RGD Reference Report - ABCC8 and ABCC9: ABC transporters that regulate K+ channels. - Rat Genome Database

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ABCC8 and ABCC9: ABC transporters that regulate K+ channels.

Authors: Bryan, J  Munoz, A  Zhang, X  Dufer, M  Drews, G  Krippeit-Drews, P  Aguilar-Bryan, L 
Citation: Bryan J, etal., Pflugers Arch. 2007 Feb;453(5):703-18. Epub 2006 Aug 8.
RGD ID: 5129880
Pubmed: PMID:16897043   (View Abstract at PubMed)
DOI: DOI:10.1007/s00424-006-0116-z   (Journal Full-text)

The sulfonylurea receptors (SURs) ABCC8/SUR1 and ABCC9/SUR2 are members of the C-branch of the transport adenosine triphosphatase superfamily. Unlike their brethren, the SURs have no identified transport function; instead, evolution has matched these molecules with K(+) selective pores, either K(IR)6.1/KCNJ8 or K(IR)6.2/KCNJ11, to assemble adenosine triphosphate (ATP)-sensitive K(+) channels found in endocrine cells, neurons, and both smooth and striated muscle. Adenine nucleotides, the major regulators of ATP-sensitive K(+) (K(ATP)) channel activity, exert a dual action. Nucleotide binding to the pore reduces the activity or channel open probability, whereas Mg-nucleotide binding and/or hydrolysis in the nucleotide-binding domains of SUR antagonize this inhibitory action to stimulate channel openings. Mutations in either subunit can alter this balance and, in the case of the SUR1/KIR6.2 channels found in neurons and insulin-secreting pancreatic beta cells, are the cause of monogenic forms of hyperinsulinemic hypoglycemia and neonatal diabetes. Additionally, the subtle dysregulation of K(ATP) channel activity by a K(IR)6.2 polymorphism has been suggested as a predisposing factor in type 2 diabetes mellitus. Studies on K(ATP) channel null mice are clarifying the roles of these metabolically sensitive channels in a variety of tissues.


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