Rabbit anti-Glutathione-S-Transferase Polyclonal antibody

Objective Copy number variants (CNVs) could explain a part of the missing heritability in rheumatoid arthritis (RA). Our goal is to investigate the association of RA with CNVs of three functional candidate genes, Glutathione S-transferase M1 (GSTM1), Glutathione S-transferase T1 (GSTT1) and Fc gamma receptor type IIIAB (FCGR3B). Methods We quantified the absolute copy number of GSTM1, GSTT1 and FCGR3B genes using droplet digital PCR. Transmission of copy number alleles was investigated in trio families with RA using family-based association tests ( Transmission Disequilibrium Test and Genotype Haplotype Relative Risk). Clinical, environmental and biological data on RA patients were also used to stratify patients sample in analysis. Results Copy numbers from zero to three were identified. Genotype combinations characterised in 182 trios allowed testing the association with RA. Genotypes without null allele of FCGR3B gene were significantly associated with RA (3.41x10(-7)). Three copy numbers of this gene is observed only in cases of RA (n=14) and a protective effect of null allele was characterised (OR=0.3 (0.17-0.53)). Conclusion CNVs in FCGR3B are associated with RA in our set of samples. This gene may play a role in physiopathology of this disease.

Background: The role of oxidative stress has been identified in the development of autism spectrum disorder (ASD), and polymorphisms of glutathione S-transferase have been associated with some diseases linked to oxidative stress. Hence, we evaluated the serum levels of oxidative stress markers and investigated genetic polymorphisms of glutathione S-transferase associated with autism. Materials and Methods: Forty-two children clinically diagnosed with ASD using the Diagnostic and Statistical Manual for Mental Disorders (DSM-5) criteria and a clinical interview were included in the study. Twenty-three age-matched controls without any known genetic/developmental disorder were also recruited. Oxidative stress markers along with the genetic polymorphisms of glutathione S-transferase were determined. Results: Reduced glutathione in ASD patients was significantly lower than the control (P = 0.008), whereas other oxidative stress markers measured were not significantly different in both the control and case populations. The frequencies of GSTT1 and GSTM1 null genotypes were lower among the controls compared with the cases, however, no association risk was observed. The observed risk of carrying Val/Val genotype among the cases was approximately six times that of the controls. Conclusion: Individuals with ASD showed a significant diminished level of reduced glutathione, however, the distribution of GSTT1, GSTM1, and GSTP1 polymorphisms was not found to be associated with autism in this study population.