Christopher Adams, MD, PhD (Associate Member)
Assistant Professor, Department of Internal Medicine, University of Iowa

http://www.int-med.uiowa.edu/Divisions/Endocrine/Directory/ChristopherAdams.html

Research Interest    

The Adams laboratory is focused on the molecular pathogenesis of skeletal muscle atrophy. One of our major projects is to determine the role of ATF4, an evolutionarily ancient regulator of genes involved in amino acid and protein metabolism. We found that ATF4 expression is increased in atrophied muscle from humans and mice, and have used gene transfer techniques to determine that ATF4 is both necessary and sufficient for muscle atrophy in mice. These studies identified a novel mechanism of skeletal muscle atrophy, and current projects aim to determine the upstream mechanism that increases ATF4 expression in atrophied muscle, and the downstream effects of ATF4 on muscle gene expression and metabolism. A second major project in our laboratory is to determine the effects of fasting, diabetes, uremia and spinal cord injury on skeletal muscle gene expression in humans. In these studies, we have identified novel changes in muscle gene expression that are associated with human muscle atrophy, and are using gene transfer techniques in mice to determine the how these changes relate to ATF4 expression and influence muscle atrophy.

Selected Publications:

Goulet CC, Volk KA, Adams CM, Prince LS, Stokes JB, and Snyder PM. Inhibition of the epithelial Na+ channel by interaction of Nedd-4 with a PY motif deleted in Liddle's syndrome. J. Biol. Chem. 273: 30012-30017, 1998.

Adams CM, Snyder PM, Price MP, and Welsh MJ. Protons activate brain Na+ channel 1 by inducing a conformational change that exposes a residue associated with neurodegeneration. J. Biol. Chem. 273: 30204-30207, 1998.

Adams CM, Price MP, Snyder PM, and Welsh MJ. Tetraethylammonium block of the BNC1 channel. Biophys. J. 76: 1377-1383, 1999.

Adams CM, Snyder PM, and Welsh MJ. Paradoxical stimulation of a DEG/ENaC channel by amiloride. J. Biol. Chem. 274: 15500-15504, 1999.

Yabe D, Xia ZP, Adams CM, and Rawson RB. Three mutations in sterol-sensing domain of SCAP block interaction with Insig and render SREBP cleavage insensitive to sterols. PNAS 99: 16672-16677, 2002.

Ainsley JA, Pettus JM, Bosenko D, Gerstein CE, Zinkevich N, Anderson MG, Adams CM, Welsh MJ, and Johnson WA. Enhanced locomotion caused by loss of the Drosophila DEG/ENaC protein Pickpocket1. Curr. Biol. 13: 1557-1563, 2003.

Adams CM, Brown MS, and Goldstein JL. Cholesterol-induced conformational change in SCAP enhanced by Insig proteins and mimicked by cationic amphiphiles. PNAS 100: 10647-10652, 2003.

Adams CM, Reitz J, De Brabander JK, Feramisco JD, Li L, Brown MS, and Goldstein JL. Cholesterol and 25-hydroxycholesterol inhibit SREBP processing by different mechanisms, both involving SCAP and Insigs. J. Biol. Chem. 279: 52772-52780, 2004.

Adams CM. Role of the transcription factor ATF4 in the anabolic actions of insulin and the anti-anabolic actions of glucocorticoids. J. Biol. Chem. 282: 16744-16753, 2007.

Malmberg SE, and Adams CM. Insulin signaling and the general amino acid control response: two distinct pathways to amino acid synthesis and uptake. J. Biol. Chem. 283: 19229-19234, 2008.

Seo, J, Fortuno ES, Suh, JM, Stenesen D, Tang W, Parks EJ, Adams CM, Townes T, and Graff JM. Atf4 Regulates Obesity, Glucose Homeostasis, and Energy Expenditure. Diabetes. Published online 8/18/09.

Publications from PubMed