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

• Published in: Molecular and cellular endocrinology Vol. 252; no. 1; pp. 184 - 190
• Main Authors: Dobkin-Bekman, Masha, Naidich, Michal, Pawson, Adam J., Millar, Robert P., Seger, Rony, Naor, Zvi
• Format: Journal Article
• Language: English
• Published: Ireland Elsevier Ireland Ltd 27.06.2006
• Subjects: Animals; Enzyme Activation; ERK; GnRH; GnRH receptor; Gonadotropin-Releasing Hormone - physiology; Gonadotropins - genetics; JNK; Mammals; Mitogen-Activated Protein Kinases - metabolism; p38; Pituitary cells; Pituitary Gland - enzymology; PKC; Prostate cancer cells; Protein Subunits - genetics; Signal Transduction; Transcription, Genetic; Prostate cancer cells; p38; Pituitary cells; JNK; PKC; GnRH; GnRH receptor; ERK
• ISSN: 0303-7207; 1872-8057
• DOI: 10.1016/j.mce.2006.03.035

The interaction of GnRH with its cognate receptor (GnRHR) in pituitary gonadotropes includes activation of Gq/G 11 and phospholipase Cβ (PLCβ), which generates the second messengers inositol 1,4,5-trisphosphate (IP 3) and diacylglycerol (DAG), which are required for Ca 2+ 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”.