Recombinant Mouse Atp7b Protein, His-tagged

• Cat.No.: Atp7b-275M
• Product Overview: Recombinant Mouse Atp7b Protein (Gln1369-Ile1462) with N-His tag was expressed in E. coli.

Specification

• Description: Enables P-type divalent copper transporter activity. Acts upstream of or within several processes, including cellular transition metal ion homeostasis; lactation; and protein maturation by copper ion transfer. Located in membrane and trans-Golgi network. Is expressed in several structures, including alimentary system; central nervous system; genitourinary system; respiratory system; and sensory organ. Used to study Wilson disease. Human ortholog(s) of this gene implicated in Wilson disease. Orthologous to human ATP7B (ATPase copper transporting beta).
• Source: E. coli
• Species: Mouse
• Tag: N-His
• Form: Freeze-dried powder
• Molecular Mass: Predicted Molecular Mass: 14.3 kDa
  Accurate Molecular Mass: 14 kDa
• Protein length: Gln1369-Ile1462
• Purity: > 97%
• Applications: Positive Control; Immunogen; SDS-PAGE; WB.
• Stability: The thermal stability is described by the loss rate. The loss rate was determined by accelerated thermal degradation test, that is, incubate the protein at 37 centigrade for 48h, and no obvious degradation and precipitation were observed. The loss rate is less than 5% within the expiration date under appropriate storage condition.
• Storage: Avoid repeated freeze/thaw cycles. Store at 2-8 centigrade for one month. Aliquot and store at -80 centigrade for 12 months.
• Storage Buffer: 20mM Tris, 150mM NaCl, pH8.0, containing 1mM EDTA, 1mM DTT, 0.01% SKL, 5% Trehalose and Proclin300.
• Reconstitution: Reconstitute in sterile water to a concentration of 0.1-1.0 mg/mL. Do not vortex.

Gene Information

• Gene Name: Atp7b ATPase, Cu++ transporting, beta polypeptide [ Mus musculus (house mouse) ]
• Official Symbol: Atp7b
• Synonyms: ATP7B; ATPase, Cu++ transporting, beta polypeptide; copper-transporting ATPase 2; toxic milk; copper pump 2; Wilson protein; wilson disease-associated protein homolog; tx; WND; Atp7a
• Gene ID: 11979
• mRNA Refseq: NM_007511
• Protein Refseq: NP_031537
• UniProt ID: Q64446

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.