Recombinant Human SUR1 protein (GST tag N-Terminus)

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This supplementary information is collated from multiple sources and compiled automatically.

The SUR1 protein also known as ABCC8 is an important subunit of ATP-sensitive potassium (K_ATP) channels. This protein has a molecular mass of approximately 158 kDa. SUR1 is expressed mainly in pancreatic beta cells although one can also find it in neurons and cardiac tissue. It plays an essential role in regulating the membrane potential and in turn controlling insulin secretion. SUR1 is a member of the ATP-binding cassette (ABC) transporter family which contributes to its ability to influence cellular responses to changes in metabolic states.

Biological function summary

SUR1 binds with the Kir6.2 channel subunits to form functional K_ATP channel complexes. These channels respond to intracellular ATP and ADP levels providing a critical link between cellular energy metabolism and electric cell function. In pancreatic beta cells the opening and closing of these channels trigger the release of insulin in response to blood glucose levels. In the brain the channels modulate neuronal excitability and play a role in neuroprotection. The coupling with Kir6.2 emphasizes the role of the SUR1-Kir6.2 complex in many cellular processes.

Pathways

The K_ATP channels containing SUR1 participate in the insulin secretion pathway and the cellular response to hypoxia. The insulin secretion pathway is important for glucose homeostasis where SUR1 interacts with proteins like Kir6.2 directly linking glucose metabolism to insulin release. In the cellular response to hypoxia SUR1 influences neuronal survival by modifying cell membrane potential regulating excitability and managing cellular energy usage in low oxygen conditions. These pathways demonstrate the importance of SUR1 in maintaining energy balance within cells and across organs.

SUR1 has a significant role in conditions such as congenital hyperinsulinism and neonatal diabetes. Mutations in the SUR1 gene (ABCC8) can lead to deregulation of insulin secretion causing the overproduction of insulin seen in congenital hyperinsulinism. Similarly other mutations might result in impaired insulin release contributing to neonatal diabetes. Additionally SUR1 interacts with Kir6.2 during these disorders and this interaction becomes a target for therapeutic strategies aimed at either activating or inhibiting K_ATP channels as needed to restore balanced insulin levels.