Role of RBM25/LUC7L3 in Abnormal Cardiac Sodium Channel Splicing Regulation in Human Heart Failure
Author(s) -
Ge Gao,
An Xie,
ShuChing Huang,
Anyu Zhou,
Jianhua Zhang,
Amanda M. Herman,
Sassan Ghassemzadeh,
EuyMyoung Jeong,
Srinivasan Kasturirangan,
Mihai Raicu,
Michael A. Sobieski,
Geetha Bhat,
Antone Tatooles,
Edward J. Benz,
Timothy J. Kamp,
Samuel C. Dudley
Publication year - 2011
Publication title -
circulation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.795
H-Index - 607
eISSN - 1524-4539
pISSN - 0009-7322
DOI - 10.1161/circulationaha.111.044495
Subject(s) - rna splicing , alternative splicing , heart failure , downregulation and upregulation , medicine , splicing factor , sudden death , sudden cardiac death , sodium channel , messenger rna , microbiology and biotechnology , biology , gene , genetics , chemistry , rna , sodium , organic chemistry
Human heart failure is associated with decreased cardiac voltage-gated Na+ channel current (encoded by SCN5A), and the changes have been implicated in the increased risk of sudden death in heart failure. Nevertheless, the mechanism of SCN5A downregulation is unclear. A number of human diseases are associated with alternative mRNA splicing, which has received comparatively little attention in the study of cardiac disease. Splicing factor expression profiles during human heart failure and a specific splicing pathway for SCN5A regulation were explored in this study.
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