Regular ArticlesInvolvement of Reactive Oxygen Species-mediated NF- κ B Activation in TNF- α -induced Cardiomyocyte Hypertrophy
References (24)
- et al.
Thyroid hormone enhances Ca2+ pumping activity of the cardiac sarcoplasmic reticulum by increasing Ca2+ ATPase and decreasing phospholamban expression
J Mol Cell Cardiol
(1994) - et al.
Calcineurin promotes protein kinase C and c-Jun NH2-terminal kinase activation in the heart
J Biol Chem
(2000) - et al.
Intercellular signaling via gap junction in connexin-43-transfected cells
J Biol Chem
(1998) - et al.
NF-κB: ten years after
Cell
(1996) - et al.
MKK6 activates myocardial cell NF-κB and inhibits apoptosis in a p38 mitogen-activated protein kinase-dependent manner
J Biol Chem
(1998) - et al.
A calcineurin-dependent transcriptional pathway for cardiac hypertrophy
Cell
(1998) - et al.
An enhancer core element mediates stimulation of rat α-myosin heavy chain promoter by an α1-adrenergic agonist and activated protein kinase C in hypertrophy of cardiac myocytes
J Biol Chem
(1994) - et al.
M-CAT, CArG, and Sp1 elements are required for α1-adrenergic induction of the skeletal α-actin promoter during cardiac myocyte hypertrophy
J Biol Chem
(1995) Tumor necrosis factor in the heart
Am J Physiol
(1998)- et al.
Tumor necrosis factor-α provokes a hypertrophic growth response in adult cardiac myocytes
Circulation
(1997)
Inhibitory effects of antioxidants on neonatal rat cardiac myocyte hypertrophy induced by tumor necrosis factor-α and angiotensin II
Circulation
(1998)
Is NF-κB the sensor of oxidative stress?
FASEB J
(1999)
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