Robert Frank Spurney, MD

Professor of Medicine
Member of the Duke Cancer Institute
Campus mail Box 103015, Duke University Medical Center, Durham, NC 27710
Phone (919) 684-9729
Email address spurn002@mc.duke.edu

Dr. Spurney’s research has focused on the role of G protein coupled receptors (GPCRs) in regulating cellular physiology both in normal and disease states as well as the regulatory mechanisms that modulate GPCR responsiveness at the molecular level. These studies have centered on two major themes. The first investigates the role of GPCR signaling pathways in regulating podocyte function using cultured podocytes and transgenic animals models. The second area of research involves the role of GPCR kinases (GRKs) and arrestin scaffolding proteins in modulating GPCR signaling in bone forming osteoblasts using cultured osteoblast cell lines as well as genetically modified mice including transgenic models and knockout animals. The long-term goal of these studies is to identify novel therapeutic targets that may useful for treating disease processes such as glomerulonephritis and osteoporosis.

Please see the Duke Nephrology Division website for more detailed information.

Education and Training

  • Fellow in Nephrology, Medicine, Duke University, 1987 - 1990
  • Senior Assistant Resident, Medicine, Duke University, 1986 - 1987
  • Resident in Pathology, Pathology, Duke University, 1985 - 1986
  • Medical Resident, Medicine, Duke University, 1983 - 1985
  • M.D., Ohio State University, 1983

Publications

Wang, Liming, Jae-Hyung Chang, Anne F. Buckley, and Robert F. Spurney. “Knockout of TRPC6 promotes insulin resistance and exacerbates glomerular injury in Akita mice..” Kidney Int 95, no. 2 (February 2019): 321–32. https://doi.org/10.1016/j.kint.2018.09.026.

PMID
30665571
Full Text

Wang, Liming, Anne F. Buckley, and Robert F. Spurney. “Regulation of cofilin phosphorylation in glomerular podocytes by testis specific kinase 1 (TESK1)..” Sci Rep 8, no. 1 (August 16, 2018). https://doi.org/10.1038/s41598-018-30115-3.

PMID
30115939
Full Text

Hall, Gentzon, Brandon M. Lane, Kamal Khan, Igor Pediaditakis, Jianqiu Xiao, Guanghong Wu, Liming Wang, et al. “The Human FSGS-Causing ANLN R431C Mutation Induces Dysregulated PI3K/AKT/mTOR/Rac1 Signaling in Podocytes..” J Am Soc Nephrol 29, no. 8 (August 2018): 2110–22. https://doi.org/10.1681/ASN.2017121338.

PMID
30002222
Full Text

Wang, Liming, Yonggang Sha, Jingyi Bai, William Eisner, Matthew A. Sparks, Anne F. Buckley, and Robert F. Spurney. “Podocyte-specific knockout of cyclooxygenase 2 exacerbates diabetic kidney disease..” Am J Physiol Renal Physiol 313, no. 2 (August 1, 2017): F430–39. https://doi.org/10.1152/ajprenal.00614.2016.

PMID
28490532
Full Text

Johnson, Stacy A., and Robert F. Spurney. “Twenty years after ACEIs and ARBs: emerging treatment strategies for diabetic nephropathy..” Am J Physiol Renal Physiol 309, no. 10 (November 15, 2015): F807–20. https://doi.org/10.1152/ajprenal.00266.2015.

PMID
26336162
Full Text

Wang, Liming, Grant Jirka, Paul B. Rosenberg, Anne F. Buckley, Jose A. Gomez, Timothy A. Fields, Michelle P. Winn, and Robert F. Spurney. “Gq signaling causes glomerular injury by activating TRPC6..” J Clin Invest 125, no. 5 (May 2015): 1913–26. https://doi.org/10.1172/JCI76767.

PMID
25844902
Full Text

Hall, Gentzon, Rasheed A. Gbadegesin, Peter Lavin, Guanghong Wu, Yangfan Liu, Edwin C. Oh, Liming Wang, et al. “A novel missense mutation of Wilms' Tumor 1 causes autosomal dominant FSGS..” J Am Soc Nephrol 26, no. 4 (April 2015): 831–43. https://doi.org/10.1681/ASN.2013101053.

PMID
25145932
Full Text

Gbadegesin, Rasheed A., Gentzon Hall, Adebowale Adeyemo, Nils Hanke, Irini Tossidou, James Burchette, Guanghong Wu, et al. “Mutations in the gene that encodes the F-actin binding protein anillin cause FSGS..” J Am Soc Nephrol 25, no. 9 (September 2014): 1991–2002. https://doi.org/10.1681/ASN.2013090976.

PMID
24676636
Full Text

Hall, Gentzon, Janelle Rowell, Federica Farinelli, Rasheed A. Gbadegesin, Peter Lavin, Guanghong Wu, Alison Homstad, et al. “Phosphodiesterase 5 inhibition ameliorates angiontensin II-induced podocyte dysmotility via the protein kinase G-mediated downregulation of TRPC6 activity..” Am J Physiol Renal Physiol 306, no. 12 (June 15, 2014): F1442–50. https://doi.org/10.1152/ajprenal.00212.2013.

PMID
24740790
Full Text

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