Contact Information

Photo of Craig January
Craig January, MD, PHD

PROFESSOR

CARDIOVASCULAR MEDICINE

CLINICAL SCIENCE CENTER
600 HIGHLAND AVE
MADISON, WI 53792-0001

(608) 262-9088




Biography

Craig January is a graduate of the MD-PhD program at the University of Iowa, where he received his medical degree in 1976 and a doctorate in Physiology and Biophysics in 1978. He completed his internship, residency and cardiology fellowship training at the University of Chicago. Dr. January remained at the University of Chicago as an instructor in Medicine, then as an assistant and as an associate professor from 1982 to 1994. He joined the faculty of the University of Wisconsin-Madison Department of Medicine, Division of Cardiovascular Medicine in 1995 (serving as division head from 1995 to 1997 and vice chair of research for the Department of Medicine from 2006-2015).

Dr. January is a clinician-scientist whose research has focused on understanding basic mechanisms of cardiac arrhythmias. In his career, he has studied several ion channels including Na+, L- and T-type Ca++ and K+, and processes involved in the regulation of cardiac contractility. His pioneering research demonstrated an essential role of the L-type Ca++ channel and its 'window current' in generating early afterdepolarizations, a trigger for potentially lethal cardiac arrhythmias. Dr. January's recent research focuses on the molecular mechanisms of the acquired and congenital long QT syndrome. In particular, his lab has been instrumental in defining how mutations in the K+ channel gene, HERG, lead to the congenital long QT syndrome (LQT2). His work has defined abnormalities in protein trafficking as the central mechanism for HERG mutations, which leads to the long QT syndrome.

Dr. January is a Fellow of the American College of Cardiology, and member of several societies including the American Heart Association Basic Sciences Council, Cardiac Electrophysiology Society, Central Society for Clinical Research, Biophysical Society, and North American Society of Pacing and Electrophysiology (now Heart Rhythm Society). He is a past-president of the Cardiac Electrophysiology Society. He has served extensively on peer-review panels including National Institutes of Health Cardiovascular Study Sections (CVA, CVB, clinical trials, K99/R00), national American Heart Association review sections, and VA merit review panels. Dr. January teaches in both clinical and basic settings. Nationally and internationally he has participated as a lecturer in many courses and invited seminars. His teaching accomplishments are well-recognized. Dr. January has been involved in various forms of service including serving as the writing chair for the ACC/AHA/HRS Atrial Fibrillation Guidelines.

Search for Craig January's literature abstracts on PubMed

SELECTED PUBLICATIONS

Zhang L, Vincent GM, Baralle M, Baralle FE, Anson BD, Benson DW, Whiting, Timothy KW, Carlquist J, January CT, Keating MT, Splawski I. 2004. An intronic mutation causes long QT Syndrome. J.A.C.C. 44:1283-1291.

Zhang L, Vincent GM, Baralle M, Baralle FE, Anson BD, Benson DW, Whiting, Timothy KW, Carlquist J, January CT, Keating MT, Splawski I. 2004. An intronic mutation causes long QT Syndrome. J.A.C.C. 44:1283-1291.

Anson BD, Weaver JG, Ackerman MJ, Akinsete O, Henry K, January CT, Badley AD. 2004. HIV protease inhibitors block HERG channels in vitro and are associated with symptomatic QT prolongation and Torsades de Pointes. Lancet. 365:682-686.

Kamp TJ, January CT. 2004. Inherited and Acquired Long QT Syndromes: New Insights and Evolving Technology. Drug Discovery Today. 1:45-51.

Kikuchi K, Nagatomo T, Abe H, Kawakami K, Makielski JC, January CT and Nakashima Y. 2005. Blockade of the HERG cardiac K+ current by antifungal drug miconazole. Br. J. Pharmacol. 144:840-848.

The hERG cardiac potassium channel: Structure, function and long QT syndrome. - Novartis Foundation Symposium 266. John Wiley & Sons, Ltd. 2005. C. January invited discussant.

Eckhardt LL, Rajamani S, January CT. 2005. Protein trafficking abnormalities: A new mechanism in drug-induced long QT syndrome. Br J Pharmacol. 145:3-4.

BP, Slind JK, Kilby JA, Anderson CL, Anson JD, Balijepalli RC, Tester DJ, Ackerman MJ, Kamp TJ, January CT. 2005. Intragenic suppression of trafficking-defective KCNH2 channels associated with long QT syndrome. Molec Pharmacol. 68:233-240.

Anderson CL*, Delisle BP*, Anson BD, Kilby JA, Will ML, Tester DJ, Gong Q, Zhou Z, Ackerman MJ, January CT. 2006. Most LQT2 Mutations Reduce K+ Current by a Class 2 (Trafficking Deficient) Mechanism. Circulation. 113:365-373.
*Joint first authors.