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

doi:10.1016/j.mce.2006.03.035

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

Biochemistry Molecular Biology

Tel Aviv University
Medical Research Council
Weizmann Institute of Science

Research output: Contribution to journal › Article › peer-review

77 Scopus citations

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
Pages (from-to)	184-190
Number of pages	7
Journal	Molecular and Cellular Endocrinology
Volume	252
Issue number	1-2
DOIs	https://doi.org/10.1016/j.mce.2006.03.035
State	Published - 27 Jun 2006

Funding

Funders	Funder number
Medical Research Council	MC_U127681325, MC_U127685842
Israel Science Foundation	221/05

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

SDG 3 Good Health and Well-being

Keywords

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

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10.1016/j.mce.2006.03.035

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

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{"}.",

keywords = "ERK, GnRH, GnRH receptor, JNK, PKC, Pituitary cells, Prostate cancer cells, p38",

author = "Masha Dobkin-Bekman and Michal Naidich and Pawson, \{Adam J.\} and Millar, \{Robert P.\} and Rony Seger and Zvi Naor",

note = "Funding Information: We thank Drs. S. Shacham, D. Harris, D. Bonfil, O. Benard and S. Kraus and Prof. N. Stern for their interest and help during the study. The studies were supported by The Israel Science Foundation (Grant No. 221/05).",

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AU - Dobkin-Bekman, Masha

AU - Naidich, Michal

AU - Pawson, Adam J.

AU - Millar, Robert P.

AU - Seger, Rony

AU - Naor, Zvi

N1 - Funding Information: We thank Drs. S. Shacham, D. Harris, D. Bonfil, O. Benard and S. Kraus and Prof. N. Stern for their interest and help during the study. The studies were supported by The Israel Science Foundation (Grant No. 221/05).

PY - 2006/6/27

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N2 - 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".

AB - 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".

KW - ERK

KW - GnRH

KW - GnRH receptor

KW - JNK

KW - PKC

KW - Pituitary cells

KW - Prostate cancer cells

KW - p38

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VL - 252

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JO - Molecular and Cellular Endocrinology

JF - Molecular and Cellular Endocrinology

IS - 1-2

ER -

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

Abstract

Funding

UN SDGs

Keywords

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