectively.	Copper	4-10	ATPase copper transporting alpha	Homo sapiens	32-37
15634671-2	2005	The copper-transporting ATPases ATP7A and ATP7B play a central role in distribution of copper in the central nervous system; genetic mutations in ATP7A and ATP7B lead to severe neurodegenerative disorders, Menkes disease and Wilson disease, respectively.	Copper	4-10	ATPase copper transporting alpha	Homo sapiens	146-151
15634671-9	2005	The induced cell-specific change in expression restores copper delivery to ceruloplasmin via ATP7A.	Copper	56-62	ATPase copper transporting alpha	Homo sapiens	93-98
15670166-2	2005	The study was carried out through titrations involving HAH1 and either the second or the fifth soluble domains of ATP7A (MNK2 and MNK5, respectively), in the presence of copper(I).	Copper	170-176	ATPase copper transporting alpha	Homo sapiens	114-119
15607932-1	2005	Recent studies have demonstrated that the major Cu influx transporter CTR1 regulates tumor cell uptake of cisplatin (DDP), carboplatin (CBDCA) and oxaliplatin (L-OHP), and that the two Cu efflux transporters ATP7A and ATP7B regulate the efflux of these drugs.	Cisplatin	106-115	ATPase copper transporting alpha	Homo sapiens	208-213
15701866-6	2005	F-DDP extensively colocalized with vesicles expressing the copper efflux protein, ATP7A, whose expression modulates the cellular pharmacology of DDP.	Copper	59-65	ATPase copper transporting alpha	Homo sapiens	82-87
15607932-1	2005	Recent studies have demonstrated that the major Cu influx transporter CTR1 regulates tumor cell uptake of cisplatin (DDP), carboplatin (CBDCA) and oxaliplatin (L-OHP), and that the two Cu efflux transporters ATP7A and ATP7B regulate the efflux of these drugs.	ddp	117-120	ATPase copper transporting alpha	Homo sapiens	208-213
15607932-1	2005	Recent studies have demonstrated that the major Cu influx transporter CTR1 regulates tumor cell uptake of cisplatin (DDP), carboplatin (CBDCA) and oxaliplatin (L-OHP), and that the two Cu efflux transporters ATP7A and ATP7B regulate the efflux of these drugs.	Oxaliplatin	160-165	ATPase copper transporting alpha	Homo sapiens	208-213
16137991-7	2005	Interestingly, copper-transport-deficient ATP7A still exhibits axonal localization.	Copper	15-21	ATPase copper transporting alpha	Homo sapiens	42-47
15239669-8	2004	Suppression of DmATP7, the putative homologue of human Cu transporter genes ATP7A and ATP7B, significantly increased Cu accumulation, demonstrating that DmATP7 is essential for efflux of excess Cu.	Copper	55-57	ATPase copper transporting alpha	Homo sapiens	76-81
15634647-3	2004	Here, we show that, of five cisplatin-resistant cell lines, only one (SR2) exhibited substantial reduction in hCtr1 expression as compared with that in its sensitive line small cell lung cancers (SCLC), whereas copper efflux transporters ATP7A and ATP7B were not significantly altered.	Cisplatin	28-37	ATPase copper transporting alpha	Homo sapiens	238-243
16240664-8	2005	Copper absorption is regulated by the transporters Ctrl, Atp7A and Atp7B, and exposure to copper at early age affects the expression and cellular localization of these proteins, affecting copper uptake and transport.	Copper	0-6	ATPase copper transporting alpha	Homo sapiens	57-62
16240664-8	2005	Copper absorption is regulated by the transporters Ctrl, Atp7A and Atp7B, and exposure to copper at early age affects the expression and cellular localization of these proteins, affecting copper uptake and transport.	Copper	90-96	ATPase copper transporting alpha	Homo sapiens	57-62
15239669-8	2004	Suppression of DmATP7, the putative homologue of human Cu transporter genes ATP7A and ATP7B, significantly increased Cu accumulation, demonstrating that DmATP7 is essential for efflux of excess Cu.	Copper	117-119	ATPase copper transporting alpha	Homo sapiens	76-81
15269138-0	2004	Increased expression of the copper efflux transporter ATP7A mediates resistance to cisplatin, carboplatin, and oxaliplatin in ovarian cancer cells.	Cisplatin	83-92	ATPase copper transporting alpha	Homo sapiens	54-59
15269138-0	2004	Increased expression of the copper efflux transporter ATP7A mediates resistance to cisplatin, carboplatin, and oxaliplatin in ovarian cancer cells.	Carboplatin	94-105	ATPase copper transporting alpha	Homo sapiens	54-59
15269138-0	2004	Increased expression of the copper efflux transporter ATP7A mediates resistance to cisplatin, carboplatin, and oxaliplatin in ovarian cancer cells.	Oxaliplatin	111-122	ATPase copper transporting alpha	Homo sapiens	54-59
15269138-1	2004	PURPOSE: The goal of this study was to determine the effect of small changes in ATP7A expression on the pharmacodynamics of cisplatin, carboplatin, and oxaliplatin in human ovarian carcinoma cells.	Cisplatin	124-133	ATPase copper transporting alpha	Homo sapiens	80-85
15269138-1	2004	PURPOSE: The goal of this study was to determine the effect of small changes in ATP7A expression on the pharmacodynamics of cisplatin, carboplatin, and oxaliplatin in human ovarian carcinoma cells.	Carboplatin	135-146	ATPase copper transporting alpha	Homo sapiens	80-85
15269138-1	2004	PURPOSE: The goal of this study was to determine the effect of small changes in ATP7A expression on the pharmacodynamics of cisplatin, carboplatin, and oxaliplatin in human ovarian carcinoma cells.	Oxaliplatin	152-163	ATPase copper transporting alpha	Homo sapiens	80-85
15269138-4	2004	RESULTS: The 1.5-fold higher expression of ATP7A in the 2008/MNK cells was sufficient to alter Cu cellular pharmacokinetics but not confer Cu resistance.	Copper	95-97	ATPase copper transporting alpha	Homo sapiens	43-48
15269138-4	2004	RESULTS: The 1.5-fold higher expression of ATP7A in the 2008/MNK cells was sufficient to alter Cu cellular pharmacokinetics but not confer Cu resistance.	Copper	95-97	ATPase copper transporting alpha	Homo sapiens	61-64
15269138-5	2004	In contrast, it was sufficient to render the 2008/MNK cells resistant to cisplatin, carboplatin, and oxaliplatin.	Cisplatin	73-82	ATPase copper transporting alpha	Homo sapiens	50-53
15269138-5	2004	In contrast, it was sufficient to render the 2008/MNK cells resistant to cisplatin, carboplatin, and oxaliplatin.	Carboplatin	84-95	ATPase copper transporting alpha	Homo sapiens	50-53
15269138-5	2004	In contrast, it was sufficient to render the 2008/MNK cells resistant to cisplatin, carboplatin, and oxaliplatin.	Oxaliplatin	101-112	ATPase copper transporting alpha	Homo sapiens	50-53
15269138-7	2004	Cu triggered relocalization of ATP7A away from the perinuclear region, whereas at equitoxic concentrations the Pt drugs did not.	Copper	0-2	ATPase copper transporting alpha	Homo sapiens	31-36
15269138-9	2004	Whereas increased expression of ATP7A reduced Cu accumulation, it did not reduce accumulation of the Pt drugs.	Copper	46-48	ATPase copper transporting alpha	Homo sapiens	32-37
15269138-10	2004	Under conditions where Cu triggered ATP7A relocalization, the Pt drugs did not.	Copper	23-25	ATPase copper transporting alpha	Homo sapiens	36-41
15269138-11	2004	Thus, although ATP7A is an important determinant of sensitivity to the Pt drugs, there are substantial differences between Cu and the Pt drugs with respect to how they interact with ATP7A and the mechanism by which ATP7A protects the cell.	Copper	123-125	ATPase copper transporting alpha	Homo sapiens	182-187
15269138-11	2004	Thus, although ATP7A is an important determinant of sensitivity to the Pt drugs, there are substantial differences between Cu and the Pt drugs with respect to how they interact with ATP7A and the mechanism by which ATP7A protects the cell.	Copper	123-125	ATPase copper transporting alpha	Homo sapiens	182-187
15035611-0	2004	Solution structure and backbone dynamics of the Cu(I) and apo forms of the second metal-binding domain of the Menkes protein ATP7A.	cuprous ion	48-53	ATPase copper transporting alpha	Homo sapiens	125-130
15135234-3	2004	Two copper transporting ATPases, Menkes (ATP7A; MNK) and Wilson (ATP7B; WND) are known to be expressed in the placenta and are thought to have a role in copper transport to the fetus.	Copper	4-10	ATPase copper transporting alpha	Homo sapiens	41-46
15135234-3	2004	Two copper transporting ATPases, Menkes (ATP7A; MNK) and Wilson (ATP7B; WND) are known to be expressed in the placenta and are thought to have a role in copper transport to the fetus.	Copper	4-10	ATPase copper transporting alpha	Homo sapiens	48-51
14985339-6	2004	To test the hypothesis, we utilized human fibroblasts overexpressing the Menkes protein (MNK), a major mammalian copper efflux protein.	Copper	113-119	ATPase copper transporting alpha	Homo sapiens	73-87
14985339-6	2004	To test the hypothesis, we utilized human fibroblasts overexpressing the Menkes protein (MNK), a major mammalian copper efflux protein.	Copper	113-119	ATPase copper transporting alpha	Homo sapiens	89-92
14985339-7	2004	MNK deletion fibroblasts have high intracellular copper, whereas MNK overexpressing fibroblasts have severely depleted intracellular copper.	Copper	49-55	ATPase copper transporting alpha	Homo sapiens	0-3
14985339-7	2004	MNK deletion fibroblasts have high intracellular copper, whereas MNK overexpressing fibroblasts have severely depleted intracellular copper.	Copper	133-139	ATPase copper transporting alpha	Homo sapiens	65-68
14985339-9	2004	Furthermore, APP promoter deletion constructs identified the copper-regulatory region between -490 and +104 of the APP gene promoter in both basal MNK overexpressing cells and in copper-chelated MNK deletion cells.	Copper	61-67	ATPase copper transporting alpha	Homo sapiens	147-150
14985339-9	2004	Furthermore, APP promoter deletion constructs identified the copper-regulatory region between -490 and +104 of the APP gene promoter in both basal MNK overexpressing cells and in copper-chelated MNK deletion cells.	Copper	61-67	ATPase copper transporting alpha	Homo sapiens	195-198
14985339-9	2004	Furthermore, APP promoter deletion constructs identified the copper-regulatory region between -490 and +104 of the APP gene promoter in both basal MNK overexpressing cells and in copper-chelated MNK deletion cells.	Copper	179-185	ATPase copper transporting alpha	Homo sapiens	147-150
14985339-9	2004	Furthermore, APP promoter deletion constructs identified the copper-regulatory region between -490 and +104 of the APP gene promoter in both basal MNK overexpressing cells and in copper-chelated MNK deletion cells.	Copper	179-185	ATPase copper transporting alpha	Homo sapiens	195-198
15213293-0	2004	Modulation of the cellular pharmacology of cisplatin and its analogs by the copper exporters ATP7A and ATP7B.	Cisplatin	43-52	ATPase copper transporting alpha	Homo sapiens	93-98
15213293-1	2004	The copper efflux transporters ATP7A and ATP7B sequester intracellular copper into the vesicular secretory pathway for export from the cell.	Copper	4-10	ATPase copper transporting alpha	Homo sapiens	31-36
15213293-7	2004	Although copper triggered relocalization of ATP7A from the perinuclear region to more peripheral locations, the platinum drugs did not.	Copper	9-15	ATPase copper transporting alpha	Homo sapiens	44-49
15213293-8	2004	These results demonstrate that both ATP7A and ATP7B modulate the pharmacodynamics of all three clinically used platinum drugs.	Platinum	111-119	ATPase copper transporting alpha	Homo sapiens	36-41
