Abstract
The interaction of GnRH with its cognate receptor (GnRHR) in pituitary gonadotropes includes activation of Gq/G11 and phospholipase Cβ (PLCβ), which generates the second messengers inositol 1,4,5-trisphosphate (IP3) and diacylglycerol (DAG), which are required for Ca2+ mobilization and PKC isoforms activation. Activation of PKC in pituitary gonadotropes leads to the activation of the major members of the mitogen-activated protein kinase superfamily (MAPK), namely: extracellular signal-regulated kinase (ERK), jun-N-terminal Kinase (JNK) and p38MAPK. The above pathways mediate GnRH-induced gonadotropin release and synthesis. Here we summarise the diverse mechanisms utilized by GnRH to activate the MAPK members and show that they depend on "cell-context".
Original language | English |
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Pages (from-to) | 184-190 |
Number of pages | 7 |
Journal | Molecular and Cellular Endocrinology |
Volume | 252 |
Issue number | 1-2 |
DOIs | |
State | Published - 27 Jun 2006 |
Keywords
- ERK
- GnRH
- GnRH receptor
- JNK
- PKC
- Pituitary cells
- Prostate cancer cells
- p38