Recombinant Human ATP7B Protein (Thr59-Val426), His tagged

• Cat.No.: ATP7B-1054H
• Product Overview: Recombinant human ATP7B (Thr59-Val426) fused with His tag was expressed in E. coli.

Specification

• Description: 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.
• Source: E. coli
• Species: Human
• Tag: His
• Form: Lyophilized powder/frozen liquid
• Molecular Mass: 38.25 kDa
• Protein Length: Thr59-Val426
• Purity: >90% as determined by SDS-PAGE.
• Notes: For research use only.
• Storage: Use a manual defrost freezer and avoid repeated freeze thaw cycles.
  Store at 2 to 8 centigrade for one week.
  Store at -20 to -80 centigrade for twelve months from the date of receipt.
• Storage Buffer: Supplied as solution form in PBS pH 7.5 or lyophilized from PBS pH 7.5.
• Reconstitution: Reconstitute in sterile water for a stock solution.
• Shipping: They are shipped out with dry ice/blue ice unless customers require otherwise.

Gene Information

• Gene Name: ATP7B ATPase, Cu++ transporting, beta polypeptide [ Homo sapiens (human) ]
• Official Symbol: ATP7B
• Synonyms: ATP7B; ATPase, Cu++ transporting, beta polypeptide; ATPase, Cu++ transporting, beta polypeptide (Wilson disease), WND; copper-transporting ATPase 2; Wilson disease; copper pump 2; Wilson disease-associated protein; ATPase, Cu (2+)- transporting, beta polypeptide; WD; PWD; WC1; WND
• Gene ID: 540
• mRNA Refseq: NM_000053
• Protein Refseq: NP_000044
• MIM: 606882
• UniProt ID: P35670

Reviews

01/15/2021

Impressed with the product quality.

05/09/2020

The product exceeded expectations.

09/28/2018

This product consistently delivers accurate results in our experiments.

Q&As

How does the ATP7B protein contribute to copper transport within cells, and what cellular compartments are involved in this process?

ATP7B facilitates copper transport from the cytoplasm to the Golgi apparatus, where copper is incorporated into proteins. It also mediates copper export from cells when copper levels are elevated, preventing toxicity.

How does ATP7B interact with other proteins involved in copper metabolism, and what are the implications of disruptions in these interactions?

ATP7B interacts with various proteins in the copper transport pathway. Disruptions in these interactions can lead to mislocalization of ATP7B and compromise its ability to regulate copper levels properly.

How does ATP7B-mediated copper transport impact the activity of copper-dependent enzymes, and what are the broader implications for cellular function?

ATP7B ensures the proper supply of copper to enzymes involved in various cellular processes, including energy production and antioxidant defense. Dysregulation can disrupt these processes, affecting cell function.

What is the role of ATP7B in copper excretion at the systemic level, and how does this relate to copper metabolism in the body?

ATP7B is crucial for copper excretion into bile, a process that contributes to systemic copper balance. Dysfunctional ATP7B results in impaired copper excretion, leading to the accumulation of copper in tissues.

Can you explain the consequences of mutations in the ATP7B gene, particularly in relation to Wilson's disease?

Mutations in the ATP7B gene lead to impaired copper transport, causing copper accumulation in tissues. This is associated with Wilson's disease, a disorder characterized by copper toxicity, especially in the liver and brain.