14998371-12	2004	Our findings were similar to those obtained for the closely related ATP7A protein, suggesting similar mechanisms for trafficking between copper-transporting CPx-type ATPases.	Copper	137-143	ATPase copper transporting alpha	Homo sapiens	68-73
15035611-0	2004	Solution structure and backbone dynamics of the Cu(I) and apo forms of the second metal-binding domain of the Menkes protein ATP7A.	Metals	82-87	ATPase copper transporting alpha	Homo sapiens	125-130
14977365-3	2004	The MNK protein is localised to the Golgi apparatus and relocalises to the plasma membrane when copper levels are elevated.	Copper	96-102	ATPase copper transporting alpha	Homo sapiens	4-7
14640979-0	2004	Copper stimulates trafficking of a distinct pool of the Menkes copper ATPase (ATP7A) to the plasma membrane and diverts it into a rapid recycling pool.	Copper	0-6	ATPase copper transporting alpha	Homo sapiens	78-83
14640979-2	2004	MNK has been shown to have a dual role in the cell: it delivers copper to cuproenzymes in the Golgi compartment and effluxes excess copper from the cell.	Copper	64-70	ATPase copper transporting alpha	Homo sapiens	0-3
14640979-2	2004	MNK has been shown to have a dual role in the cell: it delivers copper to cuproenzymes in the Golgi compartment and effluxes excess copper from the cell.	Copper	132-138	ATPase copper transporting alpha	Homo sapiens	0-3
14640979-3	2004	These roles can be achieved through copper-regulated trafficking of MNK.	Copper	36-42	ATPase copper transporting alpha	Homo sapiens	68-71
14640979-5	2004	However, the fundamental question as to whether copper influences trafficking of MNK to or from the plasma membrane remained unanswered.	Copper	48-54	ATPase copper transporting alpha	Homo sapiens	81-84
14640979-7	2004	These studies suggest that copper induces trafficking of MNK to the plasma membrane but does not affect its rate of internalization from the plasma membrane.	Copper	27-33	ATPase copper transporting alpha	Homo sapiens	57-60
14640979-8	2004	We also found that only a specific pool of MNK can traffic to the plasma membrane in response to elevated copper.	Copper	106-112	ATPase copper transporting alpha	Homo sapiens	43-46
14640979-9	2004	Significantly, copper appeared to divert MNK into a fast-recycling pool and prevented it from recycling to the Golgi compartment, thus maintaining a high level of MNK in the proximity of the plasma membrane.	Copper	15-21	ATPase copper transporting alpha	Homo sapiens	41-44
14640979-9	2004	Significantly, copper appeared to divert MNK into a fast-recycling pool and prevented it from recycling to the Golgi compartment, thus maintaining a high level of MNK in the proximity of the plasma membrane.	Copper	15-21	ATPase copper transporting alpha	Homo sapiens	163-166
15023397-1	2004	Ctr1 and Atp7A are copper (Cu) transporters that may play a role in the regulation of intestinal Cu absorption; however, intestinal regulation of these transporters by Cu in vivo has not been well defined.	Copper	27-29	ATPase copper transporting alpha	Homo sapiens	9-14
15023397-1	2004	Ctr1 and Atp7A are copper (Cu) transporters that may play a role in the regulation of intestinal Cu absorption; however, intestinal regulation of these transporters by Cu in vivo has not been well defined.	Copper	97-99	ATPase copper transporting alpha	Homo sapiens	9-14
15023397-2	2004	In this study, we hypothesized that Cu supplementation would alter the expression of intestine Ctr1 and Atp7A in vivo and further documented effects of Cu exposure on Cu transport, Ctr1 and Atp7A levels and localization in enterocyte-like Caco-2 cells.	Copper	36-38	ATPase copper transporting alpha	Homo sapiens	104-109
15023397-2	2004	In this study, we hypothesized that Cu supplementation would alter the expression of intestine Ctr1 and Atp7A in vivo and further documented effects of Cu exposure on Cu transport, Ctr1 and Atp7A levels and localization in enterocyte-like Caco-2 cells.	Copper	36-38	ATPase copper transporting alpha	Homo sapiens	190-195
15023397-2	2004	In this study, we hypothesized that Cu supplementation would alter the expression of intestine Ctr1 and Atp7A in vivo and further documented effects of Cu exposure on Cu transport, Ctr1 and Atp7A levels and localization in enterocyte-like Caco-2 cells.	Copper	152-154	ATPase copper transporting alpha	Homo sapiens	190-195
15023397-2	2004	In this study, we hypothesized that Cu supplementation would alter the expression of intestine Ctr1 and Atp7A in vivo and further documented effects of Cu exposure on Cu transport, Ctr1 and Atp7A levels and localization in enterocyte-like Caco-2 cells.	Copper	152-154	ATPase copper transporting alpha	Homo sapiens	190-195
15023397-8	2004	This study demonstrates the functional response of intestinal cells to Cu treatment and suggests that both Ctr1 and Atp7A may regulate Cu absorption.	Copper	135-137	ATPase copper transporting alpha	Homo sapiens	116-121
14977365-7	2004	MNK internalisation was inhibited in cells treated with hypertonic sucrose that not only blocked clathrin-mediated endocytosis but also fluid-phase endocytosis.	Sucrose	67-74	ATPase copper transporting alpha	Homo sapiens	0-3
12827356-3	2004	Copper export in human cells is mediated by the ATP7A and ATP7B P-type ATPases, which are, respectively, affected in the genetic disorders of copper metabolism, Menkes disease and Wilson disease.	Copper	0-6	ATPase copper transporting alpha	Homo sapiens	48-53
12827356-3	2004	Copper export in human cells is mediated by the ATP7A and ATP7B P-type ATPases, which are, respectively, affected in the genetic disorders of copper metabolism, Menkes disease and Wilson disease.	Copper	142-148	ATPase copper transporting alpha	Homo sapiens	48-53
14676106-1	2003	PURPOSE: The Cu efflux transporter ATP7A is overexpressed in some cisplatin-resistant ovarian carcinoma cell lines.	Cisplatin	66-75	ATPase copper transporting alpha	Homo sapiens	35-40
14579150-1	2004	The genes for two copper-transporting ATPases, ATP7A and ATP7B, are defective in the heritable disorders of copper imbalance, Menkes disease (MNK) and Wilson disease (WND), respectively.	Copper	18-24	ATPase copper transporting alpha	Homo sapiens	47-52
14579150-1	2004	The genes for two copper-transporting ATPases, ATP7A and ATP7B, are defective in the heritable disorders of copper imbalance, Menkes disease (MNK) and Wilson disease (WND), respectively.	Copper	18-24	ATPase copper transporting alpha	Homo sapiens	142-145
14579150-8	2004	A region of possible importance is the intervening sequence between the last copper-binding domain and the first transmembrane helix, as this region has a high percentage of MNK mutations.	Copper	77-83	ATPase copper transporting alpha	Homo sapiens	174-177
14668139-6	2004	When microtubules are depolymerized in ROCK-KIN expressing cells by nocodazole, both MNK and TGN46 are found in puncate structures throughout the cell.	Nocodazole	68-78	ATPase copper transporting alpha	Homo sapiens	85-88
14676106-3	2003	EXPERIMENTAL DESIGN: ATP7A expression was quantified by immunohistochemical staining using microarrays containing normal and malignant tissues, and standard sections of 54 paired tumor samples obtained from ovarian carcinoma patients before and after at least two cycles of platinum-based therapy.	Platinum	274-282	ATPase copper transporting alpha	Homo sapiens	21-26
14676106-11	2003	These findings are in agreement with results of in vitro studies from this laboratory demonstrating that increased expression of ATP7A renders cells resistant to cisplatin and carboplatin.	Cisplatin	162-171	ATPase copper transporting alpha	Homo sapiens	129-134
14676106-11	2003	These findings are in agreement with results of in vitro studies from this laboratory demonstrating that increased expression of ATP7A renders cells resistant to cisplatin and carboplatin.	Carboplatin	176-187	ATPase copper transporting alpha	Homo sapiens	129-134
12812980-1	2003	The Menkes disease gene encodes a P-type transmembrane ATPase (ATP7A) that translocates cytosolic copper ions across intracellular membranes of compartments along the secretory pathway.	Copper	98-104	ATPase copper transporting alpha	Homo sapiens	63-68
14635105-2	2003	MD results from mutations in the ATP7A gene, which encodes a membrane-bound copper transporting P-type ATPase located in the trans-Golgi network.	Copper	76-82	ATPase copper transporting alpha	Homo sapiens	33-38
12812980-2	2003	ATP7A moves from the trans-Golgi network (TGN) to the cell surface in response to exogenously added copper ions and recycles back to the TGN upon copper removal.	Copper	100-106	ATPase copper transporting alpha	Homo sapiens	0-5
12812980-2	2003	ATP7A moves from the trans-Golgi network (TGN) to the cell surface in response to exogenously added copper ions and recycles back to the TGN upon copper removal.	Copper	146-152	ATPase copper transporting alpha	Homo sapiens	0-5
12679332-1	2003	Excess copper is effluxed from mammalian cells by the Menkes or Wilson P-type ATPases (MNK and WND, respectively).	Copper	7-13	ATPase copper transporting alpha	Homo sapiens	87-90
12679332-2	2003	MNK and WND have six metal binding sites (MBSs) containing a CXXC motif within their N-terminal cytoplasmic region.	Metals	21-26	ATPase copper transporting alpha	Homo sapiens	0-3
12679332-6	2003	A copper-dependent interaction of Atox1 with the MBSs of MNK was observed by both approaches.	Copper	2-8	ATPase copper transporting alpha	Homo sapiens	57-60
12679332-11	2003	Therefore, a functional difference of the MBSs in the MNK N terminus cannot be attributed to cooperativity effects or varying affinities of the copper chaperone Atox1 with the MBSs.	Copper	144-150	ATPase copper transporting alpha	Homo sapiens	54-57
12594858-2	2003	Menkes disease and occipital horn syndrome (OHS) are allelic disorders of copper transport caused by defects in a X-linked gene (ATP7A) that encodes a P-type ATPase that transports copper across cellular membranes, including the trans-Golgi network.	Copper	74-80	ATPase copper transporting alpha	Homo sapiens	129-134
12730448-2	2003	The Cu-ATPases, ATP7A and ATP7B, play an important role in the physiological regulation of copper.	Copper	4-6	ATPase copper transporting alpha	Homo sapiens	16-21
12730448-2	2003	The Cu-ATPases, ATP7A and ATP7B, play an important role in the physiological regulation of copper.	Copper	91-97	ATPase copper transporting alpha	Homo sapiens	16-21
12730448-3	2003	Adequate supplies of copper are particularly important in developing animals, and in humans this is illustrated by mutations of ATP7A that cause the copper deficiency condition Menkes disease, which is fatal in early childhood.	Copper	21-27	ATPase copper transporting alpha	Homo sapiens	128-133
12565888-0	2003	Mutational analysis of the Menkes copper P-type ATPase (ATP7A).	Copper	34-40	ATPase copper transporting alpha	Homo sapiens	56-61
12565888-1	2003	The Menkes protein (ATP7A; MNK) is a ubiquitous human copper-translocating P-type ATPase and it has a key role in regulating copper homeostasis.	Copper	54-60	ATPase copper transporting alpha	Homo sapiens	20-25
12565888-1	2003	The Menkes protein (ATP7A; MNK) is a ubiquitous human copper-translocating P-type ATPase and it has a key role in regulating copper homeostasis.	Copper	54-60	ATPase copper transporting alpha	Homo sapiens	27-30
