TR-Dizin

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Cytoplasmically localized tRNA-derived fragments inhibit translation in Drosophila S2 cells
(TUBITAK, 2022) Hamid,S.M.; Akgül,B.; Akgül, Bünyamin; Moleküler Biyoloji ve Genetik Bölümü; Moleküler Biyoloji ve Genetik Bölümü
Transfer ribonucleic acids (tRNAs) serve not only as amino acid carriers during translation but also as a template for the biogenesis of short fragments that can regulate gene expression. Despite recent progress in the function of tRNA-derived fragments (tRFs), their intracellular localization, protein partners, and role in regulating translation are not well understood. We used synthetic tRFs to investigate their localization and function in Drosophila S2 cells. Under our experimental setting, all synthetic tRFs tested were localized at distinct sites within the cytoplasm in a similar manner in Drosophila S2 cells. Cytoplasmically-localized tRFs were positioned in close proximity to GW182 and XRN1 proteins. Functionally, tRFs, which slightly suppressed proliferation in S2 cells, inhibited translation without any major shift in the polysome profile. These results suggest that 5’-tRFs are cytoplasmically-localized and regulate gene expression through inhibition of translation in Drosophila. © TÜBİTAK.
Endogenous heat shock protein GroEL of A. actinomycetemcomitans preferentially targets primary human CD8+ T cells
(2015) Aldanmaz Nalbant, AYTEN; Akgül, Bünyamin; Akgül, Bünyamin; Kant, Melis
Apoptosis can be used to manipulate host cells by bacterial products such as bacterial heat shock proteins (Hsp). One of the virulence factors of periodontal pathogen Aggregatibacter actinomycetemcomitans is heat shock protein GroEL (AaGroEL), which has been shown to interact with host cells. AaGroEL (Hsp64) also has the potential to modulate immune system cells. In this study we used endogenous AaGroEL protein as an antigen to study bacterial Hsp-induced apoptosis in different immune system cells. Human peripheral blood mononuclear cells and cell lines were cultured with different doses (50-1000 ng/mL) of endogenous AaGroEL at various time points. Apoptosis of the cells was measured by Annexin V and 7AAD labeling. Apoptotic cells were analyzed by flow cytometry. Our data suggested that AaGroEL-responding primary CD8+ T cells were more susceptible to apoptosis than CD4+ T cells. Furthermore, the magnitude of apoptosis in the Jurkat T cell line was higher than that in primary CD8+ T cells. There was no statistically significant level of apoptosis in the chronic myeloid leukemia (K562) cell line, which belongs to myeloid lineages. Thus, A. actinomycetemcomitans GroEL protein has more potent apoptotic effect on cells that are derived from a lymphoid progenitor.
Citation - WoS: 0
Citation - Scopus: 0
Knockdown of death receptor 5 antisense long noncoding RNA and cisplatin treatment modulate similar macromolecular and metabolic changes in HeLa cells
(Tubitak Scientific & Technological Research Council Turkey, 2022) Gurer, Dilek Cansu; Erdogan Vatansever, Ipek; Ceylan, Cagatay; Akgul, Bunyamin; Akgül, Bünyamin
Background/aim: Despite great progress in complex gene regulatory mechanisms in the dynamic tumor microenvironment, the potential contribution of long noncoding RNAs (lncRNAs) to cancer cell metabolism is poorly understood. Death receptor 5 antisense (DR5-AS) is a cisplatin inducible lncRNA whose knockdown modulates cell morphology. However, its effect on cell metabolism is unknown. The aim of this study is to examine metabolic changes modulated by cisplatin and DR5-AS lncRNA in HeLa cells.Materials and methods: We used cisplatin as a universal cancer therapeutic drug to modulate metabolic changes in HeLa cervix cancer cells. We then examined the extent of metabolic changes by Fourier transform infrared spectroscopy (FTIR). We also performed transcriptomics analyses by generating new RNA-seq data with total RNAs isolated from cisplatin-treated HeLa cells. Then, we compared cisplatin-mediated transcriptomics and macromolecular changes with those mediated by DR5-AS knockdown.Results: Cisplatin treatment caused changes in the unsaturated fatty acid and lipid-to-protein ratios and the glycogen content. These observations in altered cellular metabolism were supported by transcriptomics analyses. FTIR spectroscopy analyses have revealed that DR5-AS knockdown causes a 20.9% elevation in the lipid/protein ratio and a 76.6% decrease in lipid peroxidation. Furthermore, we detected a 3.42% increase in the chain length of the aliphatic lipids, a higher content of RNA, and a lower amount of glycogen indicating relatively lower metabolic activity in the DR5-AS knockdown HeLa cells. Interestingly, we observed a similar gene expression pattern under cisplatin treatment and DR5-AS knockdown HeLa cells. Conclusion: These results suggest that DR5-AS lncRNA appears to account for a fraction of cisplatin-mediated macromolecular and metabolic changes in HeLa cervix cancer cells.
Citation - WoS: 9
Citation - Scopus: 9
Noncoding RNAs in apoptosis: identification and function
(Tubitak Scientific & Technological Research Council Turkey, 2022) Tuncel, Ozge; Kara, Merve; Yaylak, Bilge; Erdogan, Ipek; Akgul, Bunyamin; Akgül, Bünyamin
Apoptosis is a vital cellular process that is critical for the maintenance of homeostasis in health and disease. The derailment of apoptotic mechanisms has severe consequences such as abnormal development, cancer, and neurodegenerative diseases. Thus, there exist complex regulatory mechanisms in eukaryotes to preserve the balance between cell growth and cell death. Initially, protein coding genes were prioritized in the search for such regulatory macromolecules involved in the regulation of apoptosis. However, recent genome annotations and transcriptomics studies have uncovered a plethora of regulatory noncoding RNAs that have the ability to modulate not only apoptosis but also many other biochemical processes in eukaryotes. In this review article, we will cover a brief summary of apoptosis and detection methods followed by an extensive discussion on microRNAs, circular RNAs, and long noncoding RNAs in apoptosis.

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Browsing TR-Dizin by Author "Akgül, Bünyamin"