Background: Type of 1 diabetes (T1D) is an autoimmune disease in which the cells of immune system attack the β-cells of pancreas. Consequently, destroyed β-cells do not produce insulin to reduce blood sugar levels. This disease is very complex, the pathogenesis is contributed by both genetic factors and environmental factors. In recent years, the number of individuals with T1D is increasing worldwide. Aims: The aim of this thesis was to investigate whether it is possible to predict T1D based on the expression profile of BACH2, CDC20, IGLL3P, EIF3A and TXNDC5 genes , which are involved in the development of immune system cells and insulin production. Another aim was to compare the expression of selected genes in children, in which the first detection of the disease may be done, and adults who suffer from prolonged T1D. The final goal was to compare the expression of individual selected genes in the HLA risk alleles DR04, DR03, DQA*05:01 a DQB*03:02. Methods: The DNA and RNA of patients with T1D and healthy individuals was isolated from blood. DNA was used to HLA genotyped. Isolated RNA was reverse transcribed into cDNA and then used in real-time PCR to determine the relative levels of gene expression. Conclusion: Significant results were obtained when the expression of BACH2, CDC20 and TXNDC5 genes...

Indiana University-Purdue University Indianapolis (IUPUI) / Translation Initiation in protein synthesis is a crucial step controlling gene expression that enhanced by eukaryotic translation initiation factors (eIFs). eIF3a, the largest subunit of eIF3 complexes, has been shown to regulate protein synthesis and cellular response to cisplatin treatment. Its expression has also been shown to negatively associate with prognosis. In this study, we tested a hypothesis that eIF3a regulates synthesis of proteins important for repair of double strand DNA breaks induced by ionizing radiation (IR). We found that eIF3a up-regulation sensitizes cellular response to IR while its knockdown causes resistance to IR. We also found that eIF3a over-expression increases IR-induced DNA damage and decreases Non-Homologous End Joining (NHEJ) activity by suppressing expression level of NHEJ repair proteins such as DNA-PKcs and vice versa. Together, we conclude that eIF3a plays an important role in cellular response to DNA-damaging treatments by regulating synthesis of DNA repair proteins and, thus, eIIF3a likely plays an important role in the outcome of cancer patients treated with DNA-damaging strategies including ionizing radiation.