12565888-1	2003	The Menkes protein (ATP7A; MNK) is a ubiquitous human copper-translocating P-type ATPase and it has a key role in regulating copper homeostasis.	Copper	125-131	ATPase copper transporting alpha	Homo sapiens	20-25
12565888-1	2003	The Menkes protein (ATP7A; MNK) is a ubiquitous human copper-translocating P-type ATPase and it has a key role in regulating copper homeostasis.	Copper	125-131	ATPase copper transporting alpha	Homo sapiens	27-30
12646208-1	2003	The Menkes copper-translocating P-type ATPase (ATP7A; MNK) is a key regulator of copper homeostasis in humans.	Copper	11-17	ATPase copper transporting alpha	Homo sapiens	47-52
12646208-1	2003	The Menkes copper-translocating P-type ATPase (ATP7A; MNK) is a key regulator of copper homeostasis in humans.	Copper	11-17	ATPase copper transporting alpha	Homo sapiens	54-57
12646208-3	2003	These functions are achieved through copper-regulated trafficking of MNK between the TGN and the plasma membrane.	Copper	37-43	ATPase copper transporting alpha	Homo sapiens	69-72
12646208-5	2003	Here we investigated copper-dependent phosphorylation of MNK by a putative protein kinase(s).	Copper	21-27	ATPase copper transporting alpha	Homo sapiens	57-60
12646208-6	2003	We found that in the presence of elevated copper there was a substantial increase in phosphorylation of the wild-type MNK in vivo.	Copper	42-48	ATPase copper transporting alpha	Homo sapiens	118-121
12594858-2	2003	Menkes disease and occipital horn syndrome (OHS) are allelic disorders of copper transport caused by defects in a X-linked gene (ATP7A) that encodes a P-type ATPase that transports copper across cellular membranes, including the trans-Golgi network.	Copper	181-187	ATPase copper transporting alpha	Homo sapiens	129-134
12485191-1	2002	X-linked recessive Menkes disease is a lethal disorder of copper metabolism, caused by defects in the ATP7A gene.	Copper	58-64	ATPase copper transporting alpha	Homo sapiens	102-107
12450772-1	2003	Recently, bi-allelic mutations in the gene coding for the bi-functional enzyme UDP-N-acetylglucosamine 2-epimerase/N-acetylmannosamine kinase (GNE/MNK), symbol GNE or GLCNE (MIM: 603824), were associated with the recessively inherited phenotype of IBM2 (MIM: 600737).	Uridine Diphosphate	79-82	ATPase copper transporting alpha	Homo sapiens	147-150
12450772-1	2003	Recently, bi-allelic mutations in the gene coding for the bi-functional enzyme UDP-N-acetylglucosamine 2-epimerase/N-acetylmannosamine kinase (GNE/MNK), symbol GNE or GLCNE (MIM: 603824), were associated with the recessively inherited phenotype of IBM2 (MIM: 600737).	Acetylglucosamine	83-102	ATPase copper transporting alpha	Homo sapiens	147-150
12450772-4	2003	The dominantly inherited French type sialuria seems to result from defective allosteric feedback inhibitory regulation of GNE/MNK by cytidine monophosphate-N-acetylneuraminic acid (CMP-NANA), resulting in overproduction of cytosolic N-acetylneuraminic acid, and massive urinary excretion of free sialic acid.	Cytidine Monophosphate N-Acetylneuraminic Acid	133-179	ATPase copper transporting alpha	Homo sapiens	126-129
12450772-4	2003	The dominantly inherited French type sialuria seems to result from defective allosteric feedback inhibitory regulation of GNE/MNK by cytidine monophosphate-N-acetylneuraminic acid (CMP-NANA), resulting in overproduction of cytosolic N-acetylneuraminic acid, and massive urinary excretion of free sialic acid.	Cytidine Monophosphate N-Acetylneuraminic Acid	181-189	ATPase copper transporting alpha	Homo sapiens	126-129
12450772-4	2003	The dominantly inherited French type sialuria seems to result from defective allosteric feedback inhibitory regulation of GNE/MNK by cytidine monophosphate-N-acetylneuraminic acid (CMP-NANA), resulting in overproduction of cytosolic N-acetylneuraminic acid, and massive urinary excretion of free sialic acid.	N-Acetylneuraminic Acid	156-179	ATPase copper transporting alpha	Homo sapiens	126-129
12450772-4	2003	The dominantly inherited French type sialuria seems to result from defective allosteric feedback inhibitory regulation of GNE/MNK by cytidine monophosphate-N-acetylneuraminic acid (CMP-NANA), resulting in overproduction of cytosolic N-acetylneuraminic acid, and massive urinary excretion of free sialic acid.	N-Acetylneuraminic Acid	296-307	ATPase copper transporting alpha	Homo sapiens	126-129
12438251-8	2002	On Western blot analysis all three resistant lines exhibited increased expression of one or the other of the two copper export pumps (ATP7A or ATP7B) with no change in the HAH1 chaperone.	Copper	113-119	ATPase copper transporting alpha	Homo sapiens	134-139
12228238-2	2002	MNK is localized in the trans-Golgi network and transports copper to enzymes synthesized within secretory compartments.	Copper	59-65	ATPase copper transporting alpha	Homo sapiens	0-3
12228238-3	2002	However, in cells exposed to excessive copper, MNK traffics to the plasma membrane where it functions in copper efflux.	Copper	39-45	ATPase copper transporting alpha	Homo sapiens	47-50
12228238-3	2002	However, in cells exposed to excessive copper, MNK traffics to the plasma membrane where it functions in copper efflux.	Copper	105-111	ATPase copper transporting alpha	Homo sapiens	47-50
12228238-6	2002	Our findings suggest that mutations that block formation of the phosphorylated catalytic intermediate also prevent copper-induced relocalization of MNK from the TGN.	Copper	115-121	ATPase copper transporting alpha	Homo sapiens	148-151
11855813-4	2002	Accordingly, immunofluorescence and Western blotting revealed the occurrence of a Cu-inducible, putative homologue of human Menkes (MNK) Cu-P-type ATPase.	Copper	82-84	ATPase copper transporting alpha	Homo sapiens	124-130
12221109-4	2002	MNK is located in the trans-Golgi network where it transports copper to secreted cuproenzymes.	Copper	62-68	ATPase copper transporting alpha	Homo sapiens	0-3
12221109-5	2002	Increases in copper concentration stimulate the trafficking of MNK to the plasma membrane where it effluxes copper.	Copper	13-19	ATPase copper transporting alpha	Homo sapiens	63-66
12221109-5	2002	Increases in copper concentration stimulate the trafficking of MNK to the plasma membrane where it effluxes copper.	Copper	108-114	ATPase copper transporting alpha	Homo sapiens	63-66
12221109-8	2002	However, this mislocalization was corrected by the addition of copper to cells via a process that was dependent upon the copper binding sites at the N-terminal region of MNK.	Copper	63-69	ATPase copper transporting alpha	Homo sapiens	170-173
12221109-8	2002	However, this mislocalization was corrected by the addition of copper to cells via a process that was dependent upon the copper binding sites at the N-terminal region of MNK.	Copper	121-127	ATPase copper transporting alpha	Homo sapiens	170-173
12221109-11	2002	Our findings provide a molecular framework for understanding how mutations that affect the proper folding of the MNK transporter in Menkes patients may be responsive to parenteral copper therapy.	Copper	180-186	ATPase copper transporting alpha	Homo sapiens	113-116
12420134-1	2002	ATOX1 is a cytoplasmic copper chaperone that interacts with the copper-binding domain of the membrane copper transporters ATP7A and ATP7B.	Copper	23-29	ATPase copper transporting alpha	Homo sapiens	122-127
12420134-1	2002	ATOX1 is a cytoplasmic copper chaperone that interacts with the copper-binding domain of the membrane copper transporters ATP7A and ATP7B.	Copper	64-70	ATPase copper transporting alpha	Homo sapiens	122-127
12393797-1	2002	The Menkes disease protein (ATP7A or MNK) is a P-type transmembrane ATPase that regulates translocation of cytosolic copper ions across intracellular membranes of compartments along the secretory pathway.	Copper	117-123	ATPase copper transporting alpha	Homo sapiens	28-33
12393797-1	2002	The Menkes disease protein (ATP7A or MNK) is a P-type transmembrane ATPase that regulates translocation of cytosolic copper ions across intracellular membranes of compartments along the secretory pathway.	Copper	117-123	ATPase copper transporting alpha	Homo sapiens	37-40
12393797-2	2002	In this study, we show that endogenous MNK in cultured cell lines is localized to the distal Golgi apparatus and translocates to the plasma membrane in response to exogenous copper ions.	Copper	174-180	ATPase copper transporting alpha	Homo sapiens	39-42
12393797-4	2002	In contrast, protein kinase A inhibitors block copper-stimulated MNK delivery to the plasma membrane.	Copper	47-53	ATPase copper transporting alpha	Homo sapiens	65-68
12427520-1	2002	Carrier detection for 12 women and prenatal diagnosis for six fetuses in Japanese families with a patient with Menkes disease (MNK) were performed by gene analysis and/or measurement of the copper concentration in cultured cells.	Copper	190-196	ATPase copper transporting alpha	Homo sapiens	127-130
12427520-7	2002	In one family in which a mutation in ATP7A was not found, cultured amniocytes from a male fetus had a high copper concentration.	Copper	107-113	ATPase copper transporting alpha	Homo sapiens	37-42
12539960-1	2002	Copper transporting P-type ATPases, designated ATP7A and ATP7B, play an essential role in mammalian copper balance.	Copper	0-6	ATPase copper transporting alpha	Homo sapiens	47-52
12539960-1	2002	Copper transporting P-type ATPases, designated ATP7A and ATP7B, play an essential role in mammalian copper balance.	Copper	100-106	ATPase copper transporting alpha	Homo sapiens	47-52
12539960-2	2002	Impaired intestinal transport of copper, resulting from mutations in the ATP7A gene, lead to Menkes disease in humans.	Copper	33-39	ATPase copper transporting alpha	Homo sapiens	73-78
12539960-7	2002	Other chaperones may be important for the transport of copper into ATP7A and ATP7B.	Copper	55-61	ATPase copper transporting alpha	Homo sapiens	67-72
12539963-1	2002	The Menkes copper-translocating P-type ATPase (ATP7A; MNK) is a ubiquitous protein that regulates the absorption of copper in the gastrointestinal tract.	Copper	11-17	ATPase copper transporting alpha	Homo sapiens	47-52
12539963-1	2002	The Menkes copper-translocating P-type ATPase (ATP7A; MNK) is a ubiquitous protein that regulates the absorption of copper in the gastrointestinal tract.	Copper	11-17	ATPase copper transporting alpha	Homo sapiens	54-57
12181646-2	2002	Recently, novel components involved in copper metabolism, including Menkes disease protein (ATP7A), Wilson disease protein (ATP7B), and copper chaperones, have been identified.	Copper	39-45	ATPase copper transporting alpha	Homo sapiens	92-97
11855813-4	2002	Accordingly, immunofluorescence and Western blotting revealed the occurrence of a Cu-inducible, putative homologue of human Menkes (MNK) Cu-P-type ATPase.	Copper	82-84	ATPase copper transporting alpha	Homo sapiens	132-135
12537648-1	2002	Menkes disease and occipital horn syndrome (OHS) are allelic neurogenetic disorders of copper transport associated with mutations in an X-linked gene, ATP7A.	Copper	87-93	ATPase copper transporting alpha	Homo sapiens	151-156
11431706-7	2001	It has been demonstrated that the dileucine motif L1487L1488 functions as an endocytic signal for ATP7A cycling between the TGN and the plasma membrane.	dileucine	34-43	ATPase copper transporting alpha	Homo sapiens	98-103
