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Review
. 2007 Jan 2:260-262:244-8.
doi: 10.1016/j.mce.2005.09.016. Epub 2006 Oct 19.

Potential Leydig cell mitogenic signals generated by the wild-type and constitutively active mutants of the lutropin/choriogonadotropin receptor (LHR)

Mario Ascoli  1
Affiliations
Review

Potential Leydig cell mitogenic signals generated by the wild-type and constitutively active mutants of the lutropin/choriogonadotropin receptor (LHR)

Mario Ascoli. Mol Cell Endocrinol. .
No abstract available

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Figures

Figure 1
Figure 1. Pathways involved in the LHR-provoked phosphorylation of ERK1/2
A pathway (shown by the transparent shapes) involving the activation of the Gs/adenylyl cyclase/cAMP signaling cascade seems to be prominently involved in the LHR-provoked phosphorylation of ERK1/2 in MA-10 cells. Cyclic AMP seems to stimulate ERK1/2 phosphorylation by activating protein kinase A (PKA), which in turn activates Ras by a pathway that has not yet been characterized (indicated by the broken arrows and question marks). Additional LHR-mediated pathways for Ras activation are also possible as indicated by the curved arrow and question marks. The Ras-induced activation of the Raf1-MEK1-ERK1/2 cascade is presumed to occur by the classical pathway that has been so well described in many other cell types. A role for MEK has been documented by the inhibition of ERK1/2 phosphorylation induced by the addition of UO126, a selective MEK inhibitor. A role for cAMP can be readily documented by the inhibition of ERK1/2 phosphorylation induced by overexpression of a cAMP phosphodiesterase (PDE) and by the ability of 8Br-cAMP (a cAMP analog that activates PKA or cAMP-GEFs) to stimulate ERK1/2 phosphorylation. A role for PKA can be documented by the inhibition of ERK1/2 phosphorylation induced by overexpression of the heat stable PKA inhibitor (PKI) or by addition of H89, a selective PKA inhibitor. A role for Ras can be documented by ability of hCG to enhance the levels of Ras-GTP and by the inhibition of ERK1/2 phosphorylation induced by overexpression of a dominant-negative mutant (Ras-S17N). The involvement of cAMP-GEFs, and Rap1 can be excluded (shown by the gray shapes) by the inability of 8CPT-2Me-cAMP (a cAMP analog that selectively activates cAMP-GEFs) to stimulate ERK1/2 phosphorylation, by the inability of hCG to activate Rap1 and by the inability of a dominant negative mutant of Rap1 (Rap1b-S17N) to inhibit the hCG-induced increase in ERK1/2 phosphorylation.
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