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Kir4.1 Polyclonal Antibody
- SPECIFICATION
- CITATIONS
- PROTOCOLS
- BACKGROUND
Application 
| IHC-P |
|---|---|
| Primary Accession | P78508 |
| Reactivity | Human, Rat, Mouse |
| Host | Rabbit |
| Clonality | Polyclonal |
| Calculated MW | 42508 Da |
| Gene ID | 3766 |
|---|---|
| Other Names | ATP-sensitive inward rectifier potassium channel 10 (ATP-dependent inwardly rectifying potassium channel Kir4.1) (Inward rectifier K(+) channel Kir1.2) (Potassium channel, inwardly rectifying subfamily J member 10) |
| Dilution | IHC~~IHC 1:100-200 |
| Format | Liquid in PBS containing 50% glycerol, 0.5% BSA and 0.09% (W/V) sodium azide. |
| Storage Conditions | -20℃ |
| 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
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.
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