12372948-3	2002	ATP7A and ATP7B are genes encoding membrane copper transporters.	Copper	44-50	ATPase copper transporting alpha	Homo sapiens	0-5
12372948-4	2002	ATP7A, defective in Menkes disease (MNK), is expressed in many tissues involved primarily in copper uptake from dietary sources.	Copper	93-99	ATPase copper transporting alpha	Homo sapiens	0-5
12372948-4	2002	ATP7A, defective in Menkes disease (MNK), is expressed in many tissues involved primarily in copper uptake from dietary sources.	Copper	93-99	ATPase copper transporting alpha	Homo sapiens	36-39
12372948-6	2002	Although MNK patients have a copper deficiency in most tissues, copper accumulates in proximal tubules in the kidney.	Copper	29-35	ATPase copper transporting alpha	Homo sapiens	9-12
12540288-4	2001	The characteristic features of MNK are progressive neurological degeneration, connective tissue disorders and hair abnormalities, which are caused by a reduction in the activity of several copper-dependent enzymes, due to concomitant copper deficiency.	Copper	189-195	ATPase copper transporting alpha	Homo sapiens	31-34
11431706-7	2001	It has been demonstrated that the dileucine motif L1487L1488 functions as an endocytic signal for ATP7A cycling between the TGN and the plasma membrane.	l1487l1488	50-60	ATPase copper transporting alpha	Homo sapiens	98-103
11936860-9	2001	In conclusion, mutations of the copper transporting P-type ATPase ATP7A gene cause distinct human diseases showing some genotype/phenotype correlation and implications for treatment.	Copper	32-38	ATPase copper transporting alpha	Homo sapiens	66-71
11350187-2	2001	It is caused by a defect in the Menkes (ATP7A) gene, which encodes a transmembrane copper-transporting P-type ATPase.	Copper	83-89	ATPase copper transporting alpha	Homo sapiens	40-45
11415452-2	2001	Two related human ATPase genes, ATP7A (EC 3.6.1.36) and ATP7B (EC 3.6.1.36), have been cloned as the loci of mutations causing Menkes and Wilson diseases, diseases of copper metabolism.	Copper	167-173	ATPase copper transporting alpha	Homo sapiens	32-37
10970802-2	2000	The transcript variant that is the focus of the present study codes for a 103-residue protein containing the first heavy-metal-binding domain (Hmb1) of ATP7A, the Cu-ATPase associated with Menkes disease.	Metals	121-126	ATPase copper transporting alpha	Homo sapiens	152-157
11092760-3	2000	The MNK protein relocates to the plasma membrane in cells exposed to elevated copper where it functions in copper efflux.	Copper	78-84	ATPase copper transporting alpha	Homo sapiens	4-7
11092760-3	2000	The MNK protein relocates to the plasma membrane in cells exposed to elevated copper where it functions in copper efflux.	Copper	107-113	ATPase copper transporting alpha	Homo sapiens	4-7
11092760-5	2000	In this study, we investigated whether the MNK protein is required for the activity of tyrosinase, a copper-dependent enzyme involved in melanogenesis that is synthesized within the secretory pathway.	Copper	101-107	ATPase copper transporting alpha	Homo sapiens	43-46
11092760-8	2000	This MNK-dependent activation of tyrosinase was impaired by the chelation of copper in the medium of cells and after mutation of the invariant phosphorylation site at aspartic acid residue 1044 of MNK.	Copper	77-83	ATPase copper transporting alpha	Homo sapiens	5-8
11092760-8	2000	This MNK-dependent activation of tyrosinase was impaired by the chelation of copper in the medium of cells and after mutation of the invariant phosphorylation site at aspartic acid residue 1044 of MNK.	Aspartic Acid	167-180	ATPase copper transporting alpha	Homo sapiens	5-8
11092760-8	2000	This MNK-dependent activation of tyrosinase was impaired by the chelation of copper in the medium of cells and after mutation of the invariant phosphorylation site at aspartic acid residue 1044 of MNK.	Aspartic Acid	167-180	ATPase copper transporting alpha	Homo sapiens	197-200
11092760-9	2000	Collectively, these findings suggest that the MNK protein transports copper into the secretory pathway of mammalian cells to activate copper-dependent enzymes and reveal a second copper transport role for MNK in mammalian cells.	Copper	69-75	ATPase copper transporting alpha	Homo sapiens	46-49
11092760-9	2000	Collectively, these findings suggest that the MNK protein transports copper into the secretory pathway of mammalian cells to activate copper-dependent enzymes and reveal a second copper transport role for MNK in mammalian cells.	Copper	134-140	ATPase copper transporting alpha	Homo sapiens	46-49
11092760-9	2000	Collectively, these findings suggest that the MNK protein transports copper into the secretory pathway of mammalian cells to activate copper-dependent enzymes and reveal a second copper transport role for MNK in mammalian cells.	Copper	134-140	ATPase copper transporting alpha	Homo sapiens	205-208
11092760-9	2000	Collectively, these findings suggest that the MNK protein transports copper into the secretory pathway of mammalian cells to activate copper-dependent enzymes and reveal a second copper transport role for MNK in mammalian cells.	Copper	134-140	ATPase copper transporting alpha	Homo sapiens	46-49
11092760-9	2000	Collectively, these findings suggest that the MNK protein transports copper into the secretory pathway of mammalian cells to activate copper-dependent enzymes and reveal a second copper transport role for MNK in mammalian cells.	Copper	134-140	ATPase copper transporting alpha	Homo sapiens	205-208
11092760-10	2000	These findings describe a single cell-based system that allows both the copper transport and trafficking functions of MNK to be studied.	Copper	72-78	ATPase copper transporting alpha	Homo sapiens	118-121
10940336-3	2000	Two membrane-bound Cu-transporting ATPase enzymes, ATP7A and ATP7B, the products of the Menkes and Wilson disease genes, respectively, catalyze an ATP-dependent transfer of Cu to intracellular compartments or expel Cu from the cell.	Copper	19-21	ATPase copper transporting alpha	Homo sapiens	51-56
11040994-3	2000	They correspond to fragments of two extracellular loops ATP7A, of which one loop is apparently involved in the copper ion transfer (P16) whereas the other is not (P15).	Copper	111-117	ATPase copper transporting alpha	Homo sapiens	56-61
11040994-6	2000	The ATP7A involvement in the copper ion transfer to nonhepatocyte cells is discussed.	Copper	29-35	ATPase copper transporting alpha	Homo sapiens	4-9
10940336-3	2000	Two membrane-bound Cu-transporting ATPase enzymes, ATP7A and ATP7B, the products of the Menkes and Wilson disease genes, respectively, catalyze an ATP-dependent transfer of Cu to intracellular compartments or expel Cu from the cell.	Adenosine Triphosphate	35-38	ATPase copper transporting alpha	Homo sapiens	51-56
10940336-3	2000	Two membrane-bound Cu-transporting ATPase enzymes, ATP7A and ATP7B, the products of the Menkes and Wilson disease genes, respectively, catalyze an ATP-dependent transfer of Cu to intracellular compartments or expel Cu from the cell.	Copper	173-175	ATPase copper transporting alpha	Homo sapiens	51-56
10940336-3	2000	Two membrane-bound Cu-transporting ATPase enzymes, ATP7A and ATP7B, the products of the Menkes and Wilson disease genes, respectively, catalyze an ATP-dependent transfer of Cu to intracellular compartments or expel Cu from the cell.	Copper	173-175	ATPase copper transporting alpha	Homo sapiens	51-56
10940336-4	2000	ATP7A and ATP7B work in concert with a series of smaller peptides, the copper chaperones, that exchange Cu at the ATPase sites or incorporate the Cu directly into the structure of Cu-dependent enzymes such as cytochrome c oxidase and Cu, Zn superoxide dismutase.	Copper	71-77	ATPase copper transporting alpha	Homo sapiens	0-5
10940336-4	2000	ATP7A and ATP7B work in concert with a series of smaller peptides, the copper chaperones, that exchange Cu at the ATPase sites or incorporate the Cu directly into the structure of Cu-dependent enzymes such as cytochrome c oxidase and Cu, Zn superoxide dismutase.	Copper	104-106	ATPase copper transporting alpha	Homo sapiens	0-5
10940336-4	2000	ATP7A and ATP7B work in concert with a series of smaller peptides, the copper chaperones, that exchange Cu at the ATPase sites or incorporate the Cu directly into the structure of Cu-dependent enzymes such as cytochrome c oxidase and Cu, Zn superoxide dismutase.	Copper	146-148	ATPase copper transporting alpha	Homo sapiens	0-5
10940336-4	2000	ATP7A and ATP7B work in concert with a series of smaller peptides, the copper chaperones, that exchange Cu at the ATPase sites or incorporate the Cu directly into the structure of Cu-dependent enzymes such as cytochrome c oxidase and Cu, Zn superoxide dismutase.	Copper	146-148	ATPase copper transporting alpha	Homo sapiens	0-5
11043517-1	2000	Menkes disease is an X-linked recessive disorder of the copper membrane transport system caused by mutations in the ATP7A gene.	Copper	56-62	ATPase copper transporting alpha	Homo sapiens	116-121
10790207-1	2000	The gene ATP7B responsible for Wilson"s disease (WD) produces a protein which is predicted to be a copper-binding P-type ATPase, homologous to the Menkes disease gene (ATP7A).	Copper	99-105	ATPase copper transporting alpha	Homo sapiens	168-173
10567439-0	1999	Expression of menkes copper-transporting ATPase, MNK, in the lactating human breast: possible role in copper transport into milk.	Copper	21-27	ATPase copper transporting alpha	Homo sapiens	49-52
10567439-10	1999	Our results suggest that relocalization of the MNK is a physiological process, which may be mediated by copper levels in the breast or by hormones and other events taking place during lactation.	Copper	104-110	ATPase copper transporting alpha	Homo sapiens	47-50
10318764-1	1999	The protein encoded by the Menkes disease gene (MNK) is localised to the Golgi apparatus and cycles between the trans-Golgi network and the plasma membrane in cultured cells on addition and removal of copper to the growth medium.	Copper	201-207	ATPase copper transporting alpha	Homo sapiens	48-51
10484781-0	1999	The Menkes protein (ATP7A; MNK) cycles via the plasma membrane both in basal and elevated extracellular copper using a C-terminal di-leucine endocytic signal.	Copper	104-110	ATPase copper transporting alpha	Homo sapiens	20-25
10484781-0	1999	The Menkes protein (ATP7A; MNK) cycles via the plasma membrane both in basal and elevated extracellular copper using a C-terminal di-leucine endocytic signal.	Copper	104-110	ATPase copper transporting alpha	Homo sapiens	27-30
10484781-2	1999	MNK is normally localized pre- dominantly in the trans -Golgi network (TGN); however, when cells are exposed to excessive copper it is rapidly relocalized to the plasma membrane where it functions in copper efflux.	Copper	122-128	ATPase copper transporting alpha	Homo sapiens	0-3
10484781-2	1999	MNK is normally localized pre- dominantly in the trans -Golgi network (TGN); however, when cells are exposed to excessive copper it is rapidly relocalized to the plasma membrane where it functions in copper efflux.	Copper	200-206	ATPase copper transporting alpha	Homo sapiens	0-3
