It is an integral membrane protein. The 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) to constitute the ATP-sensitive K + channel.

Kir6.2, a pore-forming subunit of the ATP-sensitive potassium (KATP) channels, regulates the functions of metabolically active tissues and acts as an ideal therapeutic target for multiple diseases.

Here we show that the Kir6.2 pore-forming subunit is significantly overexpressed in the astrocytes of human BC specimens, and we speculate about Kir6.2's potential role in the pathophysiology of BCs and its exploitation as a potential pharmacological target in TBI.

Kir6.2 is a subtype of inwardly rectifying potassium channels that contribute to regulating the resting membrane potential and controlling excitability in various cells. It forms part of KATP channels, which link cellular metabolic status to electrical activity and are found in the brain, heart, muscles, and pancreatic cells.

Sep 1, 2005 · The discovery that Kir6.2 mutations cause neonatal diabetes has resulted in a major change in treatment, with most patients being able to improve their glycemic control when insulin injections are replaced with high-dose sulfonylurea tablets.

Apr 29, 2004 · We identified six novel, heterozygous mutations in the gene encoding Kir6.2 in 10 of the 29 probands who had permanent neonatal diabetes.

The Kir6.2/SUR1 isoform is the predominant isoform expressed by insulin-secreting β-cells of pancreatic islets, and by neurons in brain, and has essential roles in hormone secretion and learning and memory. A second pair of K ATP genes, located on human chromosome 12 (and mouse Chr 6), includes ABCC9 encoding SUR2 and KCNJ8 encoding Kir6.1.

Dec 12, 2004 · Heterozygous mutations in the human Kir6.2 gene ( KCNJ11 ), the pore-forming subunit of the ATP-sensitive (K ATP) channel, cause permanent neonatal diabetes mellitus (PNDM). For some mutations, PNDM is accompanied by marked developmental delay, muscle weakness, and epilepsy (severe disease).

Gain-of-function mutations in Kir6.2 cause permanent neonatal diabetes mellitus (PNDM) by reducing the ATP sensitivity of the K (ATP) channel and increasing the K (ATP) current, which is predicted to inhibit beta-cell electrical activity and insulin secretion.

Mar 20, 2024 · ATP-sensitive potassium (K ATP) channels, composed of four pore-lining Kir6.2 subunits and four regulatory sulfonylurea receptor 1 (SUR1) subunits, control insulin secretion in pancreatic...

Kir6.2 is a protein encoded by the KCNJ11 gene (potassium inwardly rectifying channel, subfamily J, member 11 [Homo sapiens (human)]; NCBI Reference Sequence: NG_012446.1; OMIM: 600937).

Mar 29, 2013 · Knockout of Kir6.2 results in a loss of glucose-dependent insulin secretion, modeling features of hyperinsulinism in humans. 135 Knockout of SUR1 reiterates essentially the same phenotype as Kir6.2 −/−, and again the major effects are in the pancreas.

Oct 15, 2021 · Kir6.2, a pore-forming subunit of the ATP-sensitive potassium (KATP) channels, regulates the functions of metabolically active tissues and acts as an ideal therapeutic target for multiple diseases.

Dec 25, 2023 · We recently demonstrated that neuronal KATP channels are composed of Kir6.2 subunits, are highly expressed on excitatory and inhibitory neurons, and are differentially expressed in the Alzheimer’s brain (Grizzanti et al. 2022).

Aug 10, 2006 · We show that genetic mutations, Y330C and F333I, which cause permanent neonatal diabetes mellitus, disrupt this motif and abrogate endocytosis of reconstituted mutant channels. The resultant increase in the surface density of K ATP channels would predispose β‐cells to hyperpolarise and may account for reduced insulin secretion in these patients.

Oct 25, 2016 · Altogether, our studies show that memantine modulates Kir6.2 activity, and that the Kir6.2 channel is a novel target for therapeutics to improve memory impairment in Alzheimer disease patients.

We demonstrate that cardiac sarcolemmal K ATP channels directly associate with ankyrin-B in heart via the K ATP channel α-subunit Kir6.2. We demonstrate that primary myocytes lacking ankyrin-B display defects in Kir6.2 protein expression, membrane expression, and function.

Kir6.2 variant E23K increases ATP-sensitive K + channel activity and is associated with impaired insulin release and enhanced insulin sensitivity in adults with normal glucose tolerance.

Jul 3, 2020 · We reveal, for the first time, dynamical behavior of the Kir6.2/SUR1 system, confirming a physiological role of the Kir6.2 disordered tail, and we indicate structural determinants of KATP-dependent insulin release from pancreatic β cells.

Nov 1, 2021 · Kir6.2, a pore-forming subunit of the ATP-sensitive potassium (KATP) channels, regulates the functions of metabolically active tissues and acts as an ideal therapeutic target for multiple diseases.