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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Aug 2016.

Glutamate receptor, ionotropic, kainate 2

GluR6, mGluR6, GRIK2
forms a homomeric glutamate receptor that is activated by kainate, quisqualate, and L-glutamate but not by AMPA [RGD, Feb 2006] (from NCBI)
Top mentioned proteins: ACID, metabotropic glutamate receptor, GluR2, CAN, KA2
Papers on GluR6
Toward a Valid Animal Model of Bipolar Disorder: How the Research Domain Criteria Help Bridge the Clinical-Basic Science Divide.
Suppes et al., Palo Alto, United States. In Biol Psychiatry, Feb 2016
Further, translating the biology of bipolar disorder in humans into animal models has led to greater understanding of roles for candidate biological systems such as the GRIK2 and CLOCK genes, as well as the extracellular signal-related kinase pathway involved in the pathophysiology of the illness.
Genetic assessment of additional endophenotypes from the Consortium on the Genetics of Schizophrenia Family Study.
Braff et al., San Diego, United States. In Schizophr Res, Jan 2016
Linkage analyses performed using a genome-wide SNP array further identified significant or suggestive linkage for six of the candidate endophenotypes, with several genes of interest located beneath the linkage peaks (e.g., CSMD1, DISC1, DLGAP2, GRIK2, GRIN3A, and SLC6A3).
Pharmacogenetic study of long-term response to interferon-β treatment in multiple sclerosis.
Martinelli-Boneschi et al., Milano, Italy. In Pharmacogenomics J, Jan 2016
Finally, we found an enrichment of pathways related to inflammatory processes and presynaptic membrane, the latter with involvement of genes related to glutamatergic system (GRM3 and GRIK2), confirming its potential role in the response to IFNβ.The Pharmacogenomics Journal advance online publication, 8 December 2015; doi:10.1038/tpj.2015.85.
Gene polymorphisms and oral cancer risk in tobacco habitués.
Saranath et al., Mumbai, India. In Tumour Biol, Dec 2015
The SNPs rs2124437 (RASGRP3), rs1335022 (GRIK2), rs4512367 (PREX2), rs4748011 (CCDC3), and rs1435218 (LNX1) were analyzed in 500 histopathologically confirmed oral cancers and 500 healthy controls with a minimum of 10 years of tobacco usage.
[Metabotropic glutamate receptor 8 activation promotes the apoptosis of lung carcinoma A549 cells in vitro].
Luo et al., Changsha, China. In Sheng Li Xue Bao, Nov 2015
The results showed that there were low expressions of mGluR1, mGluR5, mGluR6, mGluR7 mRNA, no expression of mGluR2 and mGluR3 mRNA, and high expressions of mGluR8 and mGluR4 mRNA in A549 cells.
Mechanism for Selective Synaptic Wiring of Rod Photoreceptors into the Retinal Circuitry and Its Role in Vision.
Martemyanov et al., Jupiter, United States. In Neuron, Oct 2015
At the synapse, ELFN1 binds in trans to mGluR6, the postsynaptic receptor on rod ON-bipolar cells.
Properties and functions of TRPM1 channels in the dendritic tips of retinal ON-bipolar cells.
Oberwinkler et al., Marburg an der Lahn, Germany. In Eur J Cell Biol, Jul 2015
The underlying transduction cascade in the dendritic tips of ON-bipolar cells involves mGluR6 glutamate receptors signaling to TRPM1 proteins that are an indispensable part of the transduction channel.
1p34.3 deletion involving GRIK3: Further clinical implication of GRIK family glutamate receptors in the pathogenesis of developmental delay.
Kosaki et al., Tokyo, Japan. In Am J Med Genet A, 2014
Among the five known GRIK family members, haploinsufficiency of GRIK1, GRIK2, and GRIK4 are known to cause developmental delay, whereas the roles of GRIK3 and GRIK5 remain unknown.
Regulation of transport across cell membranes by the serum- and glucocorticoid-inducible kinase SGK1.
