Gene-gene interactions among ADRB2, ADRB3 and ADRA2A polymorphisms were analysed using non-parametric model-free method of reducing genotype combinations called multifactor dimensionality reduction (MDR) using he MDR software package (version 3.0.2, http://sourceforge.net) (Gui et al., 2013; Ritchie et al., 2001).
All investigated polymorphisms conformed to Hardy-Weinberg expectations ([chi square] = 0.92, p = 0.337; [chi square] = 2.36, p = 0.124; [chi square] = 2.31, p = 0.129; [chi square] = 0.17, p = 0.680, for Gly16Arg, Glu27Gln of the ADRB2, Trp64Arg of the ADRB3 and G1780A of the ADRA2A, respectively.
We conducted a random-effects meta-analysis of the association between ADRb2
polymorphism in asthmatic patients compared to the healthy control.
Quantitative RT-PCR (qPCR) was conducted to analyze expression of ADRB2
with a CFX-96 RT-PCR detection system (BioRad, Hercules, CA, USA).
The searches followed the following strategy: (salmeterol OR formoterol OR LABAs OR long-acting beta 2 agonists) AND (adrenergic receptor OR ADRB2
OR adrenoceptor beta 2) AND (polymorphism OR SNP* OR variant OR mutation) AND asthma.
No statistically significant differences were found in genotype distributions of the other five loci (MS4A2 E237G, MS4A2 C-109T, ADRB2
R16G, IL4RA I75V, and IL4 C-590T) between the two groups (P>0.05).
With the use of 3 noncontinuous probes, 46/79-GG in the ADRB2
receptor and HbCmatch and HbEmatch in the HBB gene (Table 1), on templates with a variant within the template bulge, we observed Tm shifts compared to WT templates (Fig.
Here, we provide evidence to demonstrate that augmented Ang II affects EPC bioactivities and ADRB2
expression in EPCs.
The beta-2 adrenergic receptor (ADRB2
) affects cardiac autonomic function and the development of heart failure (Triposkiadis et al.
The SNP genotypes were determined by probe-extension reactions using two probes with different base sequences at their 3' termini: rs1042718 on the ADRB2
gene (5'-CCC ATT CAG ATG CAC TGG TTC N-3', where N = A or C); rs3918242 on the gelatinase B gene (5'-CTC CCG AGT AGC TGG TAT TAT AGA CN-3', where N = G or A); rs1346044 on the WRN (5'-CTC CTT TTG TTG ACA TCT CN-3', where N = A or G); and rs1801133 on the MTHFR gene (5'-CTT GAA GGA GAA GGT GTC TGC GGG TGN-3', where N = C or T).
We examined asthma prevalence and evaluated polymorphisms in genes involved in oxidative stress pathways [gluthatione S-transferases M1 (GSTM1), T1 (GSTT1), and P1 (GSTP1) and NAD(P)H:quinine oxidoreductase (NQO1)], inflammatory response [tumor necrosis factor [alpha] (TNFA)], immunologic response [Toll-like receptor 4 (TLR4)], and airway reactivity [adrenergic receptor [beta]2 (ADRB2
A total of 15 primer pairs were tested for amplification and sequencing of 13 candidate genes (PTH, CSF2, FOLR1, BDNF, LDHA, RPS13, ADM, CAT, WT1, FSHB, MYOD1, IL4 and ADRB2
The [[beta].sub.2]-adrenergic receptor (ADRB2
) is a GTP-binding-protein-coupled receptor produced by a wide variety of cell types.
OBJECTIVE: Our goal was to assess interactions between exposure to air pollution and single nucleotide polymorphisms (SNPs) in the [beta] 2-adrenergic receptor (ADRB2
), glutathione S-transferase P1 (GSTP1), and tumor necrosis factor (TNF) genes for development of childhood allergic disease.
NaI increased [beta]-adrenergic receptor (Adrb2
) gene expression in a dose-dependent manner, whereas PB and PTU increased 0q-adrenergic receptor (Adra1d) gene expression.