Hatice Humeyra Yavuz Gokce
Department of Molecular Medicine, Aziz Sancar Institute of Experimental Medicine, Istanbul University, Istanbul, Turkey.
Selcuk Dasdemir
Department of Medical Biology, Faculty of Medicine, Istanbul University, Istanbul, Turkey.
Cem Ismail Kucukali
Department of Neuroscience, Aziz Sancar Institute of Experimental Medicine, Istanbul University, Istanbul, Turkey.
Elif Sinem Iplik
Department of Biochemistry, Faculty of Pharmacy, Istanbul Yeni Yuzyil University, Istanbul, Turkey.
Bedia Cakmakoglu
Department of Molecular Medicine, Aziz Sancar Institute of Experimental Medicine, Istanbul University, Istanbul, Turkey.
Abstract:
Background: Various studies demonstrating enhanced vulnerability to apoptosis may contribute to the pathobiology of schizophrenia. Objective: Thus, G proteins may provide an intriguing link between the signal transduction, and apoptotic hypotheses of schizophrenia. In the light of these findings, we investigated whether G protein gene polymorphisms (GNAS1-T393C and GNB3-C825T) accounted for an increased risk of schizophrenia.Methods: The present analyses were based on 100 subjects diagnosed with schizophrenia, and on 100 unrelated healthy controls. The genotyping of GNAS1-T393C, and GNB3-C825T gene polymorphisms were performed using the polymerase chain reaction – restriction fragment length polymorphism (PCR-RFLP). Results: We demonstrated the positive association of GNB3-C825T gene variants with schizophrenia risk (p: 0.023). In our study, more prevalent CC genotype frequencies were detected in GNB3 in patients compared with the frequencies in the controls. The individuals with GNB3-C825T CC genotype had 2 fold increased risk for schizophrenia (p: 0.011, χ2: 6.39, OR:2.14, 95% CI: 1.18-3.90). Discussion: Our study results suggested that GNB3-C825T polymorphism might be associated with schizophrenia.
Keywords:G protein, GNB3, GNAS1, schizophrenia, polymorphisms.