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William Kutschke
Researcher at University of Iowa
Publications - 25
Citations - 3125
William Kutschke is an academic researcher from University of Iowa. The author has contributed to research in topics: Pressure overload & Ca2+/calmodulin-dependent protein kinase. The author has an hindex of 17, co-authored 22 publications receiving 2862 citations.
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Journal ArticleDOI
A dynamic pathway for calcium-independent activation of CaMKII by methionine oxidation
Jeffrey R. Erickson,Mei Ling A. Joiner,Xiaoqun Guan,William Kutschke,Jinying Yang,Carmine V. Oddis,Ryan K. Bartlett,John S. Lowe,Susan E. O'Donnell,Nukhet Aykin-Burns,Matthew C. Zimmerman,Kathy Zimmerman,Amy-Joan L. Ham,Robert M. Weiss,Douglas R. Spitz,Madeline A. Shea,Roger J. Colbran,Peter J. Mohler,Mark E. Anderson +18 more
TL;DR: It is shown that oxidation of paired regulatory domain methionine residues sustains CaMKII activity in the absence of Ca2+/CaM and highlights the critical importance of oxidation-dependent CaMK II activation to AngII and ischemic myocardial apoptosis.
Journal ArticleDOI
Activated glycogen synthase-3β suppresses cardiac hypertrophy in vivo
Christopher L. Antos,Timothy A. McKinsey,Norbert Frey,William Kutschke,John R. McAnally,John M. Shelton,James A. Richardson,Joseph A. Hill,Eric N. Olson +8 more
TL;DR: A role for GSK-3β is revealed as an inhibitor of hypertrophic signaling in the intact myocardium and it is suggested that elevation of cardiac GSK -3β activity may provide clinical benefit in the treatment of pathologic hypertrophy and heart failure.
Journal ArticleDOI
Cardiac Hypertrophy Is Not a Required Compensatory Response to Short-Term Pressure Overload
Joseph A. Hill,Mohsen Karimi,William Kutschke,Robin L. Davisson,Kathy Zimmerman,Zhengyi Wang,Richard E. Kerber,Robert M. Weiss +7 more
TL;DR: In this experimental setting, calcineurin blockade with CsA prevented LV hypertrophy due to pressure overload in mice and in vivo parameters of ventricular volume and function were examined using echocardiography.
Journal ArticleDOI
Diabetes increases mortality after myocardial infarction by oxidizing CaMKII.
Min Luo,Xiaoqun Guan,Elizabeth D. Luczak,Di Lang,William Kutschke,Zhan Gao,Jinying Yang,Patric Glynn,Samuel Sossalla,Paari Dominic Swaminathan,Robert M. Weiss,Baoli Yang,Adam G. Rokita,Adam G. Rokita,Lars S. Maier,Igor R. Efimov,Thomas J. Hund,Mark E. Anderson +17 more
TL;DR: The findings suggest that activation of a mitochondrial/ox-CaMKII pathway contributes to increased sudden death in diabetic patients after myocardial infarction.
Journal ArticleDOI
Oxidized CaMKII causes cardiac sinus node dysfunction in mice
Paari Dominic Swaminathan,Anil Purohit,Siddarth Soni,Niels Voigt,Niels Voigt,Madhu V. Singh,Alexey V. Glukhov,Zhan Gao,B. Julie He,Elizabeth D. Luczak,Mei Ling A. Joiner,William Kutschke,Jinying Yang,J. Kevin Donahue,Robert M. Weiss,Isabella M. Grumbach,Masahiro Ogawa,Masahiro Ogawa,Peng Sheng Chen,Igor R. Efimov,Dobromir Dobrev,Dobromir Dobrev,Peter J. Mohler,Thomas J. Hund,Mark E. Anderson +24 more
TL;DR: A computational model of the sinoatrial node showed that a loss of SAN cells below a critical threshold caused SND by preventing normal impulse formation and propagation, and suggested that targeted CaMKII inhibition may be useful for preventing SND in high-risk patients.