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GNB3G-Protein Beta3 Subunit
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[sup][12],[13] One commonly studied candidate gene for EH is G-protein [sz]-polypeptide 3 gene ( GNB3 ).
Genotyping of the GNB3 C825T polymorphism was performed using method of polymerase chain reaction-restriction fragment length polymorphism (PCR).
The aim of the present study was to verify whether, at A population level, the C825T polymorphism of the GNB3 influenced the response to neuropsychological tests.
Continuous variables were expressed as mean [+ or -] standard deviation and compared between groups with analysis of covariance; 95% confidence intervals were also shown for unadjusted values of the score of the neuropsychological tests across the C825T polymorphism of GNB3 gene.
The C-allele (64.1%; OR: 2.41 [95% CI: 1.58-3.68]) and CC-genotype (37.4%; OR: 72.38 [95% CI: 4.40-1190.34]) of C825T polymorphism of the GNB3 gene occurred more often in hypertensive patients than in controls.
A significantly higher frequency of the GNB3 T allele has also been reported in three independent studies in subjects with EH using unselected normotensive control subjects of European origin (Benjafield et.
Genotype distribution of GNB3 in the Patients group was not consistent with Hardy-Weinberg equilibrium (p<0.05) because of an observed increase in heterozygotes (124 vs.
In present study, we investigated the association between a GNB3 825T/C polymorphism and essential hypertension in a Turkish population.
A few of the loci were out of Hardy-Weinberg equilibrium, including GRK4 A142V (P = 0.04) and GNB3 (P = 0.04) in the low-renin population and PAI-1 (P = 0.01) and ADD (P = 0.05) in the normal-renin population.
However, the difference in GNB3 was determined to have a solid effect on how patients reacted to the diuretic.
C825T polymorphism of the gene encodes the B3 subunit of G protein (GNB3) and causes the increased intracellular signal transduction.
The GNB3 C825T polymorphism was diagnosed by restriction of the PCR amplicon with BseDI (MBI Fermentas).