Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
1994-2-28
pubmed:abstractText
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)
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0009-7330
pubmed:author
pubmed:issnType
Print
pubmed:volume
74
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
206-13
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed-meshheading:8293560-Adult, pubmed-meshheading:8293560-Aged, pubmed-meshheading:8293560-Amino Acid Sequence, pubmed-meshheading:8293560-Antigens, pubmed-meshheading:8293560-Arrestins, pubmed-meshheading:8293560-Blotting, Western, pubmed-meshheading:8293560-Cardiac Output, Low, pubmed-meshheading:8293560-Cyclic AMP-Dependent Protein Kinases, pubmed-meshheading:8293560-Eye Proteins, pubmed-meshheading:8293560-Female, pubmed-meshheading:8293560-Humans, pubmed-meshheading:8293560-Isomerism, pubmed-meshheading:8293560-Male, pubmed-meshheading:8293560-Middle Aged, pubmed-meshheading:8293560-Molecular Sequence Data, pubmed-meshheading:8293560-Myocardium, pubmed-meshheading:8293560-Peptide Fragments, pubmed-meshheading:8293560-Polymerase Chain Reaction, pubmed-meshheading:8293560-RNA, Messenger, pubmed-meshheading:8293560-Transcription, Genetic, pubmed-meshheading:8293560-beta-Adrenergic Receptor Kinases
pubmed:year
1994
pubmed:articleTitle
Expression of beta-arrestins and beta-adrenergic receptor kinases in the failing human heart.
pubmed:affiliation
Laboratorium für Molekulare Biologie, Universität München, Max-Planck-Institut für Biochemie, Martinsried, Germany.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't