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

74 Scopus citations


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


FundersFunder number
Medical Research CouncilMC_U127681325, MC_U127685842
Israel Science Foundation221/05


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


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