ADRA2C

Chr 4

adrenoceptor alpha 2C

Also known as: ADRA2L2, ADRA2RL2, ADRARL2, ALPHA2CAR

ADRA2C encodes the alpha-2C adrenergic receptor, a G protein-coupled receptor that mediates presynaptic inhibition of neurotransmitter release from noradrenergic nerve terminals in sympathetic and central nervous systems, specifically modulating neurotransmission at lower levels of nerve activity. The gene is moderately constrained against loss-of-function variants (LOEUF 0.605), but specific disease associations and inheritance patterns for ADRA2C mutations have not been established in the current clinical literature.

OMIMResearchSummary from RefSeq, UniProt
MultiplemechanismLOEUF 0.60
Clinical SummaryADRA2C
Population Constraint (gnomAD)
Moderately constrained gene (pLI 0.50) — some intolerance to loss-of-function variants.
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ClinVar Variants
119 unique Pathogenic / Likely Pathogenic· 70 VUS of 199 total submissions
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Clinical Trials
1 active or recruiting trial — potential therapeutic options may be available

Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

Moderate LoF intolerance
LoF Constraint
0.60LOEUF
pLI 0.502
Z-score 2.41
OE 0.19 (0.080.60)
Moderately constrained

Typical tolerance to LoF variation

Missense Constraint
1.64Z-score
OE missense 0.70 (0.610.79)
161 obs / 231.2 exp
Tolerant

Mild missense constraint

Observed / Expected Ratios
LoF OE0.19 (0.080.60)
00.351.4
Missense OE0.70 (0.610.79)
00.61.4
Synonymous OE1.08
01.21.6
LoF obs/exp: 2 / 10.4Missense obs/exp: 161 / 231.2Syn Z: -0.65
DN
0.6550th %ile
GOF
0.77top 25%
LOF
0.4528th %ile

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

GOFprediction above median
DNprediction above median

Note: In-silico variant effect predictors (SIFT, PolyPhen, REVEL, CADD) may underestimate pathogenicity of missense variants in genes with GOF or DN mechanisms. Consider functional evidence and clinical context.

Predictions from Badonyi M, Marsh JA. PLoS ONE. 2024;19(8):e0307312.

ClinVar Variant Classifications

199 submitted variants in ClinVar

Classification Summary

Pathogenic115
Likely Pathogenic4
VUS70
Likely Benign6
Benign4
115
Pathogenic
4
Likely Pathogenic
70
VUS
6
Likely Benign
4
Benign

Curated Variants Distribution

Classified variants from ClinVar · 5 ACMG categories

ClassificationLoFMissense + InframeNon-codingSynonymousTotal
Pathogenic
0
0
115
0
115
Likely Pathogenic
0
0
4
0
4
VUS
0
68
2
0
70
Likely Benign
0
0
1
5
6
Benign
0
2
0
2
4
Total0701227199

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

View in ClinVar →

Protein Context — Lollipop Plot

ADRA2C · protein map & ClinVar variants

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

3D Protein StructureAlphaFold
Clinical Literature
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