GRIN2B

Chr 12AD

glutamate ionotropic receptor NMDA type subunit 2B

Also known as: DEE27, EIEE27, GluN2B, MRD6, NMDAR2B, NR2B, NR3, hNR3

The protein functions as the GluN2B subunit of NMDA receptors, forming heterotetrameric calcium-permeable ion channels that bind glutamate and mediate excitatory synaptic transmission critical for synaptic plasticity, learning, and memory. Autosomal dominant mutations cause developmental and epileptic encephalopathy 27 and intellectual developmental disorder with or without seizures, predominantly through loss-of-function mechanisms. The gene shows extreme intolerance to loss-of-function variants, consistent with haploinsufficiency as a primary disease mechanism.

GeneReviewsOMIMResearchSummary from RefSeq, OMIM, UniProt, Mechanism
GOF/LOFmechanismADLOEUF 0.062 OMIM phenotypes
VCEP Guidelines: GRIN DisordersPilot
ClinGen Panel
Clinical SummaryGRIN2B
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Gene-Disease Validity (ClinGen)
complex neurodevelopmental disorder · ADDefinitive

Definitive — sufficient evidence for diagnostic panels

Population Constraint (gnomAD)
Highly constrained gene — heterozygous loss-of-function variants are very rare in the population (pLI 1.00). One damaged copy is likely sufficient to cause disease.
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ClinVar Variants
27 unique Pathogenic / Likely Pathogenic· 94 VUS of 200 total submissions
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Clinical Trials
2 active or recruiting trials — potential therapeutic options may be available
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GeneReview available — GRIN2B
Authoritative clinical overview · Recommended first read
Open GeneReview ↗
Some data sources returned errors (1)

opentargets: TimeoutError: The operation was aborted due to timeout

Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

Dual constrained — LoF & missense intolerant
LoF Constraint
0.06LOEUF
pLI 1.000
Z-score 6.48
OE 0.00 (0.000.06)
Highly constrained

Among the most LoF-intolerant genes (~top 3%)

Missense Constraint
5.42Z-score
OE missense 0.48 (0.440.52)
415 obs / 862.7 exp
Constrained

Extremely missense-constrained (top ~0.01%)

Observed / Expected Ratios
LoF OE0.00 (0.000.06)
00.351.4
Missense OE0.48 (0.440.52)
00.61.4
Synonymous OE1.14
01.21.6
LoF obs/exp: 0 / 48.9Missense obs/exp: 415 / 862.7Syn Z: -2.00
Curated Mechanism (G2P)Gene2Phenotype (DDG2P) ↗
definitiveGRIN2B-related epileptic encelopathyOTHERAD
definitiveGRIN2B-related intellectual developmental disorderLOFAD
Mechanism Note (variant-dependent)
GOFLOF— mechanism depends on specific variant

NMDA receptor GluN2B subunit. GOF variants in TM/linker regions cause severe DEE. LOF variants cause ID without epilepsy. G2P lists as undetermined/LOF but GOF is well-established for DEE variants.

References:PMID:30012257
DN
0.4289th %ile
GOF
0.5856th %ile
LOF
0.74top 10%

This gene has evidence for multiple mechanisms of pathogenicity (loss-of-function and gain-of-function). Both the Badonyi & Marsh prediction and the broader genomic evidence point to loss-of-function as the predominant mechanism. Different variants in this gene may act through different mechanisms — interpret in context of the specific variant.

LOFprediction above median · 1 literature citation · 63% of P/LP variants are LoF · LOEUF 0.06
GOF1 literature citation

Literature Evidence

GOFWe identified GRIN2B gain-of-function mutations as a cause of West syndrome with severe developmental delay as well as of ID with childhood onset focal epilepsy.PMID:24272827
LOFMultiplex targeted sequencing identifies recurrently mutated genes in autism spectrum disordersPMID:23160955

Predictions from Badonyi M, Marsh JA. PLoS ONE. 2024;19(8):e0307312. Mechanism ranking also informed by gnomAD constraint, ClinVar, and ClinGen data.

ClinVar Variant Classifications

200 submitted variants in ClinVar

Classification Summary

Pathogenic23
Likely Pathogenic4
VUS94
Likely Benign77
Benign2
23
Pathogenic
4
Likely Pathogenic
94
VUS
77
Likely Benign
2
Benign

Curated Variants Distribution

Classified variants from ClinVar · 5 ACMG categories

ClassificationLoFMissense + InframeNon-codingSynonymousTotal
Pathogenic
17
1
5
0
23
Likely Pathogenic
0
4
0
0
4
VUS
3
87
3
1
94
Likely Benign
0
6
19
52
77
Benign
0
2
0
0
2
Total201002753200

LoF = frameshift, stop gained/lost, canonical splice · Counts from ClinVar esearch · Updated hourly

View in ClinVar →

Protein Context — Lollipop Plot

GRIN2B · protein map & ClinVar variants

Showing all ClinVar variants across the protein. Search a specific variant to highlight its position.

3D Protein StructureAlphaFold
Clinical Literature
Open Research Assistant →