M
Mark E. Anderson
Researcher at Johns Hopkins University School of Medicine
Publications - 307
Citations - 20458
Mark E. Anderson is an academic researcher from Johns Hopkins University School of Medicine. The author has contributed to research in topics: Ca2+/calmodulin-dependent protein kinase & Medicine. The author has an hindex of 72, co-authored 252 publications receiving 17510 citations. Previous affiliations of Mark E. Anderson include Vanderbilt University & University of Colorado Denver.
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Journal ArticleDOI
Calmodulin kinase signaling in heart: an intriguing candidate target for therapy of myocardial dysfunction and arrhythmias.
TL;DR: The multifunctional Ca(2+)/calmodulin (CaM)-dependent protein kinase II (CaMKII) has emerged as a proarrhythmic and procardiomyopathic signal in a wide range of structural heart diseases.
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Determinants for calmodulin binding on voltage-dependent Ca2+ channels.
Patricia Pate,Javier Mochca-Morales,Yuejin Wu,Jia Zheng Zhang,George G. Rodney,Irina I. Serysheva,Barbara Y. Williams,Mark E. Anderson,Susan L. Hamilton +8 more
TL;DR: The binding of the IQ and CB peptides to calmodulin appears to be competitive, signifying that the two sequences represent either independent or alternative binding sites for cal modulin rather than both sequences contributing to a single binding site.
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Oxidative Mediated Lipid Peroxidation Recapitulates Proarrhythmic Effects on Cardiac Sodium Channels
Koji Fukuda,Sean S. Davies,Tadashi Nakajima,Boon Hooi Ong,Sabina Kupershmidt,Joshua P. Fessel,Venkataraman Amarnath,Mark E. Anderson,Penelope A. Boyden,Prakash C. Viswanathan,L. Jackson Roberts,Jeffrey R. Balser +11 more
TL;DR: It is shown here that oxidative stress reduces Na+ channel availability and synergistic functional effects of flecainide, a proarrhythmic Na+.
Journal ArticleDOI
Redox Regulation of Sodium and Calcium Handling
TL;DR: The discrimination between fine-tuned ROS signaling and unspecific ROS damage may be crucial for the understanding of heart failure development and important for the investigation of targeted treatment strategies.
Journal ArticleDOI
The mitochondrial uniporter controls fight or flight heart rate increases
Yuejin Wu,Tyler P. Rasmussen,Olha M. Koval,Mei Ling A. Joiner,Duane D. Hall,Biyi Chen,Elizabeth D. Luczak,Qiongling Wang,Adam G. Rokita,Xander H.T. Wehrens,Long-Sheng Song,Mark E. Anderson +11 more
TL;DR: This work found MCU function was essential for rapidly increasing mitochondrial calcium in pacemaker cells and that MCU enhanced oxidative phoshorylation was required to accelerate loading of an intracellular calcium compartment prior to each heartbeat.