In:
Circulation, Ovid Technologies (Wolters Kluwer Health), Vol. 92, No. 8 ( 1995-10-15), p. 2041-2043
Abstract:
Background In end-stage failing human hearts and in rat hearts after prolonged in vivo β-adrenergic treatment, several proteins involved in the cAMP-dependent signal transduction are altered on the protein, mRNA, or transcriptional level, eg, β-adrenoceptors, G-proteins, or proteins of Ca 2+ homeostasis. In many tissues, cAMP-dependent transcriptional regulation occurs through the cAMP response element binding protein (CREB) and related transcription factors binding as dimers to cAMP response elements (CREs) in the promoter regions of regulated genes. Methods and Results To investigate a possible role of CREB in the human heart, nuclear protein of explanted failing and nonfailing human hearts was used to test for CRE specific binding properties in gel mobility shift assays. CRE specific binding was found in competition studies, and CREB and its phosphorylated form were immunologically identified in supershift experiments. The alternatively spliced CREB isoforms CREB327 and CREB341 were found to be expressed on the mRNA level by the reverse transcriptase–polymerase chain reaction. Conclusions We conclude that in the failing and nonfailing human heart, CREB is expressed on the protein and mRNA levels and that CREB is phosphorylated and able to bind to CREs, indicating a functional role of CREB in the human heart.
Type of Medium:
Online Resource
ISSN:
0009-7322
,
1524-4539
DOI:
10.1161/01.CIR.92.8.2041
Language:
English
Publisher:
Ovid Technologies (Wolters Kluwer Health)
Publication Date:
1995
detail.hit.zdb_id:
1466401-X
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