%0 Journal Article %1 Ungerer1994 %A Ungerer, M. %A Parruti, G. %A Bohm, M. %A Puzicha, M. %A DeBlasi, A. %A Erdmann, E. %A Lohse, M. J. %D 1994 %J Circ Res %K *Arrestins AMP-Dependent Acid Adult Aged Amino Antigens/genetics/*metabolism Blotting, Cardiac Chain Cyclic Data Eye Female Fragments/genetics Genetic Humans Isomerism Kinases Kinases/genetics/*metabolism Low/*metabolism Male Messenger/metabolism Middle Molecular Myocardium/metabolism Output, Peptide Polymerase Protein Proteins/genetics/*metabolism RNA, Reaction Receptor Sequence Transcription, Western beta-Adrenergic %N 2 %P 206-13 %T Expression of beta-arrestins and beta-adrenergic receptor kinases in the failing human heart %U http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=8293560 %V 74 %X The beta-adrenergic receptor system of the failing human heart is markedly desensitized. We have recently postulated that this desensitization may in part be caused by an increase in beta-adrenergic receptor kinase (beta ARK) expression. beta ARK is thought to effect desensitization by acting in concert with an inhibitor protein, called beta-arrestin. Two isoforms have been identified both for beta ARK and for beta-arrestin. In the present study, we have investigated the expression of the individual isoforms of beta-arrestin and of beta ARK in left ventricles from failing and control human hearts. mRNAs for all four proteins, beta-arrestin-1, beta-arrestin-2, beta ARK-1, and beta ARK-2, were identified in human heart. Quantitation by reverse-transcription polymerase chain reactions showed that in heart failure there were no changes of the mRNA levels for beta-arrestin-1 and beta-arrestin-2, a slight (< 50%) increase of the mRNA for beta ARK-2, and a threefold increase for beta ARK-1 mRNA. At the protein level, beta-arrestin-1 was readily detected by Western blotting in human heart. Its absolute values were approximately 350 fmol/mg cytosolic protein, and its expression was not changed in heart failure. beta-Arrestin-2 levels were too low to be detectable using the same methods. beta ARK levels as determined by enzymatic activity were approximately 20 fmol/mg cytosolic protein (beta ARK-1 plus beta ARK-2) and thus almost 20-fold lower than those of beta-arrestin. beta ARK levels were increased approximately twofold in heart failure.(ABSTRACT TRUNCATED AT 250 WORDS)

@article{Ungerer1994, abstract = {The beta-adrenergic receptor system of the failing human heart is markedly desensitized. We have recently postulated that this desensitization may in part be caused by an increase in beta-adrenergic receptor kinase (beta ARK) expression. beta ARK is thought to effect desensitization by acting in concert with an inhibitor protein, called beta-arrestin. Two isoforms have been identified both for beta ARK and for beta-arrestin. In the present study, we have investigated the expression of the individual isoforms of beta-arrestin and of beta ARK in left ventricles from failing and control human hearts. mRNAs for all four proteins, beta-arrestin-1, beta-arrestin-2, beta ARK-1, and beta ARK-2, were identified in human heart. Quantitation by reverse-transcription polymerase chain reactions showed that in heart failure there were no changes of the mRNA levels for beta-arrestin-1 and beta-arrestin-2, a slight (< 50%) increase of the mRNA for beta ARK-2, and a threefold increase for beta ARK-1 mRNA. At the protein level, beta-arrestin-1 was readily detected by Western blotting in human heart. Its absolute values were approximately 350 fmol/mg cytosolic protein, and its expression was not changed in heart failure. beta-Arrestin-2 levels were too low to be detectable using the same methods. beta ARK levels as determined by enzymatic activity were approximately 20 fmol/mg cytosolic protein (beta ARK-1 plus beta ARK-2) and thus almost 20-fold lower than those of beta-arrestin. beta ARK levels were increased approximately twofold in heart failure.(ABSTRACT TRUNCATED AT 250 WORDS)}, added-at = {2010-12-14T18:12:02.000+0100}, author = {Ungerer, M. and Parruti, G. and Bohm, M. and Puzicha, M. and DeBlasi, A. and Erdmann, E. and Lohse, M. J.}, biburl = {https://www.bibsonomy.org/bibtex/252b1e5a6461d91dd8560a548b07aa295/pharmawuerz}, endnotereftype = {Journal Article}, interhash = {37e73c22225317a31a1a6e704e996055}, intrahash = {52b1e5a6461d91dd8560a548b07aa295}, issn = {0009-7330 (Print) 0009-7330 (Linking)}, journal = {Circ Res}, keywords = {*Arrestins AMP-Dependent Acid Adult Aged Amino Antigens/genetics/*metabolism Blotting, Cardiac Chain Cyclic Data Eye Female Fragments/genetics Genetic Humans Isomerism Kinases Kinases/genetics/*metabolism Low/*metabolism Male Messenger/metabolism Middle Molecular Myocardium/metabolism Output, Peptide Polymerase Protein Proteins/genetics/*metabolism RNA, Reaction Receptor Sequence Transcription, Western beta-Adrenergic}, month = Feb, note = {Ungerer, M Parruti, G Bohm, M Puzicha, M DeBlasi, A Erdmann, E Lohse, M J Research Support, Non-U.S. Gov't United states Circulation research Circ Res. 1994 Feb;74(2):206-13.}, number = 2, pages = {206-13}, shorttitle = {Expression of beta-arrestins and beta-adrenergic receptor kinases in the failing human heart}, timestamp = {2010-12-14T18:18:59.000+0100}, title = {Expression of beta-arrestins and beta-adrenergic receptor kinases in the failing human heart}, url = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=8293560}, volume = 74, year = 1994 }