J
James Gulick
Researcher at Cincinnati Children's Hospital Medical Center
Publications - 59
Citations - 4823
James Gulick is an academic researcher from Cincinnati Children's Hospital Medical Center. The author has contributed to research in topics: Myosin & Phosphorylation. The author has an hindex of 36, co-authored 58 publications receiving 4409 citations. Previous affiliations of James Gulick include University of Cincinnati & Hospital Research Foundation.
Papers
More filters
Journal ArticleDOI
Imaging cellular signals in the heart in vivo: Cardiac expression of the high-signal Ca2+ indicator GCaMP2
Yvonne Tallini,Masamichi Ohkura,Bum-Rak Choi,Guangju Ji,Keiji Imoto,Robert Doran,Jane Lee,Patricia Plan,Jason Wilson,Hong Bo Xin,Atsushi Sanbe,James Gulick,John C. Mathai,Jeffrey Robbins,Guy Salama,Junichi Nakai,Michael I. Kotlikoff +16 more
TL;DR: An improved Ca(2+) sensor, GCaMP2, its inducible expression in the mouse heart, and its use to examine signaling in heart cells in vivo are described, demonstrating that GCa MP2 will have broad utility in the dissection of numerous complex cellular interactions in mammals, in vivo.
Journal ArticleDOI
Circadian rhythms govern cardiac repolarization and arrhythmogenesis
Darwin Jeyaraj,Saptarsi M. Haldar,Xiaoping Wan,Mark McCauley,Juergen Ripperger,Kun Hu,Yuan Lu,Betty L. Eapen,Nikunj Sharma,Eckhard Ficker,Michael J. Cutler,James Gulick,Atsushi Sanbe,Jeffrey M. Robbins,Sophie Demolombe,Roman V. Kondratov,Steven Shea,Urs Albrecht,Xander H.T. Wehrens,David S. Rosenbaum,Mukesh K. Jain +20 more
TL;DR: Findings identify circadian transcription of ion channels as a mechanism for cardiac arrhythmogenesis through endogenous circadian rhythmicity under the control of a clock-dependent oscillator, krüppel-like factor 15 (Klf15).
Journal ArticleDOI
Reengineering Inducible Cardiac-Specific Transgenesis With an Attenuated Myosin Heavy Chain Promoter
TL;DR: An efficient, experimentally flexible system that enables us to reversibly affect both abundant and nonabundant cardiomyocyte proteins is developed and appears to be robust and can be used to temporally control high levels of cardiac-specific transgene expression.
Journal ArticleDOI
Enhanced autophagy ameliorates cardiac proteinopathy.
Shenuarin Bhuiyan,J. Scott Pattison,Hanna Osinska,Jeanne James,James Gulick,Patrick M. McLendon,Joseph A. Hill,Junichi Sadoshima,Jeffrey Robbins +8 more
TL;DR: It is shown that enhanced levels of autophagy induced by either autophagic gene overexpression or voluntary exercise ameliorated desmin-related cardiomyopathy (DRC) and suggest that activating Autophagy may be a viable therapeutic strategy for improving cardiac performance under proteotoxic conditions.
Journal ArticleDOI
Cardiac Myosin-Binding Protein-C Phosphorylation and Cardiac Function
Sakthivel Sadayappan,James Gulick,Hanna Osinska,Lisa A. Martin,Harvey S. Hahn,Gerald W. Dorn,Raisa Klevitsky,Christine E. Seidman,Jonathan G. Seidman,Jeffrey M. Robbins +9 more
TL;DR: The data suggest that cMyBP-C phosphorylation is essential for normal cardiac function, and not just during the development of heart failure or pathologic hypertrophy.