GnRH receptor signalling to ERK: kinetics and compartmentalization.

Reference:

Caunt, C. J., Finch, A. R., Sedgley, K. R. and McArdle, C. A., 2006. GnRH receptor signalling to ERK: kinetics and compartmentalization. Trends in Endocrinology and Metabolism, 17 (8), pp. 308-313.

Related documents:

Official URL:

http://dx.doi.org/10.1016/j.tem.2006.08.001

Abstract

Many hormones, neurotransmitters and growth factors influence their target cells by activation of mitogen-activated protein kinase cascades. The consequences of such activation reflect not only the magnitude, but also the kinetics and cellular compartmentalization of kinase activity. Gonadotropin-releasing hormone (GnRH) receptors are seven-transmembrane receptors that have undergone a period of rapidly accelerated molecular evolution in which the advent of type I mammalian GnRH receptors has been associated with the loss of the carboxyl-terminal tail, a structure present in all other seven-transmembrane receptors. Here, we review spatiotemporal aspects of extracellular-signal-regulated kinase activation by gonadotropin-releasing hormone receptors, emphasizing how the absence or presence of the carboxyl-terminal tail dictates the receptors' ability to engage and signal via arrestins.

Export

Actions (login required)