10484781-5	1999	In cells stably expressing the tagged MNK protein (MNK-tag), extracellular antibodies were internalized to the perinuclear region, indicating that MNK-tag at the TGN constitutively cycles via the plasma membrane in basal copper conditions.	Copper	221-227	ATPase copper transporting alpha	Homo sapiens	38-41
10484781-5	1999	In cells stably expressing the tagged MNK protein (MNK-tag), extracellular antibodies were internalized to the perinuclear region, indicating that MNK-tag at the TGN constitutively cycles via the plasma membrane in basal copper conditions.	Copper	221-227	ATPase copper transporting alpha	Homo sapiens	51-54
10484781-5	1999	In cells stably expressing the tagged MNK protein (MNK-tag), extracellular antibodies were internalized to the perinuclear region, indicating that MNK-tag at the TGN constitutively cycles via the plasma membrane in basal copper conditions.	Copper	221-227	ATPase copper transporting alpha	Homo sapiens	51-54
10484781-6	1999	Under elevated copper conditions, MNK-tag was recruited to the plasma membrane; however, internalization of MNK-tag was not inhibited and the protein continued to recycle through cyto- plasmic membrane compartments.	Copper	15-21	ATPase copper transporting alpha	Homo sapiens	34-37
10484781-7	1999	These findings suggest that copper stimulates exocytic movement of MNK to the plasma membrane rather than reducing MNK retrieval and indicate that MNK may remove copper from the cytoplasm by transporting copper into the vesicles through which it cycles.	Copper	28-34	ATPase copper transporting alpha	Homo sapiens	67-70
10484781-9	1999	Mutation of the di-leucine, L1487 L1488, prevented uptake of anti-myc antibodies in both basal and elevated copper conditions, thereby identifying this sequence as an endocytic signal for MNK.	di-leucine	16-26	ATPase copper transporting alpha	Homo sapiens	188-191
10484781-9	1999	Mutation of the di-leucine, L1487 L1488, prevented uptake of anti-myc antibodies in both basal and elevated copper conditions, thereby identifying this sequence as an endocytic signal for MNK.	Copper	108-114	ATPase copper transporting alpha	Homo sapiens	188-191
10484781-10	1999	Analysis of the effects of the di-leucine mutation in elevated copper provided further support for copper-stimulated exocytic movement of MNK from the TGN to the plasma membrane.	Copper	63-69	ATPase copper transporting alpha	Homo sapiens	138-141
10484781-10	1999	Analysis of the effects of the di-leucine mutation in elevated copper provided further support for copper-stimulated exocytic movement of MNK from the TGN to the plasma membrane.	Copper	99-105	ATPase copper transporting alpha	Homo sapiens	138-141
10400994-2	1999	The gene defective in Menkes disease (ATP7A) encodes a copper transporting P-type ATPase (MNK or ATP7A) with six copper-binding domains at its N-terminus.	Copper	55-61	ATPase copper transporting alpha	Homo sapiens	38-43
10400994-2	1999	The gene defective in Menkes disease (ATP7A) encodes a copper transporting P-type ATPase (MNK or ATP7A) with six copper-binding domains at its N-terminus.	Copper	55-61	ATPase copper transporting alpha	Homo sapiens	90-93
10400994-2	1999	The gene defective in Menkes disease (ATP7A) encodes a copper transporting P-type ATPase (MNK or ATP7A) with six copper-binding domains at its N-terminus.	Copper	55-61	ATPase copper transporting alpha	Homo sapiens	97-102
10400994-3	1999	MNK is normally localized to the trans -Golgi network in cultured cells, but relocates to the plasma membrane in the presence of elevated extracellular copper.	Copper	152-158	ATPase copper transporting alpha	Homo sapiens	0-3
10400994-6	1999	Using the same assay with any one of the six copper-binding domains intact, MNK moves to the plasma membrane in a way indistinguishable from the wild-type protein.	Copper	45-51	ATPase copper transporting alpha	Homo sapiens	76-79
10400994-7	1999	Therefore, the copper-binding domains are vital for MNK trafficking and only a single domain is sufficient for this redistribution to occur.	Copper	15-21	ATPase copper transporting alpha	Homo sapiens	52-55
10401004-3	1999	The Menkes gene product (MNK) is a P-type ATPase and is considered to be the main copper efflux protein in most cells.	Copper	82-88	ATPase copper transporting alpha	Homo sapiens	25-28
10401004-5	1999	Here we report the first missense mutation which causes mild Menkes disease, a mutation in a successfully copper-treated classical Menkes patient and the effect of each mutation on the localization of MNK within the cell.	Copper	106-112	ATPase copper transporting alpha	Homo sapiens	201-204
10453201-10	1999	This result may support the hypothesis that ATP7A and ATP7B are involved in cellular copper transport and those proteins could be suitable models for elucidating intracellular copper metabolism.	Copper	85-91	ATPase copper transporting alpha	Homo sapiens	44-49
10453201-10	1999	This result may support the hypothesis that ATP7A and ATP7B are involved in cellular copper transport and those proteins could be suitable models for elucidating intracellular copper metabolism.	Copper	176-182	ATPase copper transporting alpha	Homo sapiens	44-49
10419525-1	1999	The Menkes protein (MNK) is a copper-transporting P-type ATPase, which has six highly conserved metal-binding sites, GMTCXXC, at the N terminus.	Metals	96-101	ATPase copper transporting alpha	Homo sapiens	4-18
10419525-1	1999	The Menkes protein (MNK) is a copper-transporting P-type ATPase, which has six highly conserved metal-binding sites, GMTCXXC, at the N terminus.	Metals	96-101	ATPase copper transporting alpha	Homo sapiens	20-23
10419525-2	1999	The metal-binding sites may be involved in MNK trafficking and/or copper-translocating activity.	Metals	4-9	ATPase copper transporting alpha	Homo sapiens	43-46
10419525-3	1999	In this study, we report the detailed functional analysis in mammalian cells of recombinant human MNK and its mutants with various metal-binding sites altered by site-directed mutagenesis.	Metals	131-136	ATPase copper transporting alpha	Homo sapiens	98-101
10419525-4	1999	The results of the study, both in vitro and in vivo, provide evidence that the metal-binding sites of MNK are not essential for the ATP-dependent copper-translocating activity of MNK.	Metals	79-84	ATPase copper transporting alpha	Homo sapiens	102-105
10419525-5	1999	Moreover, metal-binding site mutations, which resulted in a loss of ability of MNK to traffick to the plasma membrane, produced a copper hyperaccumulating phenotype.	Metals	10-15	ATPase copper transporting alpha	Homo sapiens	79-82
10419525-5	1999	Moreover, metal-binding site mutations, which resulted in a loss of ability of MNK to traffick to the plasma membrane, produced a copper hyperaccumulating phenotype.	Copper	130-136	ATPase copper transporting alpha	Homo sapiens	79-82
10419525-7	1999	The results of this study suggest that copper-translocating activity of MNK and its copper-induced relocalization to the plasma membrane represent a well coordinated copper homeostasis system.	Copper	39-45	ATPase copper transporting alpha	Homo sapiens	72-75
10419525-7	1999	The results of this study suggest that copper-translocating activity of MNK and its copper-induced relocalization to the plasma membrane represent a well coordinated copper homeostasis system.	Copper	84-90	ATPase copper transporting alpha	Homo sapiens	72-75
10419525-7	1999	The results of this study suggest that copper-translocating activity of MNK and its copper-induced relocalization to the plasma membrane represent a well coordinated copper homeostasis system.	Copper	84-90	ATPase copper transporting alpha	Homo sapiens	72-75
9817923-2	1998	MNK is an important component of the mammalian copper transport pathway, and previous studies in cultured cells have localized MNK to the final compartment of the Golgi apparatus, the trans -Golgi network (TGN).	Copper	47-53	ATPase copper transporting alpha	Homo sapiens	0-3
10196202-3	1999	MNK is normally located in the trans-Golgi network (TGN) but has been shown to relocalize to the plasma membrane when cells are cultured in media containing high concentrations of copper.	Copper	180-186	ATPase copper transporting alpha	Homo sapiens	0-3
10196202-4	1999	The experiments described in this report test the hypothesis that the six MBSs are required for this copper-induced trafficking of MNK.	Copper	101-107	ATPase copper transporting alpha	Homo sapiens	131-134
10196202-7	1999	Furthermore, the ability of the MNK variants to relocalize corresponded well with their ability to confer copper resistance.	Copper	106-112	ATPase copper transporting alpha	Homo sapiens	32-35
10196202-12	1999	These experiments demonstrated that the deleted N-terminal region from amino acid 8 to amino acid 485 was not essential for copper-induced trafficking and that one MBS close to the membrane channel of MNK was necessary and sufficient for the copper-induced redistribution.	Copper	242-248	ATPase copper transporting alpha	Homo sapiens	201-204
10036323-1	1999	The Menkes ATPase (MNK) has an essential role in the translocation of copper across cellular membranes.	Copper	70-76	ATPase copper transporting alpha	Homo sapiens	4-17
10036323-1	1999	The Menkes ATPase (MNK) has an essential role in the translocation of copper across cellular membranes.	Copper	70-76	ATPase copper transporting alpha	Homo sapiens	19-22
10036323-5	1999	The second conserved sub-domain of MNK was over-expressed, purified and its copper-binding properties characterised.	Copper	76-82	ATPase copper transporting alpha	Homo sapiens	35-38
10036323-7	1999	This is the first direct evidence of copper-binding to the MNK amino-terminal repeats.	Copper	37-43	ATPase copper transporting alpha	Homo sapiens	59-62
10319589-1	1999	Menkes disease is an X-linked recessive disorder of the copper membrane transport system caused by mutations to the Menkes (MNK) gene.	Copper	56-62	ATPase copper transporting alpha	Homo sapiens	0-6
10319589-1	1999	Menkes disease is an X-linked recessive disorder of the copper membrane transport system caused by mutations to the Menkes (MNK) gene.	Copper	56-62	ATPase copper transporting alpha	Homo sapiens	124-127
10319589-4	1999	Secondly, we found a point mutation, T2763G, resulting in a leucine-to-arginine conversion, which we predicted would cause a change in the secondary structure of the Menkes protein.	Leucine	60-67	ATPase copper transporting alpha	Homo sapiens	166-172
10319589-4	1999	Secondly, we found a point mutation, T2763G, resulting in a leucine-to-arginine conversion, which we predicted would cause a change in the secondary structure of the Menkes protein.	Arginine	71-79	ATPase copper transporting alpha	Homo sapiens	166-172
9817923-3	1998	At this location, MNK is predicted to supply copper to copper-dependent enzymes as they migrate through the secretory pathway.	Copper	45-51	ATPase copper transporting alpha	Homo sapiens	18-21
9817923-3	1998	At this location, MNK is predicted to supply copper to copper-dependent enzymes as they migrate through the secretory pathway.	Copper	55-61	ATPase copper transporting alpha	Homo sapiens	18-21
9817923-4	1998	However, under conditions of elevated extracellular copper, the MNK protein undergoes a rapid relocalization to the plasma membrane where it functions in the efflux of copper from cells.	Copper	52-58	ATPase copper transporting alpha	Homo sapiens	64-67
