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KCNJ10 Antibody (Center) Blocking Peptide
Synthetic peptide
- SPECIFICATION
- CITATIONS
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- BACKGROUND
| Primary Accession | P78508 |
|---|---|
| Clone Names | 100623188 |
| Gene ID | 3766 |
|---|---|
| Other Names | ATP-sensitive inward rectifier potassium channel 10, ATP-dependent inwardly rectifying potassium channel Kir41, Inward rectifier K(+) channel Kir12, Potassium channel, inwardly rectifying subfamily J member 10, KCNJ10 |
| Format | Peptides are lyophilized in a solid powder format. Peptides can be reconstituted in solution using the appropriate buffer as needed. |
| Storage | Maintain refrigerated at 2-8°C for up to 6 months. For long term storage store at -20°C. |
| Precautions | This product is for research use only. Not for use in diagnostic or therapeutic procedures. |
| Name | KCNJ10 |
|---|---|
| Function | May be responsible for potassium buffering action of glial cells in the brain. 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. Can be blocked by extracellular barium and cesium (By similarity). In the kidney, together with KCNJ16, mediates basolateral K(+) recycling in distal tubules; this process is critical for Na(+) reabsorption at the tubules. |
| Cellular Location | Membrane; Multi- pass membrane protein. Basolateral cell membrane. Note=In kidney distal convoluted tubules, located in the basolateral membrane where it colocalizes with KCNJ16. |
| Tissue Location | Expressed in kidney (at protein level). |
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Provided below are standard protocols that you may find useful for product applications.
Background
This gene encodes a member of the inward rectifier-typepotassium channel family, characterized by having a greatertendency to allow potassium to flow into, rather than out of, acell. The encoded protein may form a heterodimer with anotherpotassium channel protein and may be responsible for the potassiumbuffering action of glial cells in the brain. Mutations in thisgene have been associated with seizure susceptibility of commonidiopathic generalized epilepsy syndromes.
References
Jonard, L., et al. Int. J. Pediatr. Otorhinolaryngol. 74(9):1049-1053(2010)Reichold, M., et al. Proc. Natl. Acad. Sci. U.S.A. 107(32):14490-14495(2010)Heuser, K., et al. Epilepsy Res. 88(1):55-64(2010)Pawelczyk, M., et al. Ann. Hum. Genet. 73 (PT 4), 411-421 (2009) :Yang, T., et al. Am. J. Hum. Genet. 84(5):651-657(2009)
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