KCNJ18 Antibody (N-term)
Affinity Purified Rabbit Polyclonal Antibody (Pab)
- SPECIFICATION
- CITATIONS
- PROTOCOLS
- BACKGROUND
Application
| WB, E |
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Primary Accession | B7U540 |
Other Accession | NP_001181887.1 |
Reactivity | Human |
Host | Rabbit |
Clonality | Polyclonal |
Isotype | Rabbit IgG |
Calculated MW | 48880 Da |
Antigen Region | 94-122 aa |
Gene ID | 100134444 |
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Other Names | Inward rectifier potassium channel 18, Inward rectifier K(+) channel Kir26, Potassium channel, inwardly rectifying subfamily J member 18, KCNJ18 |
Target/Specificity | This KCNJ18 antibody is generated from rabbits immunized with a KLH conjugated synthetic peptide between 94-122 amino acids from the N-terminal region of human KCNJ18. |
Dilution | WB~~1:1000 |
Format | Purified polyclonal antibody supplied in PBS with 0.09% (W/V) sodium azide. This antibody is purified through a protein A column, followed by peptide affinity purification. |
Storage | Maintain refrigerated at 2-8°C for up to 2 weeks. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles. |
Precautions | KCNJ18 Antibody (N-term) is for research use only and not for use in diagnostic or therapeutic procedures. |
Name | KCNJ18 |
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Function | Inward rectifier potassium channels are characterized by a greater tendency to allow potassium to flow into the cell rather than out of it. Their voltage dependence is regulated by the concentration of extracellular potassium; as external potassium is raised, the voltage range of the channel opening shifts to more positive voltages. The inward rectification is mainly due to the blockage of outward current by internal magnesium. |
Cellular Location | Cell membrane; Multi-pass membrane protein |
Tissue Location | Specifically expressed in skeletal muscle. |
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Provided below are standard protocols that you may find useful for product applications.
Background
Inwardly rectifying potassium channels, such as KCNJ18, maintain resting membrane potential in excitable cells and aid in repolarization of cells following depolarization. KCNJ18 is primarily expressed in skeletal muscle and is transcriptionally regulated by thyroid hormone (Ryan et al., 2010 [PubMed 20074522]).
References
Ryan, D.P., et al. Cell 140(1):88-98(2010)
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