J
John S. Lowe
Researcher at Vanderbilt University
Publications - 8
Citations - 1640
John S. Lowe is an academic researcher from Vanderbilt University. The author has contributed to research in topics: NAV1.5 Voltage-Gated Sodium Channel & Sodium channel. The author has an hindex of 8, co-authored 8 publications receiving 1494 citations. Previous affiliations of John S. Lowe include University of Iowa & 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.
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Defining the Cellular Phenotype of “Ankyrin-B Syndrome” Variants Human ANK2 Variants Associated With Clinical Phenotypes Display a Spectrum of Activities in Cardiomyocytes
Peter J. Mohler,Solena Le Scouarnec,Isabelle Denjoy,John S. Lowe,Pascale Guicheney,Lise Caron,Iwona Driskell,Jean-Jacques Schott,Kris Norris,Antoine Leenhardt,Richard B. Kim,Denis Escande,Dan M. Roden +12 more
TL;DR: These data identify ANK2 variants as modulators of human arrhythmias, provide the first insight into the clinical spectrum of “ankyrin-B syndrome,” and reinforce the role of ankyrIn-B–dependent protein interactions in regulating cardiac electrogenesis.
Journal ArticleDOI
Voltage-gated Nav channel targeting in the heart requires an ankyrin-G–dependent cellular pathway
John S. Lowe,Oleg Palygin,Naina Bhasin,Thomas J. Hund,Penelope A. Boyden,Erwin Shibata,Mark E. Anderson,Peter J. Mohler +7 more
TL;DR: This data are the first report of a cellular pathway required for Nav channel trafficking in the heart and suggest that ankyrin-G is critical for cardiac depolarization and Nav channel organization in multiple excitable tissues.
Journal ArticleDOI
Striking In vivo phenotype of a disease-associated human SCN5A mutation producing minimal changes in vitro.
Hiroshi Watanabe,Tao Yang,Dina Myers Stroud,John S. Lowe,Louise Harris,Thomas C. Atack,Dao W. Wang,Susan B. Hipkens,Brenda F. Leake,Lynn Hall,Sabina Kupershmidt,Nagesh Chopra,Mark A. Magnuson,Naohito Tanabe,Bjorn C. Knollmann,Alfred L. George,Dan M. Roden +16 more
TL;DR: Although D1275N produces near-normal currents in multiple heterologous expression experiments, the data establish this variant as a pathological mutation that generates conduction slowing, arrhythmias, and a dilated cardiomyopathy phenotype by reducing cardiac sodium current.
Journal ArticleDOI
Ca2+/calmodulin-dependent kinase II triggers cell membrane injury by inducing complement factor B gene expression in the mouse heart
Madhu V. Singh,Ann M. Kapoun,Linda S. Higgins,William Kutschke,Joshua M. Thurman,Rong Zhang,Minati Singh,Jinying Yang,Xiaoqun Guan,John S. Lowe,Robert M. Weiss,Kathy Zimmermann,Fiona E. Yull,Timothy S. Blackwell,Peter J. Mohler,Mark E. Anderson +15 more
TL;DR: The findings demonstrate what the authors believe is a novel target for CaMKII in myocardial injury and suggest that CaMK II is broadly important for the genetic effects of MI in cardiomyocytes.