Inward-rectifier potassium ion channel

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Inward-rectifier potassium ion channels (Kir, IRK) are a specific subset of potassium channels. To date, seven families have been identified in various mammalian cell types. They are crucial for numerous aspects of cellular function, including maintenance of resting membrane potential, regulation of action potential duration, and the control of cell volume.

Function[edit | edit source]

Inward-rectifier potassium ion channels are named for their property to allow larger inward currents (rectification) at potentials negative to the equilibrium potential for K+ (E_K), and smaller outward currents at potentials positive to E_K. This property is due to block of the outward current by intracellular magnesium and polyamines.

Structure[edit | edit source]

Inward-rectifier potassium ion channels are composed of two subunits, each with two transmembrane domains (TMDs). The TMDs are connected by a pore-forming loop (P-loop) that dips into the membrane from the extracellular side. The P-loop contains the selectivity filter, which determines the channel's preference for potassium ions.

Families[edit | edit source]

The seven families of inward-rectifier potassium ion channels are:

  • Kir1.x: Renal outer medullary potassium channels (ROMK)
  • Kir2.x: Classical or "strong" inward-rectifier potassium channels
  • Kir3.x: G protein-activated inward-rectifier potassium channels (GIRK)
  • Kir4.x: Inward-rectifier potassium channels predominantly expressed in glial cells
  • Kir5.x: Inward-rectifier potassium channels that form heterotetramers with other Kir subunits
  • Kir6.x: ATP-sensitive potassium channels (K_ATP)
  • Kir7.x: Inward-rectifier potassium channels with unclear function

Clinical significance[edit | edit source]

Mutations in genes encoding Kir channels have been associated with several human diseases, including Andersen-Tawil syndrome, Bartter syndrome, and Long QT syndrome.

See also[edit | edit source]



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