| This Sandbox is Reserved from 26/11/2020, through 26/11/2021 for use in the course "Structural Biology" taught by Bruno Kieffer at the University of Strasbourg, ESBS. This reservation includes Sandbox Reserved 1643 through Sandbox Reserved 1664.
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To get started:
- Click the edit this page tab at the top. Save the page after each step, then edit it again.
- Click the 3D button (when editing, above the wikitext box) to insert Jmol.
- show the Scene authoring tools, create a molecular scene, and save it. Copy the green link into the page.
- Add a description of your scene. Use the buttons above the wikitext box for bold, italics, links, headlines, etc.
More help: Help:Editing
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Gonadotropin releasing hormone 1 receptor
| It is a member of the seven-transmembrane, G-protein coupled receptor (GPCR) family and is activated by the peptide hormone gonadotropin-releasing hormone (GnRH) or the synthetic agonist. The GnRHR is expressed on the surface of pituitary gonadotrope cells as well as lymphocytes, breast, ovary, and prostate. Its activity is critical for successful reproductive function. Several diseases are associated with a dysfunction of this receptor or the corresponding signaling cascade.
You may include any references to papers as in: the use of JSmol in Proteopedia [1] or to the article describing Jmol [2] to the rescue.
Biological Function
The gonadotropin releasing hormone 1 receptor is activated by GnRH which acts upon GnRHRs as the key regulator of puberty and reproduction. This peptide hormone is produced in the hypothalamus but gets secreted and acts upon GnRHRs in the anterior pituitary to exert its effects on reproductive maturation. The activation of the receptor, associates with G-proteins, leads to the releasing of gonadotropic luteinizing hormone (LH) and follicle stimulating hormone (FSH) by activating several signaling cascades. These pathways mainly corresponds to the inositol 1,4,5-triphosphate (IP3) and diacylglycerol (DAG), MAPK, and adenyl cyclase pathways. (1)
Disease
A mutation or a dysfonctionnement of the receptor could cause disease like idiopati hypogonadotropic hypogonadism (HH) which corresponds to a hypogonadism.
Relevance
One of the main using of the couple GnRH - GnRHR in the medicine field is for fertility preservation (1). Indeed a mutation of the receptor gene sometimes lead to failure of detectable ligand binding
Structural highlights
This is a sample scene created with SAT to color by Group, and another to make a transparent representation of the protein. You can make your own scenes on SAT starting from scratch or loading and editing one of these sample scenes.
- ↑ Hanson, R. M., Prilusky, J., Renjian, Z., Nakane, T. and Sussman, J. L. (2013), JSmol and the Next-Generation Web-Based Representation of 3D Molecular Structure as Applied to Proteopedia. Isr. J. Chem., 53:207-216. doi:https://dx.doi.org/10.1002/ijch.201300024
- ↑ Herraez A. Biomolecules in the computer: Jmol to the rescue. Biochem Mol Biol Educ. 2006 Jul;34(4):255-61. doi: 10.1002/bmb.2006.494034042644. PMID:21638687 doi:10.1002/bmb.2006.494034042644
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References
1. Torrealday, S., Lalioti, M. D., Guzeloglu-Kayisli, O. and Seli, E. (2013), Characterization of the Gonadotropin Releasing Hormone Receptor (GnRHR) Expression and Activity in the Female Mouse Ovary. Endocrinology. doi: 10.1210/en.2013-1341
2. Meysing 1 ,A.U., Kanasaki, H., Bedecarrats,G.Y. Acierno Jr, J.S. Conn, P.M., Martin,K.A., Seminara,S.B., Hall,J.E., Crowley Jr, W.F., Kaiser,U.K. (2004), GNRHR Mutations in a Woman with Idiopathic Hypogonadotropic Hypogonadism Highlight the Differential Sensitivity of Luteinizing Hormone and Follicle-Stimulating Hormone to Gonadotropin-Releasing Hormone. doi : 10.1210/jc.2003-031808
