Linked Life Data

8486659

Source:http://linkedlifedata.com/resource/pubmed/id/8486659

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
13
pubmed:dateCreated
1993-6-4
pubmed:databankReference
pubmed:abstractText
The cDNA for human beta-arrestin-1 was cloned by polymerase chain reaction (PCR) and identified based on its remarkably high amino acid identity (98.6%) with the bovine sequence. Two alternatively spliced isoforms of human beta-arrestin-1, differing only in the presence or absence of 24 base pairs/8 amino acids within the sequence, were identified and called beta-arrestin-1A and beta-arrestin-1B, respectively. Both isoforms were found in all tissues tested. Southern blot analysis revealed the existence of a single gene for beta-arrestin-1, suggesting that the two isoforms are generated by alternative mRNA splicing. The possible presence of similar isoforms was investigated for the other members of the arrestin/beta-arrestin gene family by PCR. Two isoforms of arrestin were revealed in bovine peripheral blood leukocytes. The expression of beta-arrestin-1 was studied in several human tissues and cell types. High levels of beta-arrestin-1 mRNA and immunoreactivity were found in peripheral blood leukocytes. The possible regulation of the expression of beta-arrestin-1 was also investigated. Our work documents for the first time that the expression of beta-arrestin-1 is modulated by intracellular cAMP. Using two cell types, human endothelial cells and smooth muscle cells, we found that 6-8-h treatments with the cAMP-inducing agents cholera toxin, forskolin, iloprost, and isoproterenol raised beta-arrestin-1 mRNA by 2-4-fold. Forskolin preferentially increased beta-arrestin-1A expression in smooth muscle cells, as assessed by PCR. beta-Arrestin-1 immunoreactivity was 2-3-fold higher in smooth muscle cells exposed to forskolin for 8 h, compared with untreated controls. We conclude that (i) the finding of alternatively spliced isoforms of beta-arrestin-1 and arrestin documents a novel mechanism to generate diversity within the arrestin/beta-arrestin gene family; (ii) the abundant expression of beta-arrestin-1 in peripheral blood leukocytes further supports our previous suggestion of a major role for the beta ARK/beta-arrestin system in regulating receptor-mediated immune functions; (iii) the increased expression of beta-arrestin-1 by cAMP suggests a new mechanism for the regulation of receptor-mediated responses.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
0021-9258
pubmed:author
pubmed:issnType
Print
pubmed:day
5
pubmed:volume
268
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
9753-61
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed-meshheading:8486659-Alternative Splicing, pubmed-meshheading:8486659-Amino Acid Sequence, pubmed-meshheading:8486659-Animals, pubmed-meshheading:8486659-Antigens, pubmed-meshheading:8486659-Arrestins, pubmed-meshheading:8486659-Base Sequence, pubmed-meshheading:8486659-Blotting, Southern, pubmed-meshheading:8486659-Cattle, pubmed-meshheading:8486659-Cells, Cultured, pubmed-meshheading:8486659-Cholera Toxin, pubmed-meshheading:8486659-Cloning, Molecular, pubmed-meshheading:8486659-DNA, pubmed-meshheading:8486659-Endothelium, Vascular, pubmed-meshheading:8486659-Eye Proteins, pubmed-meshheading:8486659-Forskolin, pubmed-meshheading:8486659-Gene Expression Regulation, pubmed-meshheading:8486659-Genetic Variation, pubmed-meshheading:8486659-Humans, pubmed-meshheading:8486659-Molecular Sequence Data, pubmed-meshheading:8486659-Organ Specificity, pubmed-meshheading:8486659-Polymerase Chain Reaction, pubmed-meshheading:8486659-RNA, Messenger, pubmed-meshheading:8486659-Sequence Homology, Amino Acid, pubmed-meshheading:8486659-Sequence Homology, Nucleic Acid, pubmed-meshheading:8486659-Umbilical Veins
pubmed:year
1993
pubmed:articleTitle
Molecular analysis of human beta-arrestin-1: cloning, tissue distribution, and regulation of expression. Identification of two isoforms generated by alternative splicing.
pubmed:affiliation
Consorzio Mario Negri Sud, Istituto di Ricerche Farmacologiche Mario Negri, Santa Maria Imbaro, Italy.
pubmed:publicationType
Journal Article, Comparative Study, Research Support, Non-U.S. Gov't