Lincoln R. Potter

1999- Biochemistry, Molecular Biology and Biophysics University of Minnesota, Twin Cities, Minneapolis, MN 
"Lincoln Ross Potter"
Lincoln Potter earned his B.S. in biology/chemistry from David Lipscomb University in Nashville. He received his Ph.D. under the direction of David Garbers from Vanderbilt University in 1994 and then conducted postdoctoral studies with Tony Hunter at the Salk Institute in San Diego. In the fall of 1999, he joined the Department of Biochemistry, Molecular Biology and Biophysics at the University of Minnesota as a tenure-track assistant professor, which is his current position.

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David Lorn Garbers grad student 1994 Vanderbilt
 (The role of dephosphorylation in the desensitization of guanylyl cylcase-linked natriuretic peptide receptors.)
Tony Hunter post-doc Salk Institute


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Sarah E. Hosch grad student 2004 UMN
Paula M. Bryan grad student 2006 UMN
Laura K. Antos grad student 2008 UMN
Darcy R. Flora grad student 2009 UMN
Andrea R. Yoder grad student 2010 UMN
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Schmidt H, Dickey DM, Dumoulin A, et al. (2018) Regulation of the natriuretic peptide receptor 2 (Npr2) by phosphorylation of juxtamembrane serine and threonine residues is essential for bifurcation of sensory axons. The Journal of Neuroscience : the Official Journal of the Society For Neuroscience
Dickey DM, Otto NM, Potter LR. (2017) Skeletal overgrowth-causing mutations mimic an allosterically activated conformation of guanylyl cyclase-B that is inhibited by 2,4,6,-trinitrophenyl ATP. The Journal of Biological Chemistry
Otto NM, McDowell WG, Dickey DM, et al. (2017) A Glutamate-Substituted Mutant Mimics the Phosphorylated and Active Form of Guanylyl Cyclase-A. Molecular Pharmacology
Dickey DM, Edmund AB, Otto NM, et al. (2016) Catalytically Active Guanylyl Cyclase-B Requires ER-mediated Glycosylation and Mutations that Inhibit this Process Cause Dwarfism. The Journal of Biological Chemistry
Shuhaibar LC, Egbert JR, Edmund AB, et al. (2015) Dephosphorylation of juxtamembrane serines and threonines of the NPR2 guanylyl cyclase is required for rapid resumption of oocyte meiosis in response to luteinizing hormone. Developmental Biology
Wang SR, Jacobsen CM, Carmichael H, et al. (2015) Heterozygous mutations in natriuretic peptide receptor-B (NPR2) gene as a cause of short stature. Human Mutation. 36: 474-81
Egbert JR, Shuhaibar LC, Edmund AB, et al. (2014) Dephosphorylation and inactivation of NPR2 guanylyl cyclase in granulosa cells contributes to the LH-induced decrease in cGMP that causes resumption of meiosis in rat oocytes. Development (Cambridge, England). 141: 3594-604
Buys ES, Potter LR, Pasquale LR, et al. (2014) Regulation of intraocular pressure by soluble and membrane guanylate cyclases and their role in glaucoma. Frontiers in Molecular Neuroscience. 7: 38
Robinson JW, Dickey DM, Miura K, et al. (2013) A human skeletal overgrowth mutation increases maximal velocity and blocks desensitization of guanylyl cyclase-B. Bone. 56: 375-82
Robinson JW, Potter LR. (2012) Guanylyl cyclases A and B are asymmetric dimers that are allosterically activated by ATP binding to the catalytic domain. Science Signaling. 5: ra65
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