Xander H.T. Wehrens
Baylor College of Medicine
301 Papers
1.3K Citations
Xander H.T. Wehrens is an academic researcher from Baylor College of Medicine. The author has contributed to research in topics: Ryanodine receptor 2 & Ryanodine receptor. The author has an hindex of 69, co-authored 252 publications. Previous affiliations of Xander H.T. Wehrens include Boston Children's Hospital & Cardiovascular Institute Hospital.
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Papers
Non-equilibrium gating in cardiac Na+ channels: an original mechanism of arrhythmia.
TL;DR: A combination of computational and experimental analysis of mutations provides a framework to understand complex mechanisms underlying a range of disorders, from molecular defect to cellular and systems function, and suggests an original mechanism for development of LQT-3 arrhythmias.
Calcium dysregulation in atrial fibrillation: the role of CaMKII.
TL;DR: The Ca2-handling derangements occurring in AF are summarized and the role of the multifunctional Ca2+/calmodulin-dependent protein kinase type-II (CaMKII), which acts as a major link between Ca2+.-dysregulation and arrhythmogenesis is focused on.
EL20, a potent antiarrhythmic compound, selectively inhibits calmodulin-deficient ryanodine receptor type 2
Robert C. Klipp,Na Li,Qiongling Wang,Tarah A. Word,Martha Sibrian-Vazquez,Robert M. Strongin,Xander H.T. Wehrens,Jonathan J. Abramson +7 more
TL;DR: This work provides a potential therapeutic mechanism for the development of antiarrhythmic compounds that inhibit leaky RyR2 resulting from CaM dissociation, which is often associated with failing hearts and may contribute to the pathogenesis of arrhythmias with the CPVT-linked R176Q mutation.
CaMKII regulation of the cardiac ryanodine receptor and sarcoplasmic reticulum calcium release.
TL;DR: The mechanisms underlying CaMKII regulation of RyR2 are reviewed, directions of current and future research are discussed, and directions of future research in this area are discussed.
Atrial Proteomic Profiling Reveals a Switch Towards Profibrotic Gene Expression Program in CREM-IbΔC-X Mice with Persistent Atrial Fibrillation
Shuai Zhao,Mohit Hulsurkar,Satadru K. Lahiri,Yuriana Aguilar-Sanchez,Elda M. Munivez,Frank Ulrich Müller,Antrix Jain,Anna Malovannaya,Kendrick Yiu,Svetlana Reilly,Xander H.T. Wehrens +10 more
TL;DR: The major findings are that in pAF, key changes were identified in proteins involved in metabolism, energy production, DNA synthesis, and cell proliferation and growth and in mice and humans with perAF, key changes were found in the expression of proteins involved in collagen production, extracellular matrix remodeling, actin cytoskeleton organization, and tissue repair.