M
Mei Ling A. Joiner
Researcher at University of Iowa
Publications - 17
Citations - 2901
Mei Ling A. Joiner is an academic researcher from University of Iowa. The author has contributed to research in topics: Ca2+/calmodulin-dependent protein kinase & Angiotensin II. The author has an hindex of 14, co-authored 17 publications receiving 2568 citations. Previous affiliations of Mei Ling A. Joiner include Johns Hopkins University School of Medicine & Roy J. and Lucille A. Carver College of Medicine.
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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
Corrigendum: 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: In this paper, the y axis values were wrongly given as 0, 20, 40, 60 and 80 in the middle and the lower panels, respectively, in Fig. 4c of this article.
Journal ArticleDOI
CaMKII determines mitochondrial stress responses in heart
Mei Ling A. Joiner,Olha M. Koval,Jingdong Li,Jingdong Li,B. Julie He,Chantal Allamargot,Zhan Gao,Elizabeth D. Luczak,Duane D. Hall,Brian D. Fink,Biyi Chen,Jinying Yang,Steven A. Moore,Thomas D. Scholz,Stefan Strack,Peter J. Mohler,Peter J. Mohler,William I. Sivitz,William I. Sivitz,Long-Sheng Song,Mark E. Anderson +20 more
TL;DR: CaMKII activity is identified as a central mechanism for mitochondrial Ca2+ entry in myocardial cell death, and indicates that mitochondrial-targeted CaMKII inhibition could prevent or reduce myocardials death and heart failure in response to common experimental forms of pathophysiological stress.
Journal ArticleDOI
Oxidation of CaMKII determines the cardiotoxic effects of aldosterone
B. Julie He,Mei Ling A. Joiner,Madhu V. Singh,Elizabeth D. Luczak,Paari Dominic Swaminathan,Olha M. Koval,William J. Kutschke,Chantal Allamargot,Jinying Yang,Xiaoqun Guan,Kathy Zimmerman,Isabella M. Grumbach,Robert M. Weiss,Douglas R. Spitz,Curt D. Sigmund,W. Matthijs Blankesteijn,Stephane Heymans,Stephane Heymans,Peter J. Mohler,Mark E. Anderson +19 more
TL;DR: It is shown that oxidized myocardial CaMKII mediates the cardiotoxic effects of aldosterone on the cardiac matrix and establish CaMK II as a nodal signal for the neurohumoral pathways associated with poor outcomes after myocardia 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.