Scopus İndeksli Yayınlar Koleksiyonu / Scopus Indexed Publications Collection

Permanent URI for this collectionhttps://hdl.handle.net/11147/7148

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  • Article
    Citation - WoS: 11
    Citation - Scopus: 10
    Redefining methods for augmenting lactic acid bacteria robustness and phenyllactic acid biocatalysis: Integration valorizes simplicity
    (Taylor & Francis, 2022) Meruvu, Haritha
    The production of phenyllactic acid (PLA) has been reported by several researchers, but so far, no mention has been made of augmented PLA production using an orchestrated assembly of simple techniques integrated to improve lactic acid bacteria (LAB) metabolism for the same. This review summarizes sequentially tailoring LAB growth and metabolism for augmented PLA catalysis through several strategies like monitoring LAB sustenance by choosing appropriate starter PLA-producing LAB strains isolated from natural environments, with desirably fastidious growth rates, properties like acidification, proteolysis, bacteriophage-resistance, aromatic/texturing-features, etc.; entrapping chosen LAB strains in novel cryogels and/or co-cultivating two/more LAB strains to improve their biotransformation potential and promote growth dependency/sustainability; adopting adaptive evolution methods designed to improve LAB strains under selection pressure inducing desired phenotypes tolerant to stress factors like heat, salt, acid, and solvent; monitoring physico-chemical LAB fermentation factors like temperature, pH, dissolved oxygen content, enzymes, and cofactors for PLA biosynthesis; and modulating purification/downstream processes to extract substantial PLA yields. This review paper serves as a comprehensive preliminary guide that can evoke a strategic experimental plan to produce industrial-scale PLA yields using simple techniques orchestrated together in the pursuit of conserving time, effort, and resources.
  • Data Paper
    Knockdown of Death Receptor 5 Antisense Long Noncoding Rna and Cisplatin Treatment Modulate Similar Macromolecular and Metabolic Changes in Hela Cells
    (TÜBİTAK - Türkiye Bilimsel ve Teknolojik Araştırma Kurumu, 2022) Gürer, Dilek Cansu; Erdoğan Vatansever, İpek; Ceylan, Çağatay; 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 ametabolic changes in HeLa cervix cancer cells.