ACKR2

Chr 3

atypical chemokine receptor 2

Also known as: CCBP2, CCR10, CCR9, CMKBR9, D6, hD6

The protein is an atypical chemokine receptor that controls chemokine levels through high-affinity binding and sequestration rather than traditional signal transduction, playing an essential role in resolving inflammatory responses and regulating adaptive immunity. Mutations cause microcephaly, lymphedema, and chorioretinal dysplasia syndrome, which is inherited in an autosomal recessive pattern. The gene shows low constraint against loss-of-function variants, consistent with the recessive inheritance pattern of the associated disorder.

OMIMResearchSummary from RefSeq, UniProt
MultiplemechanismLOEUF 1.47
Clinical SummaryACKR2
Population Constraint (gnomAD)
Low constraint (pLI 0.00) — loss-of-function variants are relatively tolerated in the population.
📋
ClinVar Variants
7 unique Pathogenic / Likely Pathogenic· 9 VUS of 21 total submissions

Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

Tolerant — LoF & missense variants common in population
LoF Constraint
1.47LOEUF
pLI 0.001
Z-score 0.71
OE 0.71 (0.371.47)
Tolerant

Highly tolerant — LoF variants common in population

Missense Constraint
0.26Z-score
OE missense 0.95 (0.851.07)
205 obs / 215.9 exp
Tolerant

Mild missense constraint

Observed / Expected Ratios
LoF OE0.71 (0.371.47)
00.351.4
Missense OE0.95 (0.851.07)
00.61.4
Synonymous OE1.00
01.21.6
LoF obs/exp: 5 / 7.0Missense obs/exp: 205 / 215.9Syn Z: -0.01
DN
0.81top 10%
GOF
0.77top 25%
LOF
0.1993th %ile

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

DNprediction above median
GOFprediction 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

21 submitted variants in ClinVar

Classification Summary

Pathogenic6
Likely Pathogenic1
VUS9
6
Pathogenic
1
Likely Pathogenic
9
VUS

Curated Variants Distribution

Classified variants from ClinVar · 5 ACMG categories

ClassificationLoFMissense + InframeNon-codingSynonymousTotal
Pathogenic
0
0
6
0
6
Likely Pathogenic
0
0
1
0
1
VUS
0
8
1
0
9
Likely Benign
0
0
0
0
0
Benign
0
0
0
0
0
Total088016

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

View in ClinVar →

Protein Context — Lollipop Plot

ACKR2 · protein map & ClinVar variants

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

3D Protein StructureAlphaFold

Clinical Trials

Active and recruiting trials from ClinicalTrials.gov

No active trials found for this gene.

Search ClinicalTrials.gov →
Clinical Literature
Open Research Assistant →
Full-Text Mentions
NLP-detected gene mentions in article bodies · via PubTator3
PubTator3
Top 5 full-text resultsSearch PubTator3 ↗