Volume 1041, Issue 1 p. 280-287

Relaxin Signaling from Natural Receptors

RICHARD IVELL

RICHARD IVELL

Institute for Hormone and Fertility Research, University of Hamburg, Hamburg, 20246, Germany

School of Molecular and Biomedical Science, University of Adelaide, SA 5005, Australia

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RAVINDER ANAND-IVELL

Corresponding Author

RAVINDER ANAND-IVELL

School of Molecular and Biomedical Science, University of Adelaide, SA 5005, Australia

Address for correspondence: Professor Richard Ivell, University of Adelaide School of Molecular and Biomedical Science, Adelaide, SA 5005, Australia. Voice: ++61-8-83033114; fax: ++61-8-83033359. [email protected]Search for more papers by this author
OLAF BARTSCH

OLAF BARTSCH

Institute for Hormone and Fertility Research, University of Hamburg, Hamburg, 20246, Germany

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First published: 09 January 2006
Citations: 7

Abstract

Abstract: The heterodimeric peptide hormone relaxin in most cells appears to signal through a G-protein-coupled receptor, LGR7. Whereas in artificial cell systems, made by transfection of receptor-expressing gene constructs into cells normally not presenting the receptor, classic activation of adenylate cyclase appears to be mediated by Gs, in cells naturally expressing the receptor, this type of coupling appears to be very weak. Instead, there is good evidence of other intermediate steps involving cytoplasmic components and tyrosine kinase activity. Part of the complexity of relaxin signaling is also manifest in the variable time course of cAMP production evident in the THP-1 cell line, which appears to depend on passage number and, hence, presumably on differentiation status. It is therefore important to distinguish between immediate early effects, short to mid-term responses, and long-term responses likely the consequences of specific gene upregulation.