Global knockout of ROMK potassium channel worsens cardiac ischemia-reperfusion injury but cardiomyocyte-specific knockout does not: Implications for the identity of mitoKATP.
ROMK is expressed in the urinary tract at both protein and mRNA levels. Significant enlargement and hypertrophy of the bladder may contribute to hydronephrosis in male ROMK KO mice.
The results provide evidence that NHERF1 mediates K(+) current activity through acceleration of the surface expression of ROMK1 K(+) channels in M-1 cells.
ENaC and ROMK channel activity in kidney tubules are inhibited in TgWnk4(pseudoaldosteronism type II) mice. Wnk4(PHAII)-induced inhibition of ENaC and ROMK may contribute to the suppression of K(+) secretion in the tubules.
animal knockouts of ROMK1 do not produce Bartter phenotype. ROMK1 is critical in response to high K intake-stimulated K+ secretion in the collecting tubule.
THGP modulation of ROMK function confers a new role of THGP on renal ion transport and may contribute to salt wasting observed in FJHN/MCKD-2/GCKD patients.
We propose that in taste buds ROMK in type I/glial-like cells may serve a homeostatic function excreting excess K(+) through the apical pore and allowing excitable taste cells to maintain a hyperpolarized resting membrane potential.
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