KATP Related Drug Discovery Products
Membrane protein stable cell lines are widely used in many areas of biomedical research. Creative Biolabs can offer membrane protein stable cell lines to stablish in vitro models for High Throughput Screening.
Creative Biolabs offers high-quality, innovative tools to help research groups accelerate membrane protein drug discovery. They can be found by targets. If there is no product that meets your needs, please contact us.
Four pore-forming Kir6.2 subunits and four regulating Sulphonylurea receptor (SUR1) subunits, make up the KATP channel. The KATP channel's ability to be inhibited by intracellular ATP, which binds to Kir6.2 and causes channel closure, is its defining characteristic. On the other hand, SUR1's interaction with intracellular MgATP and MgADP promotes channel opening. Adenine nucleotides cause KATP channel activity to be modulated, which in turn causes cell metabolism to be controlled. The difference in structure between the nucleotide binding sites on Kir6.2 and SUR1 is reflected by the fact that magnesium ions (Mg2+) are not necessary for ATP (or ADP) binding to Kir6.2 but are necessary for binding to SUR1. This property can also be used experimentally to differentiate between nucleotide effects on Kir6.2 and SUR1.
As a leader in membrane protein drug discovery, Creative Biolabs offer a series of KATP in vitro assays and products with the best quality:
Overview of KATP
- KATP channel in β cells
For insulin to be secreted in response to glucose, the KATP channel is necessary. The ambient level of intracellular ATP makes sure that KATP channel activity is strong enough to maintain the membrane hyperpolarized, inhibiting electrical activity and insulin secretion at glucose concentrations that do not activate these processes. KATP channel closure in response to metabolically produced ATP decreases the KATPcurrent, which increases the contribution of background inward currents to the membrane potential. The membrane depolarizes as a result, and electrical activity begins if this depolarization surpasses the threshold for action potential initiation firing, which in β cells is between -60mV and -50mV.
- KATP channel in α cells
A decrease in blood glucose levels or a rise in the quantities of circulating amino acids, fatty acids, hormones, and neurotransmitters cause α cells to produce glucagon. It is unclear exactly how glucose controls glucagon production. However, research on islets from mice lacking KATP channels shows that KATP channels play a crucial role, whatever the mechanism(s) at play. The issue is whether controlling KATP channel activity directly affects glucagon production or if channel activity has a permissive, indirect effect by paving the way for other mechanisms that function by altering membrane conductance.
KATP Drug Discovery
KATP channel closure controls the release of pancreatic hormones in two different ways. It can either promote (insulin) or inhibit (glucagon) the production of hormones depending on the relative magnitudes of the resting KATP current and other cell currents. Numerous studies indicate that defects in islet cell metabolism may lead to decreased hormone production in both NDM and T2DM. These defects in islet cell metabolism may also be expected to impact glucose homeostasis via alterations in KATP channel function. Future research should focus on determining how defective KATP channel regulation affects insulin and glucagon secretion in T2DM.
