Activation of Mitogen-activated protein kinase (MAPK) by GnRH is cell-context dependent
Activation of Mitogen-activated protein kinase (MAPK) by GnRH is cell-context dependent
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DOI：
10.1016/j.mce.2006.03.035
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发表时间：
2006-06-27
影响因子：
4.1
通讯作者：
Naor, Zvi
中科院分区：
文献类型：
--
作者：
Dobkin-Bekman, Masha;Naidich, Michal;Naor, Zvi
GnRH 与其在垂体促性腺激素中的同源受体 (GnRHR) 的相互作用包括激活 Gq/G(11) 和磷脂酶 CP (PLC beta)，后者生成第二信使肌醇 1,4,5-三磷酸 (IP3) 和二酰甘油 (DAG)，这是 Ca2+ 动员和 PKC 同工型激活所需的。垂体促性腺激素中 PKC 的激活导致丝裂原激活蛋白激酶超家族 (MAPK) 主要成员的激活，即：细胞外信号调节激酶 (ERK)、jun-N 末端激酶 (INK) 和 p38MAPK。上述途径介导 GnRH 诱导的促性腺激素释放和合成。在这里，我们总结了 GnRH 用于激活 MAPK 成员的多种机制，并表明它们依赖于“细胞环境”。 (c) 2006 年，爱思唯尔爱尔兰有限公司出版。
The interaction of GnRH with its cognate receptor (GnRHR) in pituitary gonadotropes includes activation of Gq/G(11) and phospholipase CP (PLC beta), 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 (INK) 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". (c) 2006 Published by Elsevier Ireland Ltd.