Alesutan et al., Tübingen, Germany. In Mol Membr Biol, 2014
The serum- and glucocorticoid-inducible kinase 1 (SGK1) is genomically upregulated by cell stress including energy depletion and hyperosmotic shock as well as a variety of hormones including glucocorticoids, mineralocorticoids and TGFβ.
Furukawa et al., Suita, Japan. In Handb Exp Pharmacol, 2013
We further demonstrated that Trpm1 is a component of the transduction cation channel negatively regulated by the metabotropic glutamate receptor 6 (mGulR6) cascade in ON-bipolar cells through a reconstitution experiment using CHO cells expressing Trpm1, mGluR6, and Goα.
Mutation screening of TRPM1, GRM6, NYX and CACNA1F genes in patients with congenital stationary night blindness.
Zhang et al., Guangzhou, China. In Int J Mol Med, 2012
The results expand the mutation spectrum of NYX, CACNA1F and GRM6. They also suggest that NYX mutations are a common cause of congenital stationary night blindness (CSNB).
TAA repeat variation in the GRIK2 gene does not influence age at onset in Huntington's disease.
Gusella et al., Boston, United States. In Biochem Biophys Res Commun, 2012
Comprehensive analytical methods applied to a much larger sample than in previous studies do not support a role for GRIK2 as a genetic modifier of age at onset of clinical symptoms in Huntington's disease.
Patterned expression of ion channel genes in mouse dorsal raphe nucleus determined with the Allen Mouse Brain Atlas.
Commons et al., Boston, United States. In Brain Res, 2012
This study demonistrated that grik2 gene expression in mouse dorsal raphe nucleus
SUMOylation and phosphorylation of GluK2 regulate kainate receptor trafficking and synaptic plasticity.
Mellor et al., Bristol, United Kingdom. In Nat Neurosci, 2012
Our results suggest a role for the dynamic control of synaptic SUMOylation in the regulation of GluK2 synaptic transmission and plasticity
nNOS downregulation attenuates neuronal apoptosis by inhibiting nNOS-GluR6 interaction and GluR6 nitrosylation in cerebral ischemic reperfusion.
Zhang et al., Xuzhou, China. In Biochem Biophys Res Commun, 2012
these results suggest that nNOS binds with GluR6 via PSD95 and then produces endogenous NO to S-nitrosylate GluR6 in cerebral ischemia-reperfusion, which provides a new approach for stroke therapy.
SUMOylation regulates kainate-receptor-mediated synaptic transmission.
Henley et al., Bristol, United Kingdom. In Nature, 2007
the kainate receptor subunit GluR6 is a SUMO substrate
(Patho)physiological significance of the serum- and glucocorticoid-inducible kinase isoforms.
Vallon et al., Tübingen, Germany. In Physiol Rev, 2006
The serum- and glucocorticoid-inducible kinase-1 (SGK1) is ubiquitously expressed and under genomic control by cell stress (including cell shrinkage) and hormones (including gluco- and mineralocorticoids).
c-fos regulates neuronal excitability and survival.
Xu et al., Cincinnati, United States. In Nat Genet, 2002
Moreover, c-Fos regulates the expression of the kainic acid receptor GluR6 and brain-derived neurotrophic factor (BDNF), both in vivo and in vitro.
Altered synaptic physiology and reduced susceptibility to kainate-induced seizures in GluR6-deficient mice.
Heinemann et al., Los Angeles, United States. In Nature, 1998
We have now generated mutant mice lacking the kainate-receptor subunit GluR6.
Phosphorylation and modulation of a kainate receptor (GluR6) by cAMP-dependent protein kinase.
Hampson et al., Toronto, Canada. In Science, 1993
The functional modulation of GluR6, a kainate-activated glutamate receptor, by adenosine 3',5'-monophosphate-dependent protein kinase A (PKA) was examined with receptors expressed in human embryonic kidney cells.
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