Open AccessLoss of p47 phox Subunit Enhances Susceptibility to Biomechanical Stress and Heart Failure Because of Dysregulation of Cortactin and Actin Filaments
Author(s) -
Vaibhav B. Patel,
Zuocheng Wang,
Fan Dong,
Pavel Zhabyeyev,
Ratnadeep Basu,
Subhash K. Das,
Wang Wang,
Jessica DesAulniers,
Steven M. Holland,
Zamaneh Kassiri,
Gavin Y. Oudit
Publication year - 2013
Publication title -
circulation research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.899
H-Index - 336
eISSN - 1524-4571
pISSN - 0009-7330
DOI - 10.1161/circresaha.111.300299
Subject(s) - cortactin , pressure overload , cytoskeleton , actin cytoskeleton , microbiology and biotechnology , biology , actin , focal adhesion , nicotinamide adenine dinucleotide phosphate , intercalated disc , medicine , endocrinology , phosphorylation , oxidase test , intracellular , biochemistry , gap junction , muscle hypertrophy , cell , cardiac hypertrophy , enzyme
The classic phagocyte nicotinamide adenine dinucleotide phosphate oxidase (gp91(phox) or Nox2) is expressed in the heart. Nox2 activation requires membrane translocation of the p47(phox) subunit and is linked to heart failure. We hypothesized that loss of p47(phox) subunit will result in decreased reactive oxygen species production and resistance to heart failure.
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