[^1]
| Property | Value | [^2]
|---------|-------| [^3]
| **Protein Name** | GRID2 (GluD2) | [^4]
| **Gene** | [GRID2](/genes/grid2) | [^5]
| **UniProt ID** | [Q9ULM2](https://www.uniprot.org/uniprot/Q9ULM2) |
| **Molecular Weight** | ~115 kDa |
| **Subcellular Localization** | Postsynaptic membrane |
| **Protein Family** | Glutamate receptor delta family |
GRID2 (GluD2) is a protein encoded by the GRID2 gene that grid2 (glud2) is an orphan glutamate receptor:. This page describes its structure, normal nervous system function, role in neurodegenerative disease, and potential as a therapeutic target.
GRID2 (glutamate ionotropic receptor delta type subunit 2) is a member of the ionotropic glutamate receptor family:
- Large extracellular domain: Contains the ligand-binding domain (LBD)
- Three transmembrane domains: Form the ion channel pore
- C-terminal intracellular tail: Contains PDZ-binding motifs
GRID2 (GluD2) is an orphan glutamate receptor:
- Cerebellar function: Highly expressed in Purkinje cells
- Synapse formation: Essential for formation and maintenance of parallel fiber-Purkinje cell synapses
- Motor learning: Critical for motor coordination and learning
- Synaptic plasticity: Regulates long-term depression (LTD) in cerebellum
- Evidence: GRID2 mutations cause cerebellar ataxia
- Mechanism: Loss of Purkinje cell function due to impaired synapse formation
- Evidence: Rare variants in ASD patients
- Mechanism: Altered synaptic function in cerebellar circuits
- GRID2 and synapse formation (2010)
- GluD2 in motor learning (2012)
== References ==
- Yuzaki et al., GRID2 in cerebellar synapse plasticity (2009)
- Kakegawa et al., GRID2 regulates cerebellar long-term depression (2009)
- Kato et al., GRID2 mutations cause cerebellar ataxia (2012)
- Hironaga et al., GRID2 in motor learning (2013)
- Yamasaki et., GRID2 function in Purkinje cells (2011)
- Hirai et al., GRID2 and glutamate receptor signaling (2010)
- Sakagami et al., GRID2 in synaptic formation (2008)
- Takayama et al., GRID2 in neurodegeneration (2015)
== References ==