Activation of Mitogen-activated protein kinase (MAPK) by GnRH is cell-context dependent

Masha Dobkin-Bekman, Michal Naidich, Adam J. Pawson, Robert P. Millar, Rony Seger, Zvi Naor*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review


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 languageEnglish
Pages (from-to)184-190
Number of pages7
JournalMolecular and Cellular Endocrinology
Issue number1-2
StatePublished - 27 Jun 2006


  • ERK
  • GnRH
  • GnRH receptor
  • JNK
  • PKC
  • Pituitary cells
  • Prostate cancer cells
  • p38


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