ROMK

The renal outer medullary potassium channel (ROMK) is an ATP-dependent potassium channel (K_ir1.1) that transports potassium out of cells. It plays an important role in potassium recycling in the thick ascending limb (TAL) and potassium secretion in the cortical collecting duct (CCD) of the nephron. In humans, ROMK is encoded by the KCNJ1 (potassium inwardly-rectifying channel, subfamily J, member 1) gene. Multiple transcript variants encoding different isoforms have been found for this gene.

Function

Potassium channels are present in most mammalian cells, where they participate in a wide range of physiologic responses. The protein encoded by this gene is an integral membrane protein and inward-rectifier type potassium channel. It is inhibited by internal ATP and probably plays an important role in potassium homeostasis. The encoded protein has a greater tendency to allow potassium to flow into a cell rather than out of a cell (hence the term "inwardly rectifying"). ROMK was identified as the pore forming component of mitoK_ATP channels that are known to have a critical role during stroke or other ischemic attacks in the protection against hypoxia-induced brain injury.

Clinical significance

Mutations in this gene have been associated with antenatal Bartter syndrome, which is characterized by salt wasting, hypokalemic alkalosis, hypercalciuria, and low blood pressure.

References

Welling, P.A. and Kevin Ho, A Comprehensive Guide to ROMK: Form and Function in Health and Disease, Am J Physiol Renal Physiol. 2009 Oct;297(4):F849-63. (Review)

External links

• ROMK1 protein, human at the US National Library of Medicine Medical Subject Headings (MeSH)
• NDI terminology page

This article incorporates text from the United States National Library of Medicine, which is in the public domain.