9817923-4	1998	However, under conditions of elevated extracellular copper, the MNK protein undergoes a rapid relocalization to the plasma membrane where it functions in the efflux of copper from cells.	Copper	168-174	ATPase copper transporting alpha	Homo sapiens	64-67
9817923-6	1998	In vitro mutagenesis of the human MNK cDNA and immunofluorescence detection of mutant forms of MNK expressed in cultured cells demonstrated that the di-leucine, L1487L1488, was essential for localization of MNK within the TGN, but not for copper efflux.	di-leucine	149-159	ATPase copper transporting alpha	Homo sapiens	34-37
9817923-6	1998	In vitro mutagenesis of the human MNK cDNA and immunofluorescence detection of mutant forms of MNK expressed in cultured cells demonstrated that the di-leucine, L1487L1488, was essential for localization of MNK within the TGN, but not for copper efflux.	di-leucine	149-159	ATPase copper transporting alpha	Homo sapiens	95-98
9817923-6	1998	In vitro mutagenesis of the human MNK cDNA and immunofluorescence detection of mutant forms of MNK expressed in cultured cells demonstrated that the di-leucine, L1487L1488, was essential for localization of MNK within the TGN, but not for copper efflux.	di-leucine	149-159	ATPase copper transporting alpha	Homo sapiens	95-98
9817923-7	1998	We suggest that this di-leucine motif is a putative endocytic targeting motif necessary for the retrieval of MNK from the plasma membrane to the TGN.	di-leucine	21-31	ATPase copper transporting alpha	Homo sapiens	109-112
8947031-2	1996	Recent evidence that the MNK P-type ATPase has a role in copper efflux has come from studies using copper-resistant variants of cultured Chinese hamster ovary (CHO) cells.	Copper	57-63	ATPase copper transporting alpha	Homo sapiens	25-28
9813047-3	1998	The ATP7A and ATP7B genes that are defective in patients with Menkes" and Wilson"s diseases, respectively, encode transmembrane, P-type ATPase proteins (ATP7A or MNK and ATP7B or WND, respectively) that function to translocate copper across cellular membranes.	Copper	227-233	ATPase copper transporting alpha	Homo sapiens	162-165
9813047-5	1998	Both MNK and WND expressed from plasmid constructs were able to correct the copper accumulation and copper retention phenotype of these cells.	Copper	76-82	ATPase copper transporting alpha	Homo sapiens	5-8
9813047-7	1998	Although MNK showed copper-induced trafficking from the trans-Golgi network to the plasma membrane, in the same cell line the intracellular location of WND did not appear to be affected by elevated copper.	Copper	20-26	ATPase copper transporting alpha	Homo sapiens	9-12
9359859-1	1997	Two P-type ATPases, MNK and WND were recently shown to be defective in the human disorders of copper transport, Menkes disease and Wilson disease respectively.	Copper	94-100	ATPase copper transporting alpha	Homo sapiens	20-23
9359859-12	1997	The results suggest a role for MNK in the secretion of copper into milk and that PMC42 cells are a valuable model for investigating the detailed cellular function of MNK and WND.	Copper	55-61	ATPase copper transporting alpha	Homo sapiens	31-34
9257713-1	1997	The Menkes ATPase is the product of the MNK gene, defective in some inherited human disorders of copper metabolism.	Copper	97-103	ATPase copper transporting alpha	Homo sapiens	40-43
9813047-3	1998	The ATP7A and ATP7B genes that are defective in patients with Menkes" and Wilson"s diseases, respectively, encode transmembrane, P-type ATPase proteins (ATP7A or MNK and ATP7B or WND, respectively) that function to translocate copper across cellular membranes.	Copper	227-233	ATPase copper transporting alpha	Homo sapiens	4-9
9813047-3	1998	The ATP7A and ATP7B genes that are defective in patients with Menkes" and Wilson"s diseases, respectively, encode transmembrane, P-type ATPase proteins (ATP7A or MNK and ATP7B or WND, respectively) that function to translocate copper across cellular membranes.	Copper	227-233	ATPase copper transporting alpha	Homo sapiens	153-158
9762903-0	1998	ATP-dependent copper transport by the Menkes protein in membrane vesicles isolated from cultured Chinese hamster ovary cells.	Adenosine Triphosphate	0-3	ATPase copper transporting alpha	Homo sapiens	38-44
9762903-0	1998	ATP-dependent copper transport by the Menkes protein in membrane vesicles isolated from cultured Chinese hamster ovary cells.	Copper	14-20	ATPase copper transporting alpha	Homo sapiens	38-44
9762903-1	1998	The Menkes (MNK) protein is a vital component of copper homeostasis in mammalian cells.	Copper	49-55	ATPase copper transporting alpha	Homo sapiens	4-10
9762903-1	1998	The Menkes (MNK) protein is a vital component of copper homeostasis in mammalian cells.	Copper	49-55	ATPase copper transporting alpha	Homo sapiens	12-15
9762903-3	1998	The enzyme activity in membrane vesicles prepared from Chinese hamster ovary cells overexpressing MNK was ATP-dependent, correlated with the amount of MNK and followed Michaelis-Menten kinetics with respect to copper.	Adenosine Triphosphate	106-109	ATPase copper transporting alpha	Homo sapiens	98-101
9762903-3	1998	The enzyme activity in membrane vesicles prepared from Chinese hamster ovary cells overexpressing MNK was ATP-dependent, correlated with the amount of MNK and followed Michaelis-Menten kinetics with respect to copper.	Adenosine Triphosphate	106-109	ATPase copper transporting alpha	Homo sapiens	151-154
9762903-4	1998	The copper transport was observed only under reducing conditions suggesting MNK transports Cu(I).	Copper	4-10	ATPase copper transporting alpha	Homo sapiens	76-79
9762903-4	1998	The copper transport was observed only under reducing conditions suggesting MNK transports Cu(I).	cuprous ion	91-96	ATPase copper transporting alpha	Homo sapiens	76-79
9668172-1	1998	The Menkes protein (MNK or ATP7A) is an important component of the mammalian copper transport pathway and is defective in Menkes disease, a fatal X-linked disorder of copper transport.	Copper	77-83	ATPase copper transporting alpha	Homo sapiens	4-18
9668172-1	1998	The Menkes protein (MNK or ATP7A) is an important component of the mammalian copper transport pathway and is defective in Menkes disease, a fatal X-linked disorder of copper transport.	Copper	77-83	ATPase copper transporting alpha	Homo sapiens	20-23
9668172-1	1998	The Menkes protein (MNK or ATP7A) is an important component of the mammalian copper transport pathway and is defective in Menkes disease, a fatal X-linked disorder of copper transport.	Copper	77-83	ATPase copper transporting alpha	Homo sapiens	27-32
9668172-2	1998	To study the structure and function of this protein and to elucidate its role in cellular copper homeostasis, a cDNA construct encoding the full-length MNK protein was cloned into a mammalian expression vector under the control of the CMV promoter.	Copper	90-96	ATPase copper transporting alpha	Homo sapiens	152-155
9668172-4	1998	Detailed characterization of four clones showed that an increase in MNK protein expression led to a corresponding increase in the level of copper resistance of the cells.	Copper	139-145	ATPase copper transporting alpha	Homo sapiens	68-71
9668172-6	1998	When the extracellular copper concentration was increased, MNK in the clones as well as in CHO-K1 cells was redistributed to the cytoplasm and plasma membrane, but returned to the TGN under basal, low copper conditions.	Copper	23-29	ATPase copper transporting alpha	Homo sapiens	59-62
9668172-6	1998	When the extracellular copper concentration was increased, MNK in the clones as well as in CHO-K1 cells was redistributed to the cytoplasm and plasma membrane, but returned to the TGN under basal, low copper conditions.	Copper	201-207	ATPase copper transporting alpha	Homo sapiens	59-62
9668172-8	1998	It also demonstrates the stable expression of a functional MNK protein from a cDNA construct in mammalian cells, as well as the copper-induced redistribution of MNK in a cell line (CHO-K1) that was not selected for copper resistance or overexpression of MNK.	Copper	128-134	ATPase copper transporting alpha	Homo sapiens	161-164
9668172-8	1998	It also demonstrates the stable expression of a functional MNK protein from a cDNA construct in mammalian cells, as well as the copper-induced redistribution of MNK in a cell line (CHO-K1) that was not selected for copper resistance or overexpression of MNK.	Copper	128-134	ATPase copper transporting alpha	Homo sapiens	161-164
9686355-0	1998	Investigation of the copper binding sites in the Menkes disease protein, ATP7A.	Copper	21-27	ATPase copper transporting alpha	Homo sapiens	73-78
9467005-1	1998	The ATP7A gene encodes a copper-transporting ATPase.	Copper	25-31	ATPase copper transporting alpha	Homo sapiens	4-9
9467005-8	1998	These findings indicate that endoplasmic reticulum localization only of a variant ATP7A protein is insufficient to effect normal copper transport.	Copper	129-135	ATPase copper transporting alpha	Homo sapiens	82-87
9147644-0	1997	Immunocytochemical localization of the Menkes copper transport protein (ATP7A) to the trans-Golgi network.	Copper	46-52	ATPase copper transporting alpha	Homo sapiens	72-77
9147644-1	1997	We have generated polyclonal antibodies against the amino-terminal third of the Menkes protein (ATP7A; MNK) by immunizing rabbits with a histidine-tagged MNK fusion construct containing metal-binding domains 1-4.	Histidine	137-146	ATPase copper transporting alpha	Homo sapiens	103-106
9147644-1	1997	We have generated polyclonal antibodies against the amino-terminal third of the Menkes protein (ATP7A; MNK) by immunizing rabbits with a histidine-tagged MNK fusion construct containing metal-binding domains 1-4.	Histidine	137-146	ATPase copper transporting alpha	Homo sapiens	154-157
9147644-1	1997	We have generated polyclonal antibodies against the amino-terminal third of the Menkes protein (ATP7A; MNK) by immunizing rabbits with a histidine-tagged MNK fusion construct containing metal-binding domains 1-4.	Metals	186-191	ATPase copper transporting alpha	Homo sapiens	103-106
9147644-7	1997	Using brefeldin A, a fungal inhibitor of protein secretion, we further demonstrated that the MNK protein is localized to the trans-Golgi network.	Brefeldin A	6-17	ATPase copper transporting alpha	Homo sapiens	93-96
9147644-9	1997	In light of the proposed role of MNK both in subcellular copper trafficking and in copper efflux, these data suggest a model for how these two processes are linked and represent an important step in the functional analysis of the MNK protein.	Copper	57-63	ATPase copper transporting alpha	Homo sapiens	33-36
9147644-9	1997	In light of the proposed role of MNK both in subcellular copper trafficking and in copper efflux, these data suggest a model for how these two processes are linked and represent an important step in the functional analysis of the MNK protein.	Copper	57-63	ATPase copper transporting alpha	Homo sapiens	230-233
9147644-9	1997	In light of the proposed role of MNK both in subcellular copper trafficking and in copper efflux, these data suggest a model for how these two processes are linked and represent an important step in the functional analysis of the MNK protein.	Copper	83-89	ATPase copper transporting alpha	Homo sapiens	230-233
