GRIA4 Membrane Protein Introduction

Introduction of GRIA4

Glutamate receptor 4 (GRIA4), also known as AMPA-selective glutamate receptor 4, is a protein that in humans is encoded by the GRIA4 gene. The GRIA4 gene belongs to the L-glutamate-gated ion channels which mediate fast synaptic excitatory neurotransmission. These channels are also responsive to the glutamate agonist, alpha-amino-3-hydroxy-5-methyl-4-isoxazolpropionate (AMPA). Spliced transcript variants encoding different isoforms have been found for this gene.

Glutamate receptors are the predominant excitatory neurotransmitter receptors in the mammalian brain and are activated in a variety of normal neurophysiologic processes. These receptors are heteromeric protein complexes composed of multiple subunits, arranged to form ligand-gated ion channels. The classification of glutamate receptors is based on their activation by different pharmacologic agonists. The subunit encoded by this gene belongs to a family of AMPA (alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionate)-sensitive glutamate receptors and is subject to RNA editing (AGA->GGA; R->G).

Basic Information of GRIA4
Protein Name Glutamate receptor 4
Gene Name GRIA4
Aliases GluR-4, GluR4, AMPA-selective glutamate receptor 4, GluR-D, Glutamate receptor ionotropic, AMPA 4, GLUR4
Organism Homo sapiens (Human)
UniProt ID P48058
Transmembrane Times 3
Length (aa) 902

Function of GRIA4 Membrane Protein

Alternative splicing of the GRIA4 gene results in transcript variants encoding different isoforms, which may vary in their signal transduction properties. Some haplotypes of this gene show a positive association with schizophrenia. Among its related pathways are Circadian entrainment and Post NMDA receptor activation events. Gene Ontology (GO) annotations related to this gene include ionotropic glutamate receptor activity and AMPA glutamate receptor activity.

AMPAR are heterotetrameric assemblies containing various arrangements of GluA subunits 1-4 (GluA 1-4). OPC express all four subunits (GluA1-4). GluA4 is the predominant subunit expressed by OPC in the developing white matter of rodents and humans. Importantly, the timing of GluA4 expression in these systems corresponds with an established window of vulnerability during which OPC is selectively injured by hypoxicischemic conditions, and GluA4 is highly expressed in neural cells vulnerable to excitotoxic cell death. GluA4 signaling is therefore strongly connected to excitotoxicity.

Interacting Proteins for GRIA4 Gene.Fig.1 Interacting proteins for GRIA4 gene.

Application of GRIA4 Membrane Protein in Literature

  1. Begum G., et al. NF-Y-dependent regulation of glutamate receptor 4 expression and cell survival in cells of the oligodendrocyte lineage. Glia. 2018, 66(9): 1896-1914. PubMed ID: 29704264

    This article provides the first definition of a trans-acting mechanism regulating Gria4 and identify the NF-Y network as a potential source of pharmacological targets for promoting OPC survival.

  2. Martin S., et al. De Novo Variants in GRIA4 Lead to Intellectual Disability with or without Seizures and Gait Abnormalities. Am J Hum Genet. 2017, 101(6): 1013-1020. PubMed ID: 29220673

    Authors in this group demonstrate that pathogenic de novo variants in GRIA4 lead to intellectual disability with or without seizures, gait abnormalities, problems of social behavior, and other variable features.

  3. Frankel W.N., et al. Unraveling genetic modifiers in the gria4 mouse model of absence epilepsy. PLoS Genet. 2014, 10(7): e1004454. PubMed ID: 25010494

    The article explores the genetic modifiers in the gria4 mouse model of absence epilepsy. The results expand our knowledge of how natural variation modulates seizures.

  4. Gasparini C.F., et al. Genetic analysis of GRIA2 and GRIA4 genes in migraine. Headache. 2014, 54(2): 303-12. PubMed ID: 24512576

    The article reveals that no association between migraine and the GRIA2 and GRIA4 polymorphisms investigated are exist.

  5. Paz J.T., et al. A new mode of corticothalamic transmission revealed in the Gria4(-/-) model of absence epilepsy. Nat Neurosci. 2011, 14(9): 1167-73. PubMed ID: 21857658

    This article reports a new mode of corticothalamic transmission in the Gria4(-/-) model of absence epilepsy. This mode represents a previously unknown channel of cortico-thalamo-cortical information processing.

GRIA4 Preparation Options

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