|1.||Koch, Walter J: 13 articles (10/2010 - 06/2002)|
|2.||Koch, W J: 7 articles (11/2001 - 05/2000)|
|3.||Eckhart, Andrea D: 4 articles (08/2008 - 06/2002)|
|4.||Glower, D D: 3 articles (11/2001 - 05/2000)|
|5.||White, D C: 3 articles (11/2001 - 05/2000)|
|6.||Shah, A S: 3 articles (11/2001 - 05/2000)|
|7.||Rockman, H A: 3 articles (05/2001 - 11/2000)|
|8.||Lefkowitz, R J: 3 articles (05/2001 - 05/2000)|
|9.||Molina, Ezequiel J: 2 articles (06/2009 - 10/2008)|
|10.||Palma, Jon: 2 articles (06/2009 - 10/2008)|
04/06/2004 - "Previously, expression of a peptide inhibitor of betaARK1 (betaARKct) has proven beneficial in several animal models of heart failure (HF). "
08/15/2008 - "Preventing GRK2 translocation to activated betaAR with a GRK2-derived peptide that binds G(beta)gamma (betaARKct) has benefited some models of heart failure, but the precise mechanism is uncertain, because GRK2 is still present and betaARKct has other potential effects. "
02/08/2005 - "Our previous studies have shown that inhibition of betaARK1 with the use of the Gbetagamma sequestering peptide of betaARK1 (betaARKct) can prevent cardiac dysfunction in models of heart failure. "
10/01/2010 - "Over the past two decades the GRK2 inhibitory peptide betaARKct has been identified as a potential therapy that is able to break this vicious cycle of self-perpetuating deregulation of the beta-AR system and subsequent myocardial malfunction, thus halting development of cardiac failure. "
02/08/2005 - "TG mice with low betaARKct expression developed severe heart failure, whereas mice with high betaARKct expression showed significantly less cardiac deterioration than wild-type (WT) mice. "
10/23/2001 - "Ventricular dysfunction after cardioplegic arrest is improved after myocardial gene transfer of a beta-adrenergic receptor kinase inhibitor."
11/01/2002 - "Myocardial gene-mediated inhibition of betaARK1 via betaARKct expression avoids ventricular dysfunction after prolonged preservation. "
03/06/2001 - "In vivo delivery of Adeno-betaARKct is feasible in the infarcted/failing heart by coronary catheterization; expression of betaARKct results in marked reversal of ventricular dysfunction. "
03/01/2004 - "We sought to determine whether selective right ventricular expression of a transgene encoding a beta-adrenergic receptor kinase inhibitor can improve right ventricular remodeling early after pulmonary artery banding. "
01/06/2009 - "betaARKct significantly improved cardiac contractility and reversed left ventricular remodeling, which was accompanied by a normalization of the neurohormonal (catecholamines and aldosterone) status of the chronic HF animals, including normalization of cardiac betaAR signaling. "
05/08/2001 - "Thus, overexpression of the betaARKct resulted in a marked prolongation in survival and improved cardiac function in a mouse model of severe cardiomyopathy that can be potentiated with beta-blocker therapy. "
10/17/2003 - "To uncover genomic changes associated with cardiomyopathy and/or its phenotypic rescue by the betaARKct, oligonucleotide microarray analysis of left ventricular (LV) gene expression was performed in a total of 53 samples, including 12 each of Normal, HF, and Rescue. "
10/01/2008 - "Genetic modulation of heart failure using the betaARKct gene was associated with improved exercise capacity and cardiac function as well as amelioration in heart failure-associated profiles of systemic inflammation and volume overload."
10/01/2008 - "We hypothesized that intracoronary adenoviral-mediated delivery of betaARKct would improve heart failure associated pathophysiologic abnormalities related to exercise capacity, cardiac contractility, systemic inflammation and volume overload. "
10/01/2008 - "Adenoviral beta-adrenergic receptor kinase inhibitor gene transfer improves exercise capacity, cardiac contractility, and systemic inflammation in a model of pressure overload hypertrophy."
06/01/2009 - "These results suggest that attenuation of the pathologic mechanisms of beta adrenergic receptor desensitization, SERCA(2a) expression, inflammation and apoptosis, not only occur in the left ventricle but also in the right ventricular myocardium after intracoronary gene transfer of betaARKct during heart failure."
|3.||beta-Adrenergic Receptor Kinases
|4.||Protein Kinases (Protein Kinase)
|6.||glucuronyl glucosamine glycan sulfate (Vessel)
|7.||Adrenergic Receptors (Adrenergic Receptor)
|8.||Carrier Proteins (Binding Protein)
|9.||G-Protein-Coupled Receptor Kinase 2