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Validated All-in-One™ qPCR Primer for GRM5(NM_001143831.3) Search again
Powered by BiozBy default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Summary
L-glutamate is the major excitatory neurotransmitter in the central nervous system and activates both ionotropic and metabotropic glutamate receptors. Glutamatergic neurotransmission is involved in most aspects of normal brain function and can be perturbed in many neuropathologic conditions. The metabotropic glutamate receptors are a family of G protein-coupled receptors, that have been divided into 3 groups on the basis of sequence homology, putative signal transduction mechanisms, and pharmacologic properties. Group I includes GRM1 and GRM5 and these receptors have been shown to activate phospholipase C. Group II includes GRM2 and GRM3 while Group III includes GRM4, GRM6, GRM7 and GRM8. Group II and III receptors are linked to the inhibition of the cyclic AMP cascade but differ in their agonist selectivities. Multiple transcript variants encoding different isoforms have been found for this gene. [provided by RefSeq].
Gene References into function
- mGLUR5 and 1,4,5-InsP3 signaling control calcium release
- Data report the isolation of a novel gene termed metabotropic glutamate receptor 5-related (mGluR5R) [mGluR5R].
- Data report the identification of a novel variant of the G-protein coupled metabotropic glutamate receptor mGlu5 (hmGlu5d) generated by alternative splicing at the C-terminal domain.
- mGlu5 on nuclear membranes has a role in mediating intranuclear Ca2+ changes in heterologous cell types and neurons
- alternative 5'-splicing and usage of multiple promoters may contribute to regulatory mechanisms for tissue- and context-specific expression of the mGluR5 gene
- mGluR3 and mGluR5 can critically and differentially modulate the expression of glutamate transporters and may represent interesting pharmacological targets to regulate the extracellular levels of glutamate in pathological conditions.
- activation of mGluR5 causes translocation of both gammaPKC and deltaPKC to the plasma membrane. deltaPKC, but not gammaPKC, phosphorylates mGluR5 Thr(840), leading to the blockade of both Ca2+ oscillations and gammaPKC cycling.
- We found a selective expression of the group I receptor mGluR5 in human parasympathetic Onuf's nucleus, strengthening the hypothesis that mGluR expression may provide a possible clue to the selective vulnerability in ALS.
- glial progenitor cells present in the adult human CNS express mGluR3 and mGluR5a
- metabotropic glutamate receptors 1 and 5 mediate opposite glutamate effects in human lymphocyte activation
- it is phosphorylation of Ser-839, not Thr-840, that is absolutely required for the unique Ca2+ oscillations produced by mGluR5 activation
- there is an alpha-actinin-1-dependent mGlu(5b) receptor association with the actin cytoskeleton modulating receptor cell surface expression and functioning
- We documented for the first time the expression of the mGluR5 and EAAT1 in MG-63 cells, as well as the ability of dexamethasone to upregulate the expression of the mGluR5 and EAAT1 in the MG-63 cells.
- This study provides the first quantitative demonstration and direct comparison of a PET tracer candidate identifying mGluR5 binding sites in mammalian cerebellum.
- deletion of the C terminus of the mGlu5a receptor abolishes both its interaction with the NMDA receptor and reciprocal inhibition of the receptors
- the nucleus can function as an autonomous organelle independent of signals originating in the cytoplasm, and nuclear mGlu5 receptors play a dynamic role in mobilizing Ca2+ in a specific, localized fashion
- These results provide insight into a glutamate-induced regulatory pathway distinct from that described for cytokine-induced NF-kappaB activation and have important implications with regard to both normal glial cell physiology and pathogenesis.
- Review. The structure and function of mGLUR5 and the mechanisms and SARs of its antagonists are reviewed.