Quantification of the cAMP response element binding protein in ventricular nuclear protein from failing and nonfailing human hearts.
Alterations in the expression of myocardial regulatory proteins (e.g. beta-adrenoceptor, inhibitory G-proteins) in human heart failure are associated with excessive stimulation of the cAMP signalling pathway by endogenous catecholamines. The transcription factor cAMP response element binding protein (CREB) mediates cAMP-dependent transcriptional activation and is expressed in the human heart. Here, CREB protein was immunologically quantified in ventricular nuclear protein preparations from nonfailing donor hearts (n = 8) and from failing hearts transplanted due to dilative (n = 10) or ischemic cardiomyopathy (n = 6). CREB expression was unchanged in ventricular nuclei from failing hearts compared to the nonfailing controls suggesting that expressional alterations in human heart failure cannot be explained by altered expression of CREB.
Müller
F U
FU
Institut für Pharmakologie und Toxikologie, Universität Münster, Germany. mullerf@uni-muenster.de
Bokník
P
P
Knapp
J
J
Lüss
H
H
Neumann
J
J
Vahlensieck
U
U
Böhm
M
M
Deng
M C
MC
Scheld
H H
HH
Schmitz
W
W
D017362:Cyclic AMP Response Element-Binding Protein / Q000378:metabolism*; D006333:Heart Failure / Q000378:metabolism*; D006352:Heart Ventricles / Q000378:metabolism; D006801:Humans; D007158:Immunologic Techniques; D009687:Nuclear Proteins / Q000378:metabolism
D017362:Cyclic AMP Response Element-Binding Protein; D009687:Nuclear Proteins