8947031-2	1996	Recent evidence that the MNK P-type ATPase has a role in copper efflux has come from studies using copper-resistant variants of cultured Chinese hamster ovary (CHO) cells.	Copper	99-105	ATPase copper transporting alpha	Homo sapiens	25-28
8947031-3	1996	These variants have MNK gene amplification and consequently overexpress MNK, the extents of which correlate with the degree of elevated copper efflux.	Copper	136-142	ATPase copper transporting alpha	Homo sapiens	20-23
8947031-3	1996	These variants have MNK gene amplification and consequently overexpress MNK, the extents of which correlate with the degree of elevated copper efflux.	Copper	136-142	ATPase copper transporting alpha	Homo sapiens	72-75
8947031-4	1996	Here, we report on the localization of MNK in these copper-resistant CHO cells when cultured in different levels of copper.	Copper	52-58	ATPase copper transporting alpha	Homo sapiens	39-42
8947031-4	1996	Here, we report on the localization of MNK in these copper-resistant CHO cells when cultured in different levels of copper.	Copper	116-122	ATPase copper transporting alpha	Homo sapiens	39-42
8947031-6	1996	In elevated copper conditions there was a rapid trafficking of MNK from the Golgi to the plasma membrane.	Copper	12-18	ATPase copper transporting alpha	Homo sapiens	63-66
8947031-8	1996	In media containing basal copper, MNK accumulated in cytoplasmic vesicles after treatment of cells with a variety of agents that inhibit endosomal recycling.	Copper	26-32	ATPase copper transporting alpha	Homo sapiens	34-37
8589689-0	1995	Gene amplification of the Menkes (MNK; ATP7A) P-type ATPase gene of CHO cells is associated with copper resistance and enhanced copper efflux.	Copper	97-103	ATPase copper transporting alpha	Homo sapiens	26-32
8923001-1	1996	Occipital horn syndrome (OHS), an X-linked connective tissue disorder, has recently been shown to result from mutations in the Menkes disease gene (MNK), which encodes a copper-transporting ATPase.	Copper	170-176	ATPase copper transporting alpha	Homo sapiens	148-151
8812725-1	1996	Classical Menkes disease is a fatal X-linked neurodegenerative disorder caused by defects in a gene (MNK) that encodes a copper-transporting ATPase.	Copper	121-127	ATPase copper transporting alpha	Homo sapiens	101-104
8589689-6	1995	The degree of increase in MNK mRNA and protein correlated well with the level of copper resistance and extent of copper efflux.	Copper	81-87	ATPase copper transporting alpha	Homo sapiens	26-29
8589689-6	1995	The degree of increase in MNK mRNA and protein correlated well with the level of copper resistance and extent of copper efflux.	Copper	113-119	ATPase copper transporting alpha	Homo sapiens	26-29
8589689-8	1995	These data, combined with the clinical and cellular phenotype in Menkes disease, provide strong evidence that the MNK protein is involved in transmembrane copper efflux, and demonstrate a new system of gene amplification in mammalian cells.	Copper	155-161	ATPase copper transporting alpha	Homo sapiens	114-117
8589689-0	1995	Gene amplification of the Menkes (MNK; ATP7A) P-type ATPase gene of CHO cells is associated with copper resistance and enhanced copper efflux.	Copper	97-103	ATPase copper transporting alpha	Homo sapiens	34-37
8589689-0	1995	Gene amplification of the Menkes (MNK; ATP7A) P-type ATPase gene of CHO cells is associated with copper resistance and enhanced copper efflux.	Copper	128-134	ATPase copper transporting alpha	Homo sapiens	26-32
8589689-0	1995	Gene amplification of the Menkes (MNK; ATP7A) P-type ATPase gene of CHO cells is associated with copper resistance and enhanced copper efflux.	Copper	128-134	ATPase copper transporting alpha	Homo sapiens	34-37
8589689-3	1995	As cultured cells from patients with Menkes disease (mutations in MNK; ATP7A gene) accumulate copper, probably due to defective copper efflux, we investigated the possible role of the MNK gene in the molecular basis of copper resistance.	Copper	94-100	ATPase copper transporting alpha	Homo sapiens	66-69
8589689-3	1995	As cultured cells from patients with Menkes disease (mutations in MNK; ATP7A gene) accumulate copper, probably due to defective copper efflux, we investigated the possible role of the MNK gene in the molecular basis of copper resistance.	Copper	94-100	ATPase copper transporting alpha	Homo sapiens	71-76
8589689-5	1995	The MNK protein, which has not been previously demonstrated experimentally in mammalian cells, was observed to have an apparent molecular weight of 178 kDa on SDS gels.	Sodium Dodecyl Sulfate	159-162	ATPase copper transporting alpha	Homo sapiens	4-7
33235918-3	2020	This adaptation renders tumor cells critically dependent on the copper transporter ATP7A, which reveals copper metabolism as a promising therapeutic target for KRAS-driven colorectal cancers.	Copper	64-70	ATPase copper transporting alpha	Homo sapiens	83-88
8091505-2	1994	Recently, however, two human diseases that disrupt copper transport, Menkes disease and Wilson disease, were found to be caused by mutations in two closely related genes, MNK and WND, which encode proteins belonging to the P-type ATPase family of cation transporters.	Copper	51-57	ATPase copper transporting alpha	Homo sapiens	171-174
8091505-3	1994	The MNK and WND proteins are unique in having at their amino termini six copies of a sequence that is remarkably similar to sequences previously found in bacterial heavy-metal-resistance proteins and in a P-type ATPase that appears to form part of a bacterial copper homeostatic system.	Metals	170-175	ATPase copper transporting alpha	Homo sapiens	4-7
8091505-3	1994	The MNK and WND proteins are unique in having at their amino termini six copies of a sequence that is remarkably similar to sequences previously found in bacterial heavy-metal-resistance proteins and in a P-type ATPase that appears to form part of a bacterial copper homeostatic system.	Copper	260-266	ATPase copper transporting alpha	Homo sapiens	4-7
34958799-10	2022	We found that Leishmania infection triggers upregulation of major mammalian copper exporter, ATP7A, in macrophages, and trafficking of ATP7A from the trans-Golgi network to endolysosomes in macrophages harboring amastigotes.	Copper	76-82	ATPase copper transporting alpha	Homo sapiens	93-98
28766096-5	2018	MEK inhibitor U0126 inhibits basal and chemodrug-induced phosphorylation of ERK as well as Mnk1 and eIF4E, suggesting that Mnk1/eIF4E are the downstream signaling of ERK pathway and chemotherapy agents activate ERK/MNK/eIF4E in a MEK-dependent manner.	U 0126	14-19	ATPase copper transporting alpha	Homo sapiens	215-218
34390123-0	2021	Elesclomol induces copper-dependent ferroptosis in colorectal cancer cells via degradation of ATP7A.	elesclomol	0-10	ATPase copper transporting alpha	Homo sapiens	94-99
34390123-4	2021	Elesclomol alone promotes the degradation of the copper transporter ATP7A, which retards the proliferation of colorectal cancer cells.	elesclomol	0-10	ATPase copper transporting alpha	Homo sapiens	68-73
34390123-6	2021	Combinational treatment of elesclomol and copper leads to copper retention within mitochondria due to ATP7A loss, leading to ROS accumulation, which in turn promotes the degradation of SLC7A11, thus further enhancing oxidative stress and consequent ferroptosis in CRC cells.	elesclomol	27-37	ATPase copper transporting alpha	Homo sapiens	102-107
34390123-6	2021	Combinational treatment of elesclomol and copper leads to copper retention within mitochondria due to ATP7A loss, leading to ROS accumulation, which in turn promotes the degradation of SLC7A11, thus further enhancing oxidative stress and consequent ferroptosis in CRC cells.	Copper	42-48	ATPase copper transporting alpha	Homo sapiens	102-107
34390123-6	2021	Combinational treatment of elesclomol and copper leads to copper retention within mitochondria due to ATP7A loss, leading to ROS accumulation, which in turn promotes the degradation of SLC7A11, thus further enhancing oxidative stress and consequent ferroptosis in CRC cells.	ros	125-128	ATPase copper transporting alpha	Homo sapiens	102-107
34390123-8	2021	In summary, our findings indicate that elesclomol-induced copper chelation inhibits colorectal cancer by targeting ATP7A and regulating ferroptosis.	elesclomol	39-49	ATPase copper transporting alpha	Homo sapiens	115-120
34390123-8	2021	In summary, our findings indicate that elesclomol-induced copper chelation inhibits colorectal cancer by targeting ATP7A and regulating ferroptosis.	Copper	58-64	ATPase copper transporting alpha	Homo sapiens	115-120
34734631-7	2021	The Cu transporters SLC31A1 (CTR1), SLC31A2 (CTR2), ATP7A and ATP7B regulate Cu content in cellular compartments and maintain Cu homeostasis.	Copper	77-79	ATPase copper transporting alpha	Homo sapiens	52-57
34533854-0	2021	FGF13 Enhances Resistance to Platinum Drugs by Regulating hCTR1 and ATP7A via a Microtubule-Stabilizing Effect.	Platinum	29-37	ATPase copper transporting alpha	Homo sapiens	68-73
34734631-7	2021	The Cu transporters SLC31A1 (CTR1), SLC31A2 (CTR2), ATP7A and ATP7B regulate Cu content in cellular compartments and maintain Cu homeostasis.	Copper	126-128	ATPase copper transporting alpha	Homo sapiens	52-57
34613798-2	2021	The Menkes ATPase ATP7A plays a key role in copper efflux, by trafficking from the Golgi to the plasma membrane upon cell exposure to elevated copper, but the mechanisms that target ATP7A to the cell periphery are poorly understood.	Copper	44-50	ATPase copper transporting alpha	Homo sapiens	18-23
34613798-2	2021	The Menkes ATPase ATP7A plays a key role in copper efflux, by trafficking from the Golgi to the plasma membrane upon cell exposure to elevated copper, but the mechanisms that target ATP7A to the cell periphery are poorly understood.	Copper	44-50	ATPase copper transporting alpha	Homo sapiens	182-187
34613798-2	2021	The Menkes ATPase ATP7A plays a key role in copper efflux, by trafficking from the Golgi to the plasma membrane upon cell exposure to elevated copper, but the mechanisms that target ATP7A to the cell periphery are poorly understood.	Copper	143-149	ATPase copper transporting alpha	Homo sapiens	18-23
34613798-2	2021	The Menkes ATPase ATP7A plays a key role in copper efflux, by trafficking from the Golgi to the plasma membrane upon cell exposure to elevated copper, but the mechanisms that target ATP7A to the cell periphery are poorly understood.	Copper	143-149	ATPase copper transporting alpha	Homo sapiens	182-187
34613798-7	2021	However, WW-PLEKHAs and PDZD11 are not necessary for ATP7A Golgi localization in basal copper, ATP7A copper-induced exit from the Golgi, and ATP7A retrograde trafficking to the Golgi.	Copper	101-107	ATPase copper transporting alpha	Homo sapiens	95-100
34613798-9	2021	These data indicate that WW-PLEKHAs-PDZD11 complexes regulate the localization and function of ATP7A to promote copper extrusion in elevated copper.	Copper	112-118	ATPase copper transporting alpha	Homo sapiens	95-100
34613798-9	2021	These data indicate that WW-PLEKHAs-PDZD11 complexes regulate the localization and function of ATP7A to promote copper extrusion in elevated copper.	Copper	141-147	ATPase copper transporting alpha	Homo sapiens	95-100
34461106-3	2021	While all the metal-binding domains are quite similar in structure, their spacing differs markedly between ATP7A and ATP7B.	Metals	14-19	ATPase copper transporting alpha	Homo sapiens	107-112
