KCNJ1 Antibody - Azide and BSA Free Summary
Immunogen |
A synthetic peptide from the cytoplasmic domain of human KCNJ1 conjugated to blue carrier protein was used as the antigen. |
Predicted Species |
Mouse (92%), Rat (92%). Backed by our 100% Guarantee. |
Isotype |
IgG |
Clonality |
Polyclonal |
Host |
Rabbit |
Gene |
KCNJ1 |
Purity |
Ammonium sulfate precipitation |
Innovator's Reward |
Test in a species/application not listed above to receive a full credit towards a future purchase. |
Applications/Dilutions
Dilutions |
- Immunohistochemistry 10-50 ug/ml
- Immunohistochemistry-Frozen 10-50 ug/ml
- Immunohistochemistry-Paraffin 10-50 ug/ml
- Western Blot 10-50 ug/ml
|
Packaging, Storage & Formulations
Storage |
Store at 4C short term. Aliquot and store at -20C long term. Avoid freeze-thaw cycles. |
Buffer |
Sterilized water |
Preservative |
No Preservative |
Concentration |
LYOPH |
Purity |
Ammonium sulfate precipitation |
Reconstitution Instructions |
Reconstitute 0.5 mg size in 0.5 ml of sterile water. Centrifuge to remove any insoluble material. Glycerol may be added (1:1) for additional stability. Please note the 0.1 mg size is provided in reconstituted format. |
Alternate Names for KCNJ1 Antibody - Azide and BSA Free
Background
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.
Limitations
This product is for research use only and is not approved for use in humans or in clinical diagnosis. Primary Antibodies are
guaranteed for 1 year from date of receipt.
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