HTR2A

Chr 13AD

5-hydroxytryptamine receptor 2A

Also known as: 5-HT2A, HTR2

This gene encodes a G-protein coupled receptor for serotonin that activates phospholipase C-beta signaling and affects neural activity, perception, cognition and mood. Mutations are associated with susceptibility to schizophrenia and obsessive-compulsive disorder, as well as altered response to antidepressant therapy in major depressive disorder. The inheritance pattern is autosomal dominant.

GeneReviewsOMIMResearchSummary from RefSeq, OMIM, UniProt
MultiplemechanismADLOEUF 0.523 OMIM phenotypes
Clinical SummaryHTR2A
Population Constraint (gnomAD)
Moderately constrained gene (pLI 0.51) — some intolerance to loss-of-function variants.
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ClinVar Variants
56 unique Pathogenic / Likely Pathogenic· 31 VUS of 106 total submissions
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Clinical Trials
5 active or recruiting trials — potential therapeutic options may be available
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GeneReview available — HTR2A
Authoritative clinical overview · Recommended first read
Open GeneReview ↗

Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

Moderate LoF intolerance
LoF Constraint
0.52LOEUF
pLI 0.511
Z-score 2.86
OE 0.20 (0.090.52)
Moderately constrained

More LoF-intolerant than ~75% of genes

Missense Constraint
1.75Z-score
OE missense 0.69 (0.610.78)
177 obs / 255.7 exp
Tolerant

Mild missense constraint

Observed / Expected Ratios
LoF OE0.20 (0.090.52)
00.351.4
Missense OE0.69 (0.610.78)
00.61.4
Synonymous OE1.02
01.21.6
LoF obs/exp: 3 / 14.9Missense obs/exp: 177 / 255.7Syn Z: -0.15
DN
0.7036th %ile
GOF
0.78top 25%
LOF
0.3941th %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

106 submitted variants in ClinVar

Classification Summary

Pathogenic55
Likely Pathogenic1
VUS31
Likely Benign10
Benign4
55
Pathogenic
1
Likely Pathogenic
31
VUS
10
Likely Benign
4
Benign

Curated Variants Distribution

Classified variants from ClinVar · 5 ACMG categories

ClassificationLoFMissense + InframeNon-codingSynonymousTotal
Pathogenic
0
0
55
0
55
Likely Pathogenic
0
0
1
0
1
VUS
1
27
3
0
31
Likely Benign
0
1
1
8
10
Benign
0
0
2
2
4
Total1286210101

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

View in ClinVar →

Protein Context — Lollipop Plot

HTR2A · 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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