A synthetic peptide from the cytoplasmic domain of human KCNJ1 (ROMK1, Kir1.1) conjugated to blue carrier protein was used as the antigen. The peptide is shares 92% identity with rat and mouse sequences.
KCNJ1
Reactivity: Human, Rat, Mouse
WB, IHC, IF, ICC, IP
Host: Rabbit
Polyclonal
unconjugated
Application Notes
IHC, WB. A concentration of 10-50 μg,ml is recommended. The optimal concentration should be determined by the end user. Not yet tested in other applications.
Restrictions
For Research Use only
Format
Lyophilized
Reconstitution
Reconstitute in 500 µL of sterile water. Centrifuge to remove any insoluble material.
Handling Advice
Avoid freeze and thaw cycles.
Storage
4 °C/-20 °C
Storage Comment
Maintain the lyophilised/reconstituted antibodies frozen at -20°C for long term storage and refrigerated at 2-8°C for a shorter term. When reconstituting, glycerol (1:1) may be added for an additional stability. Avoid freeze and thaw cycles.
Expiry Date
12 months
Target
KCNJ1
(Potassium Inwardly-Rectifying Channel, Subfamily J, Member 1 (KCNJ1))
FUNCTION: In the kidney, probably plays a major role in potassium homeostasis. 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. This channel is activated by internal ATP and can be blocked by external barium. Tissue specificity: In the kidney and pancreatic islets. Lower levels in skeletal muscle, pancreas, spleen, brain, heart and liver. Subcellular location: Membrane, Multi-pass membrane protein. Involvement in disease: Defects in KCNJ1 are the cause of Bartter syndrome type 2 (BS2) also termed hyperprostanglandin E syndrome 2. BS refers to a group of autosomal recessive disorders characterized by impaired salt reabsorption in the thick ascending loop of Henle with pronounced salt wasting, hypokalemic metabolic alkalosis, and varying degrees of hypercalciuria. BS2 is a life-threatening condition beginning in utero, with marked fetal polyuria that leads to polyhydramnios and premature delivery. Another hallmark of BS2 is a marked hypercalciuria and, as a secondary consequence, the development of nephrocalcinosis and osteopenia.,Inward Rectifier,ATP-sensitive inward rectifier potassium channel 1, Potassium channel, inwardly rectifying subfamily J member 1, ATP-regulated potassium channel ROM-K, Kir1.1, ROMK1