Copyright © 2007, European Society of Cardiology
Derepression of pathological cardiac genes by members of the CaM kinase superfamily
Myogen, Inc./Gilead Colorado, Inc., 7575 West 103rd Ave., Westminster, Colorado 80021, USA
* Tel.: +1 303 533 1736; fax: +1 303 410 6669. Email address: timothy.mckinsey{at}gilead.com
In response to pathologic stresses such as hypertension or myocardial infarction, the heart undergoes a remodeling process that is characterized by myocyte hypertrophy, myocyte death and fibrosis, resulting in impaired cardiac function and heart failure. Cardiac remodeling is associated with derepression of genes that contribute to disease progression. This review focuses on evidence linking members of the Ca2+/calmodulin-dependent protein kinase (CaMK) superfamily, specifically CaMKII, protein kinase D (PKD) and microtubule associated kinase (MARK), to stress-induced derepression of pathological cardiac gene expression through their effects on class IIa histone deacetylases (HDACs).
KEYWORDS Transcription; Signaling; CaM kinase; Histone deacetylase; Chromatin
Time for primary review 27 days
CiteULike 
Connotea 
Del.icio.us What's this?
This article has been cited by other articles:
|
|
 |
|
  Y. Fu, M. Ren, H. Feng, L. Chen, Z. F. Altun, and C. S. Rubin Neuronal and Intestinal Protein Kinase D Isoforms Mediate Na+ (Salt Taste)-Induced Learning Sci. Signal., August 11, 2009; 2(83): ra42 - ra42. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 Y. Liu, M. Contreras, T. Shen, W. R. Randall, and M. F. Schneider {alpha}-Adrenergic signalling activates protein kinase D and causes nuclear efflux of the transcriptional repressor HDAC5 in cultured adult mouse soleus skeletal muscle fibres J. Physiol., March 1, 2009; 587(5): 1101 - 1115. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. Backs, T. Backs, S. Neef, M. M. Kreusser, L. H. Lehmann, D. M. Patrick, C. E. Grueter, X. Qi, J. A. Richardson, J. A. Hill, et al. The {delta} isoform of CaM kinase II is required for pathological cardiac hypertrophy and remodeling after pressure overload PNAS, February 17, 2009; 106(7): 2342 - 2347. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. Hsu, T. Nagayama, N. Koitabashi, M. Zhang, L. Zhou, D. Bedja, K. L. Gabrielson, J. D. Molkentin, D. A. Kass, and E. Takimoto Phosphodiesterase 5 inhibition blocks pressure overload-induced cardiac hypertrophy independent of the calcineurin pathway Cardiovasc Res, February 1, 2009; 81(2): 301 - 309. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 E. R. Sharlow, K. V. Giridhar, C. R. LaValle, J. Chen, S. Leimgruber, R. Barrett, K. Bravo-Altamirano, P. Wipf, J. S. Lazo, and Q. J. Wang Potent and Selective Disruption of Protein Kinase D Functionality by a Benzoxoloazepinolone J. Biol. Chem., November 28, 2008; 283(48): 33516 - 33526. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. S. Martini, P. Raake, L. E. Vinge, B. R. DeGeorge Jr., J. K. Chuprun, D. M. Harris, E. Gao, A. D. Eckhart, J. A. Pitcher, and W. J. Koch Uncovering G protein-coupled receptor kinase-5 as a histone deacetylase kinase in the nucleus of cardiomyocytes PNAS, August 26, 2008; 105(34): 12457 - 12462. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. Backs, T. Backs, S. Bezprozvannaya, T. A. McKinsey, and E. N. Olson Histone Deacetylase 5 Acquires Calcium/Calmodulin-Dependent Kinase II Responsiveness by Oligomerization with Histone Deacetylase 4 Mol. Cell. Biol., May 15, 2008; 28(10): 3437 - 3445. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 H. Su, L. Altucci, and Q. You Competitive or noncompetitive, that's the question: research toward histone deacetylase inhibitors Mol. Cancer Ther., May 1, 2008; 7(5): 1007 - 1012. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. Bossuyt, K. Helmstadter, X. Wu, H. Clements-Jewery, R. S. Haworth, M. Avkiran, J. L. Martin, S. M. Pogwizd, and D. M. Bers Ca2+/Calmodulin-Dependent Protein Kinase II{delta} and Protein Kinase D Overexpression Reinforce the Histone Deacetylase 5 Redistribution in Heart Failure Circ. Res., March 28, 2008; 102(6): 695 - 702. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
C. H. George Sarcoplasmic reticulum Ca2+ leak in heart failure: mere observation or functional relevance? Cardiovasc Res, January 15, 2008; 77(2): 302 - 314. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
L. S. Maier, D. M. Bers, and J. H. Brown Calmodulin and Ca2+/calmodulin kinases in the heart - Physiology and pathophysiology Cardiovasc Res, March 1, 2007; 73(4): 629 - 630. [Full Text] [PDF]
|
|