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William H. Thiel
Researcher at Roy J. and Lucille A. Carver College of Medicine
Publications - 7
Citations - 802
William H. Thiel is an academic researcher from Roy J. and Lucille A. Carver College of Medicine. The author has contributed to research in topics: Ca2+/calmodulin-dependent protein kinase & Cardiac function curve. The author has an hindex of 5, co-authored 7 publications receiving 707 citations. Previous affiliations of William H. Thiel include Vanderbilt University.
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Journal ArticleDOI
Calmodulin kinase II inhibition protects against structural heart disease
Rong Zhang,Michelle S.C. Khoo,Yuejin Wu,Yingbo Yang,Chad E. Grueter,Gemin Ni,Edward Price,William H. Thiel,Silvia Guatimosim,Silvia Guatimosim,Long-Sheng Song,Ernest C. Madu,Anisha N Shah,Tatiana A. Vishnivetskaya,James B. Atkinson,Vsevolod V. Gurevich,Guy Salama,W. J. Lederer,Roger J. Colbran,Mark E. Anderson +19 more
TL;DR: CaMKII inhibition substantially prevented maladaptive remodeling from excessive βAR stimulation and myocardial infarction, and induced balanced changes in excitation-contraction coupling that preserved baseline and βAR-stimulated physiological increases in cardiac function.
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E-C coupling structural protein junctophilin-2 encodes a stress-adaptive transcription regulator
Ang Guo,Yihui Wang,Yihui Wang,Biyi Chen,Yunhao Wang,Jinxiang Yuan,Liyang Zhang,Duane D. Hall,Jennifer Wu,Yun Shi,Qi Zhu,Qi Zhu,Cheng Chen,Cheng Chen,William H. Thiel,Xin Zhan,Robert M. Weiss,Fenghuang Zhan,Catherine A. Musselman,Miles A. Pufall,Weizhong Zhu,Kin Fai Au,Jiang Hong,Mark E. Anderson,Chad E. Grueter,Long-Sheng Song,Long-Sheng Song +26 more
TL;DR: The hypothesis that JP2 encodes a stress-adaptive transcriptional regulator, which transduces mechanical information (E-C uncoupling) into transcriptional reprogramming in the myocardium in the setting of cardiac stress is tested.
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Proarrhythmic Defects in Timothy Syndrome Require Calmodulin Kinase II
William H. Thiel,Biyi Chen,Thomas J. Hund,Olha M. Koval,Anil Purohit,Long-Sheng Song,Peter J. Mohler,Mark E. Anderson,Mark E. Anderson +8 more
TL;DR: In Timothy syndrome, the loss of voltage-dependent inactivation is an upstream initiating event for arrhythmia phenotypes that are ultimately dependent on CaMKII activation.
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CaMKII (Ca2+/Calmodulin-Dependent Kinase II) in Mitochondria of Smooth Muscle Cells Controls Mitochondrial Mobility, Migration, and Neointima Formation.
Emily K. Nguyen,Olha M. Koval,Paige Noble,Kim Broadhurst,Chantal Allamargot,Meng Wu,Meng Wu,Stefan Strack,William H. Thiel,Isabella M. Grumbach,Isabella M. Grumbach +10 more
TL;DR: Mitochondrial CaMKII is identified as a key regulator of mitochondrial Ca2+ uptake via MCU, thereby controlling mitochondrial translocation and VSMC migration after vascular injury and neointimal hyperplasia was significantly reduced.
Journal ArticleDOI
Identification of RNA Aptamers that Internalize into HPV-16 E6/E7 Transformed Tonsillar Epithelial Cells
Francoise A. Gourronc,William M. Rockey,William H. Thiel,Paloma H. Giangrande,Aloysius J. Klingelhutz +4 more
TL;DR: Aptamers that internalize into cells may be useful for delivering therapeutic agents to HPV-16 associated malignancies.