Genetic polymorphisms of the beta 2-adrenergic receptor in nocturnal and nonnocturnal asthma. Evidence that Gly16 correlates with the nocturnal phenotype.

Turki, Jamal; Pak, Juno; Green, S A; Martin, Richard J.; Liggett, Stephen B.

doi:10.1172/jci117838

Cited by 371 publications

(213 citation statements)

References 27 publications

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“…31 These in vitro observations are consistent with many clinical studies examining potential roles of ␤ 2 AR polymorphisms in asthma. Some of these clinical studies have examined potential disease modifying effects, such as severity, 32 phenotype, 33,34 and physiologic parameters. 35 A few studies have examined pharmacogenetic relationships between these polymorphisms and the response to ␤-agonists.…”

Section: Pharmacogenetics Of ␤-Agonists In Asthmamentioning

confidence: 99%

The pharmacogenetics of asthma: a candidate gene approach

et al. 2001

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Section: Pharmacogenetics Of ␤-Agonists In Asthmamentioning

confidence: 99%

The pharmacogenetics of asthma: a candidate gene approach

et al. 2001

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“…Met 34, Thr?Ile 164). Three of these mutations (codon 16, 27 and 164) are functionally relevant, the ®rst two altering agonist induced downregulation of the receptor and the third altering ligand binding (Green et al, 1993;1995;Reishaus et al, 1993;Turki et al, 1995b). Control of human b 2 adrenergic receptor gene expression is regulated in part by the 5' anking region immediately upstream from the gene.…”

mentioning

confidence: 99%

Identification of novel polymorphisms within the promoter region of the human β₂ adrenergic receptor gene

Scott

Swan

Wheatley

et al. 1999

British J Pharmacology

107

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By screening the 1470 bp 5′ to the start codon of the human β2 adrenergic receptor gene, we have identified a total of eight polymorphisms (−20 T→C, −47 T→C, −367 T→C, −468 C→G, −654 G→A, −1023 G→A, −1343 A→G and −1429 T→A c.f. β2 adrenergic receptor start codon). Transient transfection of 5′ flanking deletion luciferase reporter constructs demonstrated the majority of activity of the human β2 adrenergic gene 5′ flanking region to be present within a 549 bp fragment immediately upstream from the start codon. Because of linkage disequilibrium, some combinations of polymorphisms were particularly frequent. We transiently transfected COS‐7 cells with luciferase constructs under the control of the 549 bp of 5′ flanking DNA containing the two most frequent extended haplotypes in this region. Luciferase activity was significantly reduced in cells transfected with the ‘mutant’ construct (−20C, −47C, −367C, −468G) c.f. the ‘wild‐type’ construct (−20T, −47T, −367T, −468C). These data suggest that polymorphisms have the potential to alter human β2 adrenergic receptor gene expression.British Journal of Pharmacology (1999) 126, 841–844; doi:10.1038/sj.bjp.0702385

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“…The ADRB2 polymorphism remains an area of focus stemming from initial links to asthma morbidity and mortality [19][20][21][22]. Associations with specific ADRB2 polymorphisms may predict response to long acting beta agonists (LABA), inhaled corticosteroids (ICS) and anticholinergics [23,24].…”

Section: Discussionmentioning

confidence: 99%

No Correlation between Beta2-Adrenergic Receptor Polymorphisms and the Severity and Clinical Control of Geriatric Asthma and COPD

Pham¹

2014

J Allergy Ther

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Background: Polymorphisms of the β2-adrenergic receptor (ADRB2) have previously been associated with non-specific bronchial hyper-responsiveness, adverse response to β2-agonists and variable effects on lung function. The objective of this study was to determine whether genotypic variance in ADRB2 polymorphisms in a cohort of geriatric men and women with asthma and/or COPD correlate with disease severity, baseline pulmonary function, and the ability to maintain clinical control of their disease.Methods: This comparative, prospective cohort study sequenced two ADRB2 polymorphisms, Arg16 --> Gly and Gln27 --> Glu, in 103 geriatric patients with a clinical history of asthma and/or COPD. Primary endpoints included pulmonary exacerbation rate, hospitalization rate, and quality of life scores.Results: Arg/Arg genotype comprised 13.6% of the cohort. No significant differences in baseline pulmonary functions were noted across genotypic variants. No significant difference was associated with genotype and change in lung function, exacerbations, clinical hospitalizations, exercise tolerance and subjective quality of life assessment over 6 months of follow-up. Conclusion:We conclude that in a geriatric asthma and/or COPD population, ADRB2 polymorphisms are not a factor in the ability to control disease.

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Genetic polymorphisms of the beta 2-adrenergic receptor in nocturnal and nonnocturnal asthma. Evidence that Gly16 correlates with the nocturnal phenotype.

Cited by 371 publications

References 27 publications

The pharmacogenetics of asthma: a candidate gene approach

The pharmacogenetics of asthma: a candidate gene approach

Identification of novel polymorphisms within the promoter region of the human β₂ adrenergic receptor gene

No Correlation between Beta2-Adrenergic Receptor Polymorphisms and the Severity and Clinical Control of Geriatric Asthma and COPD

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Genetic polymorphisms of the beta 2-adrenergic receptor in nocturnal and nonnocturnal asthma. Evidence that Gly16 correlates with the nocturnal phenotype.

Cited by 371 publications

References 27 publications

The pharmacogenetics of asthma: a candidate gene approach

The pharmacogenetics of asthma: a candidate gene approach

Identification of novel polymorphisms within the promoter region of the human β2 adrenergic receptor gene

No Correlation between Beta2-Adrenergic Receptor Polymorphisms and the Severity and Clinical Control of Geriatric Asthma and COPD

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Identification of novel polymorphisms within the promoter region of the human β₂ adrenergic receptor gene