Mouse Anti-ATP7B Recombinant Antibody (CBYY-1597) (CBMAB-1668-YY)

Name: Mouse Anti-ATP7B Recombinant Antibody (CBYY-1597)
SKU: CBMAB-1668-YY
Rating: 5 (1 reviews)

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Datasheet

SDS

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Datasheet Target References Q & As Review & reward Protocols Associated Products

Basic Information

Host Animal

Mouse

Clone

CBYY-1597

Application

WB, ELISA

Immunogen

ATP7B (NP_000044, 1372 a.a. ~ 1465 a.a) partial recombinant protein with GST tag.

Specificity

Human

Antibody Isotype

IgG1, κ

Clonality

Monoclonal

Application Notes

The COA includes recommended starting dilutions, optimal dilutions should be determined by the end user.

Formulations & Storage [For reference only, actual COA shall prevail!]

Format

Liquid

Buffer

PBS, pH 7.4

Preservative

None

Concentration

Batch dependent

Storage

Store at +4°C short term (1-2 weeks). Aliquot and store at -20°C long term. Avoid repeated freeze/thaw cycles.

More Infomation

Target

Full Name

ATPase Copper Transporting Beta

Introduction

This gene is a member of the P-type cation transport ATPase family and encodes a protein with several membrane-spanning domains, an ATPase consensus sequence, a hinge domain, a phosphorylation site, and at least 2 putative copper-binding sites. This protein functions as a monomer, exporting copper out of the cells, such as the efflux of hepatic copper into the bile. Alternate transcriptional splice variants, encoding different isoforMouse with distinct cellular localizations, have been characterized. Mutations in this gene have been associated with Wilson disease (WD).

Entrez Gene ID

Cattle
Goat	102183524
Sheep	443046

UniProt ID

Cattle	F1MKI1
Goat	A0A452FX39
Sheep	Q9XT50

Alternative Names

ATPase Copper Transporting Beta; Copper Pump 2; ATPase, Cu++ Transporting, Beta Polypeptide; Wilson Disease-Associated Protein; Copper-Transporting ATPase 2; WND; PWD; WC1;

Function

Copper ion transmembrane transporter involved in the export of copper out of the cells. It is involved in copper homeostasis in the liver, where it ensures the efflux of copper from hepatocytes into the bile in response to copper overload.

Biological Process

Cellular copper ion homeostasis Source: GO_Central
Copper ion export Source: GO_Central
Copper ion import Source: UniProtKB
Copper ion transport Source: UniProtKB
Ion transmembrane transport Source: Reactome
Response to copper ion Source: UniProtKB
Sequestering of calcium ion Source: UniProtKB
Xenobiotic detoxification by transmembrane export across the plasma membrane Source: GO_Central

Cellular Location

Late endosome; Trans-Golgi network membrane. Predominantly found in the trans-Golgi network (TGN). Localized in the trans-Golgi network under low copper conditions, redistributes to cytoplasmic vesicles when cells are exposed to elevated copper levels, and then recycles back to the trans-Golgi network when copper is removed (PubMed:10942420).
Isoform 1: Golgi apparatus membrane
Isoform 2: Cytoplasm
WND/140 kDa: Mitochondrion

Involvement in disease

Wilson disease (WD): An autosomal recessive disorder of copper metabolism in which copper cannot be incorporated into ceruloplasmin in liver, and cannot be excreted from the liver into the bile. Copper accumulates in the liver and subsequently in the brain and kidney. The disease is characterized by neurologic manifestations and signs of cirrhosis.

Topology

Cytoplasmic: 1-653 aa
Helical: 654-675 aa
Extracellular: 676-697 aa
Helical: 698-717 aa
Cytoplasmic: 718-724 aa
Helical: 725-745 aa
Extracellular: 746-764 aa
Helical: 765-785 aa
Cytoplasmic: 786-919 aa
Helical: 920-942 aa
Extracellular: 943-972 aa
Helical: 973-994 aa
Cytoplasmic: 995-1322 aa
Helical: 1323-1340 aa
Extracellular: 1341-1351 aa
Helical: 1352-1371 aa
Cytoplasmic: 1372-1465 aa

PTM

Isoform 1 may be proteolytically cleaved at the N-terminus to produce the WND/140 kDa form.

Mamoor, S. (2021). ATP7B is a differentially expressed gene in brain metastatic human breast cancer.

Li, J., Lu, Q., Yu, J., Ji, M., & Lu, L. (2021). Osteoarticular manifestations as initial symptoms of WD with novel compound heterozygote mutations in the ATP7B gene: a case report. Translational Pediatrics, 10(4), 1026.

Wang, J., Tang, L., Xu, A., Zhang, S., Jiang, H., Pei, P., ... & Yang, W. (2021). Identification of mutations in the ATP7B gene in 14 Wilson disease children: Case series. Medicine, 100(16).

Abdelmoula, N. (2021). Toxic accumulation of copper and neuropsychiatric symptoms due to a familial tunisian compound heterozygous ATP7B missense mutation. European Psychiatry, 64(S1), S717-S718.

Ryumon, S., Okui, T., Kunisada, Y., Kishimoto, K., Shimo, T., Hasegawa, K., ... & Sasaki, A. (2019). Ammonium tetrathiomolybdate enhances the antitumor effect of cisplatin via the suppression of ATPase copper transporting beta in head and neck squamous cell carcinoma. Oncology reports, 42(6), 2611-2621.

Wang, X., Guo, L., Zhang, S., Chen, Y., Chen, Y. T., Zheng, B., ... & Lu, W. (2019). Copper sulfide facilitates hepatobiliary clearance of gold nanoparticles through the copper-transporting ATPase ATP7B. ACS nano, 13(5), 5720-5730.

Xiao, H., Deng, S., Deng, X., Gu, S., Yang, Z., Yin, H., & Deng, H. (2019). Mutation analysis of the ATP7B gene in seven Chinese families with Wilson’s disease. Digestion, 99(4), 319-326.

Schmidt, K., Ralle, M., Schaffer, T., Jayakanthan, S., Bari, B., Muchenditsi, A., & Lutsenko, S. (2018). ATP7A and ATP7B copper transporters have distinct functions in the regulation of neuronal dopamine-β-hydroxylase. Journal of Biological Chemistry, 293(52), 20085-20098.

Moinuddin, F. M., Hirano, H., Shinsato, Y., Higa, N., Arita, K., & Furukawa, T. (2017). ATP7B expression in human glioblastoma is related to temozolomide resistance. Oncology letters, 14(6), 7777-7782.

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Please try the standard protocols which include: protocols, troubleshooting and guide.

Enzyme-linked Immunosorbent Assay (ELISA)
Flow Cytometry
Immunofluorescence (IF)
Immunohistochemistry (IHC)
Immunoprecipitation (IP)
Western Blot (WB)
Enzyme-Linked Immunospot (ELISpot)
Proteogenomics
Other Protocols

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Isotype control

For research use only. Not intended for any clinical use.

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