34185060-3	2021	Therefore, intracellular Cu levels are strictly regulated by proteins related to Cu-trafficking, including ATP7A.	Copper	25-27	ATPase copper transporting alpha	Homo sapiens	107-112
34461106-0	2021	At sixes and sevens: a cryptic domain in the metal binding chain of the human copper transporter ATP7A.	Metals	45-50	ATPase copper transporting alpha	Homo sapiens	97-102
34461106-1	2021	ATP7A and ATP7B are structurally similar but functionally distinct active copper transporters that regulate copper levels in the human cells and deliver copper to the biosynthetic pathways.	Copper	74-80	ATPase copper transporting alpha	Homo sapiens	0-5
34461106-1	2021	ATP7A and ATP7B are structurally similar but functionally distinct active copper transporters that regulate copper levels in the human cells and deliver copper to the biosynthetic pathways.	Copper	108-114	ATPase copper transporting alpha	Homo sapiens	0-5
34461106-1	2021	ATP7A and ATP7B are structurally similar but functionally distinct active copper transporters that regulate copper levels in the human cells and deliver copper to the biosynthetic pathways.	Copper	153-159	ATPase copper transporting alpha	Homo sapiens	0-5
34390520-5	2021	Malfunctions of the Cu+ -transporting ATPases ATP7A and ATP7B cause Menkes disease and Wilson disease, respectively.	Copper	20-22	ATPase copper transporting alpha	Homo sapiens	46-51
34568338-2	2021	WW-PLEKHAs contribute to the trafficking and retention of transmembrane proteins, including nectins, Tspan33, and the copper pump ATP7A, at cell-cell junctions and lateral membranes.	Copper	118-124	ATPase copper transporting alpha	Homo sapiens	130-135
34185060-3	2021	Therefore, intracellular Cu levels are strictly regulated by proteins related to Cu-trafficking, including ATP7A.	Copper	81-83	ATPase copper transporting alpha	Homo sapiens	107-112
34185060-8	2021	6-OHDA reduced the protein levels of the Cu exporter ATP7A and the Cu chaperone Atox1, but not CTR1, a Cu importer; however, it did not affect the expression of ATP7A and Atox1 mRNAs.	Oxidopamine	0-6	ATPase copper transporting alpha	Homo sapiens	53-58
34185060-9	2021	The decreased levels of ATP7A and Atox1 proteins were restored by the antioxidant N-acetylcysteine and the lysosomal inhibitor bafilomycin A1.	Acetylcysteine	82-98	ATPase copper transporting alpha	Homo sapiens	24-29
34185060-9	2021	The decreased levels of ATP7A and Atox1 proteins were restored by the antioxidant N-acetylcysteine and the lysosomal inhibitor bafilomycin A1.	bafilomycin A1	127-141	ATPase copper transporting alpha	Homo sapiens	24-29
35604085-2	2022	Here, we comprehensively summarize the potential origins of copper accumulation in diseases especially in cancers by dysregulating copper transporter 1 (CTR1) or ATPase copper transporting alpha/beta (ATP7A/B) and further demonstrate the underlying mechanism of copper contributing to tumorigenesis.	Copper	60-66	ATPase copper transporting alpha	Homo sapiens	162-199
34069220-1	2021	Menkes disease (MD) is a rare and often lethal X-linked recessive syndrome, characterized by generalized alterations in copper transport and metabolism, linked to mutations in the ATPase copper transporting alpha (ATP7A) gene.	Copper	120-126	ATPase copper transporting alpha	Homo sapiens	180-212
34069220-1	2021	Menkes disease (MD) is a rare and often lethal X-linked recessive syndrome, characterized by generalized alterations in copper transport and metabolism, linked to mutations in the ATPase copper transporting alpha (ATP7A) gene.	Copper	120-126	ATPase copper transporting alpha	Homo sapiens	214-219
34430447-1	2021	Menkes disease (MD) is a rare congenital copper deficiency disease caused by an adenosine triphosphatase copper transporting alpha (ATP7A) gene mutation.	Adenosine	80-89	ATPase copper transporting alpha	Homo sapiens	132-137
34430447-1	2021	Menkes disease (MD) is a rare congenital copper deficiency disease caused by an adenosine triphosphatase copper transporting alpha (ATP7A) gene mutation.	Copper	105-111	ATPase copper transporting alpha	Homo sapiens	132-137
34201235-5	2021	While many mechanisms have been proposed for Pt-drug transport, the high-affinity copper transporter (hCtr1), Cu chaperone (Atox1), and Cu exporters (ATP7A and ATP7B) are also involved in cDDP transport, highlighting Cu homeostasis regulation in Pt-based cancer therapy.	cddp	188-192	ATPase copper transporting alpha	Homo sapiens	150-155
34747666-0	2021	MiR-495 Inhibits Cisplatin Resistance and Angiogenesis in Esophageal Cancer by Targeting ATP7A.	Cisplatin	17-26	ATPase copper transporting alpha	Homo sapiens	89-94
34747666-2	2021	In this study, we investigated the possible regulation of 1 copper ion transporter (ATP7A; ATPase copper transporting alpha) by microRNA miR-495 and its implications in cisplatin resistance and angiogenesis in esophageal cancer.	Copper	60-66	ATPase copper transporting alpha	Homo sapiens	84-89
34747666-12	2021	ATP7A overexpression substantially abrogated the changes in proliferation, apoptosis, angiogenesis, and above-mentioned gene expression in cisplatin-resistant Eca-109 and TE1 cells.	Cisplatin	139-148	ATPase copper transporting alpha	Homo sapiens	0-5
34747666-13	2021	Conclusions: MiR-495 suppressed cisplatin resistance and angiogenesis in esophageal cancer cells by targeting ATP7A gene expression.	Cisplatin	32-41	ATPase copper transporting alpha	Homo sapiens	110-115
35604085-2	2022	Here, we comprehensively summarize the potential origins of copper accumulation in diseases especially in cancers by dysregulating copper transporter 1 (CTR1) or ATPase copper transporting alpha/beta (ATP7A/B) and further demonstrate the underlying mechanism of copper contributing to tumorigenesis.	Copper	60-66	ATPase copper transporting alpha	Homo sapiens	201-208
35604085-2	2022	Here, we comprehensively summarize the potential origins of copper accumulation in diseases especially in cancers by dysregulating copper transporter 1 (CTR1) or ATPase copper transporting alpha/beta (ATP7A/B) and further demonstrate the underlying mechanism of copper contributing to tumorigenesis.	Copper	262-268	ATPase copper transporting alpha	Homo sapiens	162-199
35604085-2	2022	Here, we comprehensively summarize the potential origins of copper accumulation in diseases especially in cancers by dysregulating copper transporter 1 (CTR1) or ATPase copper transporting alpha/beta (ATP7A/B) and further demonstrate the underlying mechanism of copper contributing to tumorigenesis.	Copper	262-268	ATPase copper transporting alpha	Homo sapiens	201-208
35417652-3	2022	Using rational design, we identified and validated the 4,6-diaryl-pyrazolo(3,4-b)pyridin-3-amine scaffold as the core for MNK inhibitors.	4,6-diaryl-pyrazolo(3,4-b)pyridin-3-amine	55-96	ATPase copper transporting alpha	Homo sapiens	122-125
35367340-8	2022	In addition, we found that low SLC7A11-AS1 expression activated the p38MAPK-JNK signaling pathway, and increased the expression of cisplatin export gene ATP7A and the GSH biosynthesis gene GCLM in GC.	Cisplatin	131-140	ATPase copper transporting alpha	Homo sapiens	153-158
35393273-0	2022	Copper-histidine therapy in an infant with novel splice-site variant in the ATP7A gene of Menkes disease: the first experience in South East Asia and literature review.	copper histidine	0-16	ATPase copper transporting alpha	Homo sapiens	76-81
35393273-10	2022	These findings suggest that the benefit of Cu-His in our case is limited which might be related to severe presentations and degree of ATP7A mutation.	copper histidine	43-49	ATPase copper transporting alpha	Homo sapiens	134-139
35265524-5	2022	While the lower expression of ATP7A by siRNA knockdown resulted in enhancement of OXA sensitivity and increased OXA-induced apoptosis.	2-phenyloxazolone	112-115	ATPase copper transporting alpha	Homo sapiens	30-35
35265524-3	2022	Here, we identified ATP7A as a potentially key gene of OXA resistance in CRC.	2-phenyloxazolone	55-58	ATPase copper transporting alpha	Homo sapiens	20-25
35265524-4	2022	The patients with higher expression of ATP7A tended to have platinum drug resistance.	Platinum	60-68	ATPase copper transporting alpha	Homo sapiens	39-44
35433682-3	2022	The essential requirement for copper in humans is illustrated by Menkes disease, a fatal neurodegenerative disorder of early childhood caused by mutations in the ATP7A copper transporter.	Copper	30-36	ATPase copper transporting alpha	Homo sapiens	162-167
35433682-3	2022	The essential requirement for copper in humans is illustrated by Menkes disease, a fatal neurodegenerative disorder of early childhood caused by mutations in the ATP7A copper transporter.	Copper	168-174	ATPase copper transporting alpha	Homo sapiens	162-167
35327466-5	2022	Our studies demonstrate the role of cellular copper transporters CTR1 and ATP7A in the survival dynamics of malignant cells post-EGCG exposure.	epigallocatechin gallate	129-133	ATPase copper transporting alpha	Homo sapiens	74-79
35245129-1	2022	ATP7A and ATP7B, two homologous copper-transporting P1B-type ATPases, play crucial roles in cellular copper homeostasis, and mutations cause Menkes and Wilson diseases, respectively.	Copper	32-38	ATPase copper transporting alpha	Homo sapiens	0-5
35245129-1	2022	ATP7A and ATP7B, two homologous copper-transporting P1B-type ATPases, play crucial roles in cellular copper homeostasis, and mutations cause Menkes and Wilson diseases, respectively.	Copper	101-107	ATPase copper transporting alpha	Homo sapiens	0-5
35245129-2	2022	ATP7A/B contains a P-type ATPase core consisting of a membrane transport domain and three cytoplasmic domains, the A, P, and N domains, and a unique amino terminus comprising six consecutive metal-binding domains.	Metals	191-196	ATPase copper transporting alpha	Homo sapiens	0-7
35265524-5	2022	While the lower expression of ATP7A by siRNA knockdown resulted in enhancement of OXA sensitivity and increased OXA-induced apoptosis.	2-phenyloxazolone	82-85	ATPase copper transporting alpha	Homo sapiens	30-35
35136028-0	2022	Exosome-mediated miR-7-5p delivery enhances the anticancer effect of Everolimus via blocking MNK/eIF4E axis in non-small cell lung cancer.	Everolimus	69-79	ATPase copper transporting alpha	Homo sapiens	93-96
35136028-2	2022	Activated mitogen-activated protein kinase interacting kinases/eukaryotic translation initiation factor 4E (MNK/eIF4E) axis plays a crucial role in resistance to Everolimus in non-small cell lung cancer (NSCLC).	Everolimus	162-172	ATPase copper transporting alpha	Homo sapiens	108-111
35136028-13	2022	The combination of miR-7-5p with Everolimus induced apoptosis to exhibit a synergistic anticancer therapeutic efficacy through dual abrogation of MNK/eIF4E and mTOR in NSCLC.	Everolimus	33-43	ATPase copper transporting alpha	Homo sapiens	146-149
35136028-15	2022	Either endogenous miR-7-5p or exo-miR-7-5p combined with Everolimus can enhance the anticancer efficacy by targeting MNK/eIF4E axis and mTOR.	exo-mir-7-5p	30-42	ATPase copper transporting alpha	Homo sapiens	117-120
35136028-15	2022	Either endogenous miR-7-5p or exo-miR-7-5p combined with Everolimus can enhance the anticancer efficacy by targeting MNK/eIF4E axis and mTOR.	Everolimus	57-67	ATPase copper transporting alpha	Homo sapiens	117-120