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American Journal of Physiology. Renal Physiology|December 10, 2019
Hypertension-causing cullin 3 mutations disrupt COP9 signalosome bindingRyan J Cornelius, Chao-Ling Yang, David H EllisonAmerican Journal of Physiology. Renal Physiology|May 9, 2022
COP9 signalosome deletion promotes renal injury and distal convoluted tubule remodelingRyan J Cornelius, Jonathan W Nelson, Xiao-Tong Su, et al.American Journal of Physiology. Renal Physiology|August 29, 2024
Distal convoluted tubule-specific disruption of the COP9 signalosome but not its regulatory target cullin 3 causes tubular injuryYujiro Maeoka, Tanner Bradford, Xiao-Tong Su, et al.The Journal of Clinical Investigation|November 3, 2007
The thiazide-sensitive Na-Cl cotransporter is regulated by a WNK kinase signaling complexChao-Ling Yang, Xiaoman Zhu, David H EllisonBiochemical and Biophysical Research Communications|April 15, 2004
Comparison of WNK4 and WNK1 kinase and inhibiting activitiesZhaohong Wang, Chao-Ling Yang, David H EllisonJournal of the American Society of Nephrology : JASN|October 11, 2018
Renal COP9 Signalosome Deficiency Alters CUL3-KLHL3-WNK Signaling PathwayRyan J Cornelius, Jinge Si, Catherina A Cuevas, et al.American Journal of Physiology. Renal Physiology|June 14, 2018
Dual gain and loss of cullin 3 function mediates familial hyperkalemic hypertensionRyan J Cornelius, Chong Zhang, Kayla J Erspamer, et al.Current Cardiology Reports|August 14, 2020
Kidney Is Essential for Blood Pressure Modulation by Dietary PotassiumXiao-Tong Su, Chao-Ling Yang, David H EllisonThe Journal of Clinical Investigation|April 3, 2003
WNK kinases regulate thiazide-sensitive Na-Cl cotransportChao-Ling Yang, Jordan Angell, Rose Mitchell, et al.American Journal of Physiology. Renal Physiology|October 6, 2005
Dominant-negative regulation of WNK1 by its kidney-specific kinase-defective isoformArohan R Subramanya, Chao-Ling Yang, Xiaoman Zhu, et al.Pageof 15