C
Carmen R. Valdivia
Researcher at University of Wisconsin-Madison
Publications - 72
Citations - 4846
Carmen R. Valdivia is an academic researcher from University of Wisconsin-Madison. The author has contributed to research in topics: Ryanodine receptor & Long QT syndrome. The author has an hindex of 32, co-authored 65 publications receiving 4522 citations. Previous affiliations of Carmen R. Valdivia include National Institutes of Health & University of Michigan.
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Journal ArticleDOI
Postmortem molecular analysis of SCN5A defects in sudden infant death syndrome.
Michael J. Ackerman,Benjamin L. Siu,William Q. Sturner,David J. Tester,Carmen R. Valdivia,Jonathan C. Makielski,Jeffrey A. Towbin +6 more
TL;DR: Almost 2% of this prospective, population-based cohort of SIDS cases had an identifiable SCN5A channel defect, suggesting that mutations in cardiac ion channels may provide a lethal arrhythmogenic substrate in some infants at risk for SIDS.
Journal ArticleDOI
Increased late sodium current in myocytes from a canine heart failure model and from failing human heart.
Carmen R. Valdivia,William W. Chu,Jielin Pu,Jason D. Foell,Robert A. Haworth,Mathew R. Wolff,Timothy J. Kamp,Jonathan C. Makielski +7 more
TL;DR: It is concluded that a peak I(Na) is decreased, and non-inactivating late I( Na) is increased in heart failure and this may contribute to action potential prolongation and the generation of arrhythmia.
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SCN4B-Encoded Sodium Channel β4 Subunit in Congenital Long-QT Syndrome
Argelia Medeiros-Domingo,Toshihiko Kaku,David J. Tester,Pedro Iturralde-Torres,Ajit Itty,Bin Ye,Carmen R. Valdivia,Kazuo Ueda,Samuel Canizales-Quinteros,María Teresa Tusié-Luna,Jonathan C. Makielski,Michael J. Ackerman +11 more
TL;DR: A case of a 21-month-old Mexican-mestizo female with intermittent 2:1 atrioventricular block and a corrected QT interval and the seminal report of SCN4B-encoded Nav&bgr;4 as a novel LQT3-susceptibility gene is provided.
Journal ArticleDOI
Syntrophin mutation associated with long QT syndrome through activation of the nNOS–SCN5A macromolecular complex
Kazuo Ueda,Carmen R. Valdivia,Argelia Medeiros-Domingo,David J. Tester,Matteo Vatta,Gianrico Farrugia,Michael J. Ackerman,Jonathan C. Makielski +7 more
TL;DR: It is concluded that the A390V mutation disrupted binding with PMCA4b, released inhibition of nNOS, caused S-nitrosylation of SCN5A, and was associated with increased late sodium current, which is the characteristic biophysical dysfunction for sodium-channel-mediated LQTS (LQT3).
Journal ArticleDOI
A ubiquitous splice variant and a common polymorphism affect heterologous expression of recombinant human SCN5A heart sodium channels.
Jonathan C. Makielski,Bin Ye,Carmen R. Valdivia,Matthew D. Pagel,Jielin Pu,David J. Tester,Michael J. Ackerman +6 more
TL;DR: Four variant sequences for SCN5A are commonly present in human myocardium and they exhibit functional differences among themselves and with the previous standard clone, which has implications for the choice of background sequence for experiments with heterologous expression systems, and possibly implications for electrophysiological function in vivo.