Metabotropic glutamate receptor: Difference between revisions
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[[Metabotropic glutamate receptor|Metabotropic glutamate receptors]] are [[Glutamate Receptors|glutamate receptors]] that activate ion channels indirectly through a signaling cascade involving G proteins<ref>PMID:20716669</ref>. They are members of the large class of seven-transmembrane domain receptors, the [[G protein-coupled receptor|G protein-coupled receptors]]. Glutamate receptors are classified into 3 groups based on their homology, mechanism and pharmacological properties. See also [[Ligand Binding N-Terminal of Metabotropic Glutamate Receptors]]. | [[Metabotropic glutamate receptor|Metabotropic glutamate receptors]] are [[Glutamate Receptors|glutamate receptors]] that activate ion channels indirectly through a signaling cascade involving G proteins<ref>PMID:20716669</ref>. They are members of the large class of seven-transmembrane domain receptors, the [[G protein-coupled receptor|G protein-coupled receptors]]. Glutamate receptors are classified into 3 groups based on their homology, mechanism and pharmacological properties. See also [[Ligand Binding N-Terminal of Metabotropic Glutamate Receptors]]. | ||
*'''Metabotropic glutamate receptor 1''' and '''metabotropic glutamate receptor 5''' belong to group I and activate phospholipase C.<br /> | *'''Metabotropic glutamate receptor 1''' and '''metabotropic glutamate receptor 5''' belong to group I and activate phospholipase C. For details see [[Metabotropic glutamate receptor 5]].<br /> | ||
*'''Metabotropic glutamate receptor 2''' and '''metabotropic glutamate receptor 3''' belong to group II and inhibit the cyclic AMP cascade.<br /> | *'''Metabotropic glutamate receptor 2''' and '''metabotropic glutamate receptor 3''' belong to group II and inhibit the cyclic AMP cascade.<br /> | ||
*'''Metabotropic glutamate receptor 7''' belongs to group III and inhibits adenylate cyclase activity.<br /> | *'''Metabotropic glutamate receptor 7''' belongs to group III and inhibits adenylate cyclase activity.<br /> | ||
Revision as of 17:39, 14 January 2017
FunctionMetabotropic glutamate receptors are glutamate receptors that activate ion channels indirectly through a signaling cascade involving G proteins[1]. They are members of the large class of seven-transmembrane domain receptors, the G protein-coupled receptors. Glutamate receptors are classified into 3 groups based on their homology, mechanism and pharmacological properties. See also Ligand Binding N-Terminal of Metabotropic Glutamate Receptors.
Articles in Proteopedia concerning Toll-like Receptors include:
RelevanceGluR are targets for Parkinson's disease drugs[2] as well as for Alzheimer's disease, depression, anxiety and schizophrenia[3]. Structural highlightsin the crevice between the N-terminal and C-terminal domains[4]. Water molecules shown as red spheres.
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3D structures of metabotropic glutamate receptor3D structures of metabotropic glutamate receptor
Updated on 14-January-2017
See AlsoSee Also
Membrane Channels & Pumps
Ionotropic_Glutamate_Receptors
Alzheimer's Disease
ReferencesReferences
- ↑ Traynelis SF, Wollmuth LP, McBain CJ, Menniti FS, Vance KM, Ogden KK, Hansen KB, Yuan H, Myers SJ, Dingledine R. Glutamate receptor ion channels: structure, regulation, and function. Pharmacol Rev. 2010 Sep;62(3):405-96. doi: 10.1124/pr.109.002451. PMID:20716669 doi:http://dx.doi.org/10.1124/pr.109.002451
- ↑ Johnson KA, Conn PJ, Niswender CM. Glutamate receptors as therapeutic targets for Parkinson's disease. CNS Neurol Disord Drug Targets. 2009 Dec;8(6):475-91. PMID:19702565
- ↑ Niswender CM, Conn PJ. Metabotropic glutamate receptors: physiology, pharmacology, and disease. Annu Rev Pharmacol Toxicol. 2010;50:295-322. doi:, 10.1146/annurev.pharmtox.011008.145533. PMID:20055706 doi:http://dx.doi.org/10.1146/annurev.pharmtox.011008.145533
- ↑ Kunishima N, Shimada Y, Tsuji Y, Sato T, Yamamoto M, Kumasaka T, Nakanishi S, Jingami H, Morikawa K. Structural basis of glutamate recognition by a dimeric metabotropic glutamate receptor. Nature. 2000 Oct 26;407(6807):971-7. PMID:11069170 doi:10.1038/35039564