Rabbit anti-Human KCNJ11 Polyclonal Antibody

Uniprot Id

Q14654

Target Species

Human

Target Name

KCNJ11

Target Full Name

ATP-sensitive inward rectifier potassium channel 11

Target Function

This receptor is controlled by G proteins. 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. Subunit of ATP-sensitive potassium channels (KATP). Can form cardiac and smooth muscle-type KATP channels with ABCC9. KCNJ11 forms the channel pore while ABCC9 is required for activation and regulation.

Target Involvement

Familial hyperinsulinemic hypoglycemia 2 (HHF2); Diabetes mellitus, permanent neonatal (PNDM); Transient neonatal diabetes mellitus 3 (TNDM3); Maturity-onset diabetes of the young 13 (MODY13)

Target Subcellular Location

Membrane; Multi-pass membrane protein.

Target Protein Families

Inward rectifier-type potassium channel (TC 1.A.2.1) family, KCNJ11 subfamily

Target Synonyms

KCNJ11; ATP-sensitive inward rectifier potassium channel 11; IKATP; Inward rectifier K(+ channel Kir6.2; Potassium channel, inwardly rectifying subfamily J member 11

Target 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 transcript variants that encode different protein isoforms have been described for this gene.