Data suggest underlying pathology for some patients with type II Bartter syndrome is linked to stability of ROMK1 in ERAD pathway; using a yeast expression system cells can be rescued by wild-type (rat) ROMK1 but not by ROMK1 containing any one of four mutations found in (human) type II Bartter syndrome; mutant ROMKs are significantly less stable than wild-type ROMK. (ERAD = endoplasmic reticulum-associated degradation)
Blockade of ROMK or Na(+)-K(+)-2Cl(-) transport inhibits tubuloglomerular feedback yet increases renal vascular resistance. The renal vasoconstriction was independent of volume depletion blood pressure TGF or proximal tubule hydrostatic pressure.
The TPNQ toxin-rKir1.1 channel complex structure not only revealed their unique interaction mechanism but also elucidate the relative insensitivity of rKir1.1 channel towards animal toxins.
The large increase in the Rb/K conductance ratio with no change in K/Na permeability or rectification is consistent with R128Y-Kir1.1b causing a subtle change in the selectivity filter
hydrophobic leucines at the cytoplasmic end of the inner transmembrane helices comprise the principal pH gate of Kir1.1 a gate that can be relocated from 160-Kir1.1b to 157-Kir1.1b.
May participate in the regulation of epithelial and smooth muscle cell volume and osmolality and in bidirectional potassium transport across urinary tract epithelia.
CD63 plays a role in the regulation of ROMK channels through its association with RPTPalpha which in turn interacts with and activates Src family PTK thus reducing ROMK activity.
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