KIR6.2 rabbit pAb
ENT-A3031
Description
| REF | ENT-A3031 |
|---|---|
| Category | Antibody Polyclonal |
| Description | KIR6.2 rabbit pAb |
| Source | Rabbit |
| Applications | WB;IHC;IF;ELISA |
| Reactivity | Human;Mouse;Rat |
| Reactivity | Human;Mouse;Rat |
| Dilution | Western Blot: 1/500 – 1/2000. Immunohistochemistry: 1/100 – 1/300. Immunofluorescence: 1/200 – 1/1000. ELISA: 1/10000. Not yet tested in other applications. |
| Immunogen | The antiserum was produced against synthesized peptide derived from human Kir6.2. AA range:190-239 |
| Storage Stability | -20°C/1 year |
| Clonality | Polyclonal |
| Isotype | IgG |
| Concentration | 1 mg/ml |
| Observed Band KD | 40kD |
| Human Gene ID | 3767 |
| Human Swiss Prot Nº | Q14654 |
| Subcellular Location | Membrane; Multi-pass membrane protein. |
Other Name: KCNJ11; ATP-sensitive inward rectifier potassium channel 11; IKATP; Inward rectifier K(+) channel Kir6.2; Potassium channel; inwardly rectifying subfamily J member 11
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