GO curators for mouse genes have assigned the following annotations to the gene product of Kcnj11. (This text reflects annotations as of Wednesday, January 23, 2013.) Summary from NCBI RefSeq
[Summary is not available for the mouse gene. This summary is for the human ortholog.] 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. [provided by RefSeq, Oct 2009]Summary text based on GO annotations supported by experimental evidence in mouse
Researchers have inferred from direct assay, that the gene product of Kcnj11
participates in the following biological processes:
The gene product of Kcnj11 has been shown to bind to the gene products of Ank2. [3] Researchers have inferred, based on physical interactions, that the gene product of Kcnj11
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Li J et al. (2010) Ankyrin-B regulates Kir6.2 membrane expression and function in heart. J Biol Chem, 285:28723-30. (PubMed:20610380)
Morrissey A et al. (2005) Expression of ATP-sensitive K+ channel subunits during perinatal maturation in the mouse heart. Pediatr Res, 58:185-92. (PubMed:16085792)