GRID2

Source: Wikipedia, the free encyclopedia.
GRID2
Available structures
Gene ontology
Molecular function
Cellular component
Biological process
Sources:Amigo / QuickGO
Ensembl
UniProt
RefSeq (mRNA)

NM_001286838
NM_001510

NM_008167
NM_001370966

RefSeq (protein)

NP_001273767
NP_001501

NP_032193
NP_001357895

Location (UCSC)Chr 4: 92.3 – 93.81 MbChr 6: 63.23 – 64.68 Mb
PubMed search[3][4]
Wikidata
View/Edit HumanView/Edit Mouse

Glutamate receptor, ionotropic, delta 2, also known as GluD2, GluRδ2, or δ2, is a

glutamate or various other glutamate agonists.[7]

delta iGluRs have long been considered

endogenous ligand was unknown. They are now believed to bind glycine and D-serine but these do not result in channel opening.[8][9]

Function

GluD2-containing receptors are selectively/predominantly expressed in Purkinje cells in the cerebellum[7][10] where they play a key role in synaptogenesis, synaptic plasticity, and motor coordination.[11]

GluD2 induces synaptogenesis through interaction of its N-terminal domain with Cbln1, which in turn interacts with presynaptic

neurexins, forming a bridge across cerebellar synapses.[11][12]

The main functions of GluD2 in synaptic plasticity are carried out by its intracellular C-terminus.

protein-protein interactions
.

Pathology

A heterozygous deletion in GRID2 in humans causes a complicated spastic paraplegia with ataxia, frontotemporal dementia, and lower motor neuron involvement[16] whereas a homozygous biallelic deletion leads to a syndrome of cerebellar ataxia with marked developmental delay, pyramidal tract involvement[17] and tonic upgaze,[18] that can be classified as an ataxia with oculomotor apraxia (AOA) and has been named spinocerebellar ataxia, autosomal recessive type 18 (SCAR18).

A gain of channel function, resulting from a point mutation in mouse GRID2, is associated with the phenotype named 'lurcher', which in the heterozygous state leads to ataxia and motor coordination deficits resulting from selective, cell-autonomous apoptosis of cerebellar Purkinje cells during postnatal development.

embryogenesis
.

Ligands

9-Aminoacridine, 9-tetrahydroaminoacridine, N1-dansyl-spermine, N1-dansyl-spermidine, and pentamidine have been shown to act as antagonists of δ2-containing receptors.[21]

Interactions

GRID2 has been shown to

interact with GOPC,[22] GRIK2,[23] PTPN4[24] and GRIA1.[23] A possible correlation between GRID2 and the pre-B lymphocyte protein 3 (VPREB3) has been suggested, due to the apparent importance of B-lymphocytes in the origins of cerebellar Purkinje neurons in humans.[25][26][27][28][29] Morphological studies conducted in GRID2-knockout mice suggest that GRID2 may be present in lymphocytes as well as in the adrenal cortex, however further studies must be conducted to confirm these claims.[28][30]

See also

References

  1. ^ a b c GRCh38: Ensembl release 89: ENSG00000152208Ensembl, May 2017
  2. ^ a b c GRCm38: Ensembl release 89: ENSMUSG00000071424Ensembl, May 2017
  3. ^ "Human PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
  4. ^ "Mouse PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
  5. ^ "Entrez Gene: GRID2 glutamate receptor, ionotropic, delta 2".
  6. PMID 9465309
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Further reading

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