rs1800888

This is a variant in the ADRB2 gene that changes a threonine to an isoleucine.

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GWAS Catalog Trait Associations (7)

Genome-wide significant associations (p < 5×10⁻⁸) from the NHGRI-EBI GWAS Catalog.

FEV/FVC ratio

Shrine N et al. “Multi-ancestry genome-wide association analyses improve resolution of genes and pathways influencing lung function and chronic obstructive pulmonary disease risk.” Nature Genetics 55(3):410-422 (2023)
Allele T
OR 10.91
p 1.0e-27
N 588,452
Large GWAS
multi-ancestry
Loya H et al. “A scalable variational inference approach for increased mixed-model association power.” Nature Genetics 57(2):461-468 (2025)
Allele T
OR 0.09
p 2.0e-27
N 394,642
Large GWAS
European
Shrine N et al. “New genetic signals for lung function highlight pathways and chronic obstructive pulmonary disease associations across multiple ancestries.” Nature Genetics 51(3):481-493 (2019)
Allele T
OR 0.11
p 2.0e-27
N 321,047
Large GWAS
European

forced expiratory volume

Shrine N et al. “New genetic signals for lung function highlight pathways and chronic obstructive pulmonary disease associations across multiple ancestries.” Nature Genetics 51(3):481-493 (2019)
Allele T
OR 0.08
p 6.0e-18
N 321,047
Large GWAS
European
Loya H et al. “A scalable variational inference approach for increased mixed-model association power.” Nature Genetics 57(2):461-468 (2025)
Allele T
OR 0.06
p 6.0e-15
N 394,642
Large GWAS
European
Schoeler T et al. “Combining cross-sectional and longitudinal genomic approaches to identify determinants of cognitive and physical decline.” Nature Communications 16(1):4524 (2025)
Allele T
OR 0.05
p 2.0e-11
N 373,397
Large GWAS
European

chronic obstructive pulmonary disease

Moll M et al. “A systematic analysis of protein-altering exonic variants in chronic obstructive pulmonary disease.” American Journal of Physiology. Lung Cellular and Molecular Physiology 321(1):L130-L143 (2021)
Allele T
OR 1.32
p 9.0e-13
N 251,091
Large GWAS
multi-ancestry

eosinophil percentage of leukocytes

Vuckovic D et al. “The Polygenic and Monogenic Basis of Blood Traits and Diseases.” Cell 182(5):1214-1231.e11 (2020)
Allele T
OR 0.06
p 1.0e-9
N 408,112
Large GWAS
European

diastolic blood pressure

Koskeridis F et al. “Multi-trait association analysis reveals shared genetic loci between Alzheimer's disease and cardiovascular traits.” Nature Communications 15(1):9827 (2024)
Allele T
OR 0.04
p 1.0e-8
N 1,212,859
Large GWAS
European
Keaton JM et al. “Genome-wide analysis in over 1 million individuals of European ancestry yields improved polygenic risk scores for blood pressure traits.” Nature Genetics 56(5):778-791 (2024)
Allele T
OR 0.36
p 3.0e-8
N 1,028,980
Large GWAS
multi-ancestry

health trait

Schoeler T et al. “Combining cross-sectional and longitudinal genomic approaches to identify determinants of cognitive and physical decline.” Nature Communications 16(1):4524 (2025)
Allele C
OR 0.02
p 2.0e-8
N 405,979
Large GWAS
European
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ClinVar annotation

Drug Response★☆☆☆
2 submitters2 publications

Beta-2-adrenoreceptor agonist, reduced response to

View on ClinVar →
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Research that mentions this SNP (2)

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Genetic variation in the beta‐2 adrenergic receptor is associated with chronic musculoskeletal complaints in adolescents
AssociationN=1,004Skouen JS et al.(2012)· European Journal of Pain

This candidate gene association study examined 14 SNPs in ADRB2 and COMT genes in 1,004 Western Australian adolescents (age 17) to identify genetic variants associated with chronic musculoskeletal complaints. Of the SNPs tested, only rs2053044 in ADRB2 (recessive model) showed association with chronic disabling neck and low back pain (OR = 2.49; 95% CI = 1.25-4.98; p = 0.01) and pain in 3-4 body areas (OR = 1.86; 95% CI = 1.13-3.06; p = 0.02). The findings suggest that genetic variants in ADRB2 may be involved in regulating chronic musculoskeletal pain in adolescents.

Traits studied:Chronic disabling neck and low back painChronic musculoskeletal complaintsChronic widespread painNumber of pain areasPain in 3-4 body areas
PubMedDOIMetascience Observatory
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Three major haplotypes of the β2 adrenergic receptor define psychological profile, blood pressure, and the risk for development of a common musculoskeletal pain disorder
AssociationN=202Luda Diatchenko et al.(2006)· American Journal of Medical Genetics Part B: Neuropsychiatric Genetics

Study of 202 female subjects examining ADRB2 haplotypes defined by 8 SNPs and their associations with psychological traits, resting blood pressure, and temporomandibular disorder (TMD) risk. Three major haplotypes (H1, H2, H3) were identified representing 97.4% of variants. Heterozygotes carrying one H1 haplotype showed protective effects: highest positive psychological traits, higher resting blood pressure, and ~10-fold lower TMD risk (1.3% incidence vs 20% in H2/H2 homozygotes; RR=8.0-11.3 for homozygotes vs heterozygotes).

Traits studied:AnxietyBlood pressureDepressionPsychological traitsSomatizationTemporomandibular disorder
PubMedDOIMetascience Observatory

About ADRB2

This gene encodes beta-2-adrenergic receptor which is a member of the G protein-coupled receptor superfamily. This receptor is directly associated with one of its ultimate effectors, the class C L-type calcium channel Ca(V)1.2. This receptor-channel complex also contains a G protein, an adenylyl cyclase, cAMP-dependent kinase, and the counterbalancing phosphatase, PP2A. The assembly of the signaling complex provides a mechanism that ensures specific and rapid signaling by this G protein-coupled receptor. This receptor is also a transcription regulator of the alpha-synuclein gene, and together, both genes are believed to be associated with risk of Parkinson's Disease. This gene is intronless. Different polymorphic forms, point mutations, and/or downregulation of this gene are associated with nocturnal asthma, obesity, type 2 diabetes and cardiovascular disease. [provided by RefSeq, Oct 2019]

View all ADRB2 variants →

Gene information from NCBI Gene. Variant classifications from ClinVar.

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