Photo of James McCormick, Ph.D.

James McCormick Ph.D.

    • Associate Professor of Medicine, Division of Nephrology and Hypertension School of Medicine
    • Program in Molecular and Cellular Biosciences School of Medicine

Dr. McCormick completed his PhD in the laboratory of Dr. Jonathan Seckl in Edinburgh, UK.  During his graduate work, he focused on transcriptional regulation of the  glucocorticoid receptor, a key mediator of perinatal “programming” of adult  diseases such as hypertension and dementia. He completed an American Heart  Association-funded postdoctoral fellowship with Dr. David Pearce in the  Division of Nephrology at UCSF, studying the physiological roles of serum and  glucocorticoid-induced kinase (SGK)  isoforms, and how they differentially regulate renal sodium transport. He  joined the Division of Nephrology & Hypertension at OHSU in 2005. His  current work uses mouse models to examine mechanisms of blood pressure regulation.

Education

  • B.S., University of Edinburgh, Edinburgh United Kingdom 1996
  • Ph.D., University of Edinburgh, Edinburgh United Kingdom 2000
  • Fellowship:

    • Nephrology - University of California, San Francisco, 2000-2004

Memberships and associations

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Publications

  • "Optical Clearing in the Kidney Reveals Potassium-Mediated Tubule Remodeling." Cell Reports  In: , Vol. 25, No. 10, 04.12.2018, p. 2668-2675.e3.
  • "With no lysine kinase 4 modulates sodium potassium 2 chloride cotransporter activity in vivo." American Journal of Physiology - Renal Physiology  In: , Vol. 315, No. 4, 01.10.2018, p. F781-F790.
  • "Endothelial transcriptomics reveals activation of fibrosis-related pathways in hypertension." Physiological Genomics  In: , Vol. 50, No. 2, 01.02.2018, p. 104-116.
  • "Potassium intake modulates the thiazide-sensitive sodium-chloride cotransporter (NCC) activity via the Kir4.1 potassium channel." Kidney International  In: , 01.01.2018.
  • "Nephron remodeling underlies hyperkalemia in familial hyperkalemic hypertension." Journal of the American Society of Nephrology  In: , Vol. 28, No. 9, 01.09.2017, p. 2555-2557.
  • "Potassium sensing by renal distal tubules requires Kir4.1." Journal of the American Society of Nephrology  In: , Vol. 28, No. 6, 01.06.2017, p. 1814-1825.
  • "Calcineurin inhibitor cyclosporine A activates renal NA-K-CL cotransporters via local and systemic mechanisms." American Journal of Physiology - Renal Physiology  In: , Vol. 312, No. 3, 01.03.2017, p. F489-F501.
  • "SPAK and OSR1 play essential roles in potassium homeostasis through actions on the distal convoluted tubule." Journal of Physiology  In: , Vol. 594, No. 17, 01.09.2016, p. 4945-4966.
  • "The CUL3/KLHL3-WNK-SPAK/OSR1 pathway as a target for antihypertensive therapy." American Journal of Physiology - Renal Physiology  In: , Vol. 310, No. 11, 01.06.2016, p. F1389-F1396.
  • "Calcineurin and Sorting-Related Receptor with A-Type Repeats Interact to Regulate the Renal Na-K-2Cl Cotransporter." Journal of the American Society of Nephrology  In: , Vol. 27, No. 1, 01.01.2016, p. 107-119.
  • "Direct and indirect mineralocorticoid effects determine distal salt transport." Journal of the American Society of Nephrology  In: , Vol. 27, No. 8, 2016, p. 2436-2445.
  • "Potassium modulates electrolyte balance and blood pressure through effects on distal cell voltage and chloride." Cell Metabolism  In: , Vol. 21, No. 1, 06.01.2015, p. 39-50.
  • "Distal convoluted tubule." Comprehensive Physiology  In: , Vol. 5, No. 1, 01.01.2015, p. 45-98.
  • "Hyperkalemic hypertension-associated cullin 3 promotes WNK signaling by degrading KLHL3." Journal of Clinical Investigation  In: , Vol. 124, No. 11, 03.11.2014, p. 4723-4736.
  • "Sympathetic stimulation of thiazide-sensitive sodium chloride cotransport in the generation of salt-sensitive hypertension." Hypertension  In: , Vol. 64, No. 1, 2014, p. 178-184.
  • "Regulation of NKCC2 activity by inhibitory SPAK isoforms : KS-SPAK is a more potent inhibitor than SPAK2." American Journal of Physiology - Renal Physiology  In: , Vol. 305, No. 12, 15.12.2013.
  • "SPAK differentially mediates vasopressin effects on sodium cotransporters." Journal of the American Society of Nephrology  In: , Vol. 24, No. 3, 28.02.2013, p. 407-418.
  • "Enhanced phosphorylation of Na+ -Cl- co-transporter in experimental metabolic syndrome : Role of insulin." Clinical Science  In: , Vol. 123, No. 11, 12.2012, p. 635-647.
  • "Pathogenesis of calcineurin inhibitor-induced hypertension." Journal of Nephrology  In: , Vol. 25, No. 3, 06.2012, p. 269-275.
  • "Novel role for SGK3 in glucose homeostasis revealed in SGK3/Akt2 double-null mice." Molecular Endocrinology  In: , Vol. 25, No. 12, 12.2011, p. 2106-2118.
  • "Overexpression of the sodium chloride cotransporter is not sufficient to cause familial hyperkalemic hypertension." Hypertension  In: , Vol. 58, No. 5, 11.2011, p. 888-894.
  • "The calcineurin inhibitor tacrolimus activates the renal sodium chloride cotransporter to cause hypertension." Nature Medicine  In: , Vol. 17, No. 10, 10.2011, p. 1304-1309.
  • "A SPAK isoform switch modulates renal salt transport and blood pressure." Cell Metabolism  In: , Vol. 14, No. 3, 07.09.2011, p. 352-364.
  • "High tail-cuff blood pressure in mice 1 week after shipping : The need for longer acclimation." American Journal of Hypertension  In: , Vol. 24, No. 5, 05.2011, p. 534-536.
  • "The WNK kinase network regulating sodium, potassium, and blood pressure." Journal of the American Society of Nephrology  In: , Vol. 22, No. 4, 04.2011, p. 605-614.
  • "The WNKs : Atypical protein kinases with pleiotropic actions." Physiological Reviews  In: , Vol. 91, No. 1, 01.2011, p. 177-219.
  • "Altered renal FGF23-mediated activity involving MAPK and Wnt : Effects of the Hyp mutation." Journal of Endocrinology  In: , Vol. 207, No. 1, 2010, p. 67-75.
  • "Akt2 and SGK3 are both determinants of postnatal hair follicle development." FASEB Journal  In: , Vol. 23, No. 9, 09.2009, p. 3193-3202.
  • "WNK kinases and renal sodium transport in health and disease : an integrated view." Hypertension  In: , Vol. 51, No. 3, 03.2008, p. 588-596.
  • "NH2 terminus of serum and glucocorticoid-regulated kinase 1 binds to phosphoinositides and is essential for isoform-specific physiological functions." American Journal of Physiology - Renal Physiology  In: , Vol. 292, No. 6, 06.2007.

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