| Product name: |
KIR6.2 (phospho Thr224) rabbit pAb |
| Reactivity: |
Human;Mouse;Rat |
| Alternative Names: |
KCNJ11; ATP-sensitive inward rectifier potassium channel 11; IKATP; Inward rectifier K(+) channel Kir6.2; Potassium channel; inwardly rectifying subfamily J member 11 |
| Source: |
Rabbit |
| Dilutions: |
Western Blot: 1/500 – 1/2000. Immunohistochemistry: 1/100 – 1/300. Immunofluorescence: 1/200 – 1/1000. ELISA: 1/5000. Not yet tested in other applications. |
| Immunogen: |
The antiserum was produced against synthesized peptide derived from human Kir6.2 around the phosphorylation site of Thr224. AA range:190-239 |
| Storage: |
-20C/1 year |
| Clonality: |
Polyclonal |
| Isotype: |
IgG |
| Concentration: |
1 mg/ml |
| Observed Band: |
40kD |
| GeneID: |
3767 |
| Human Swiss-Prot No: |
Q14654 |
| Cellular localization: |
Membrane; Multi-pass membrane protein. |
| Background: |
Potassium channels are present in most mammalian cells, where they participate in a wide range of physiologic responses. The protein encoded by this gene is an integral membrane protein and inward-rectifier type potassium channel. The encoded protein, which has a greater tendency to allow potassium to flow into a cell rather than out of a cell, is controlled by G-proteins and is found associated with the sulfonylurea receptor SUR. Mutations in this gene are a cause of familial persistent hyperinsulinemic hypoglycemia of infancy (PHHI), an autosomal recessive disorder characterized by unregulated insulin secretion. Defects in this gene may also contribute to autosomal dominant non-insulin-dependent diabetes mellitus type II (NIDDM), transient neonatal diabetes mellitus type 3 (TNDM3), and permanent neonatal diabetes mellitus (PNDM). Multiple alternatively spliced trans |
