ATP7B
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Official Full Name
ATPase, Cu++ transporting, beta polypeptide
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Overview
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 isoforms with distinct cellular localizations, have been characterized. Mutations in this gene have been associated with Wilson disease (WD). -
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 poly;
- Recombinant Proteins
- Cell & Tissue Lysates
- Protein Pre-coupled Magnetic Beads
- Human
- Mouse
- E.coli
- HEK293
- HEK293T
- Mammalian Cell
- Mammalian cells
- Wheat Germ
- Flag
- GST
- His
- His (Fc)
- Avi
- Myc
- DDK
- MYC
- N/A
- N
- Involved Pathway
- Protein Function
- Interacting Protein
- ATP7B Related Articles
ATP7B involved in several pathways and played different roles in them. We selected most pathways ATP7B participated on our site, such as Ion channel transport, Ion transport by P-type ATPases, Transmembrane transport of small molecules, which may be useful for your reference. Also, other proteins which involved in the same pathway with ATP7B were listed below. Creative BioMart supplied nearly all the proteins listed, you can search them on our site.
| Pathway Name | Pathway Related Protein |
|---|---|
| Ion channel transport | TRPA1A;TRPM1A;FXYD7;BEST4;ANO10;TRPM6;ANO8;TRPC4APB;CLCA1 |
| Ion transport by P-type ATPases | CCC2;ATP2B1B;ATP2C1;ATP8B1;ATP13A;ATP13A5;ATP2B3A;ATP1A1A.5;FXYD3 |
| Transmembrane transport of small molecules | ANO4;SLC9A8;SLC5A2;SLC22A12;SLC29A2;SLC13A5;SLC13A1;TRPC4B;MFSD7B |
ATP7B has several biochemical functions, for example, ATP binding, copper ion binding, copper-exporting ATPase activity. Some of the functions are cooperated with other proteins, some of the functions could acted by ATP7B itself. We selected most functions ATP7B had, and list some proteins which have the same functions with ATP7B. You can find most of the proteins on our site.
| Function | Related Protein |
|---|---|
| ATP binding | POMK;MVDA;MCM3L;ATP1A1A.4;CASKA;TWF2;DAPK2;GRK1A;NSFA |
| copper ion binding | IL1A;HIST2H3A;ADNP;GPC1;S100U;COMMD1;POLR1B;PRNP;SOD1 |
| copper-exporting ATPase activity | ATP7A;ATP7B |
| protein binding | EFNB2;WHRN;IFRD2;ID2;SERPINF1;CORO1B;HDLBP;SAP30;ZNF514 |
ATP7B has direct interactions with proteins and molecules. Those interactions were detected by several methods such as yeast two hybrid, co-IP, pull-down and so on. We selected proteins and molecules interacted with ATP7B here. Most of them are supplied by our site. Hope this information will be useful for your research of ATP7B.
- Q&As
- Reviews
Q&As (5)
Ask a questionATP7B 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.
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.
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.
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.
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.
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