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Defects in KCNJ16 Cause a Novel Tubulopathy with Hypokalemia, Salt Wasting, Disturbed Acid-Base Homeostasis, and Sensorineural Deafness. , Schlingmann KP., J Am Soc Nephrol. June 1, 2021; 32 (6): 1498-1512.
A novel method for inducing nerve growth via modulation of host resting potential: gap junction-mediated and serotonergic signaling mechanisms. , Blackiston DJ ., Neurotherapeutics. January 1, 2015; 12 (1): 170-84.
KCNJ10 mutations display differential sensitivity to heteromerisation with KCNJ16. , Parrock S., Nephron Physiol. January 1, 2013; 123 (3-4): 7-14.
KCNJ10 mutations disrupt function in patients with EAST syndrome. , Freudenthal B., Nephron Physiol. January 1, 2011; 119 (3): p40-8.
Kir5.1 underlies long-lived subconductance levels in heteromeric Kir4.1/ Kir5.1 channels from Xenopus tropicalis. , Shang L., Biochem Biophys Res Commun. October 23, 2009; 388 (3): 501-5.
Interaction of the Ca2+-sensing receptor with the inwardly rectifying potassium channels Kir4.1 and Kir4.2 results in inhibition of channel function. , Huang C., Am J Physiol Renal Physiol. March 1, 2007; 292 (3): F1073-81.