Akdeniz, Esra Şahin

Profile URL
https://hdl.handle.net/11147/16311
Name Variants
Şahin Akdeniz, Esra
Akdeniz, Esra Sahin
Sahin Akdeniz, Esra
Job Title
Email Address
esrasahin@iyte.edu.tr
Main Affiliation
04.03. Department of Molecular Biology and Genetics
Status
Current Staff
Website
ORCID ID
0000-0003-2795-9652
Scopus Author ID
20436778100
Turkish CoHE Profile ID
CF1D327835B63A66
Google Scholar ID
xU71gHUAAAAJ
WoS Researcher ID
AHB-9054-2022

Sustainable Development Goals

SDG data is not available
Documents

6

Citations

97

h-index

5

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Documents

4

Citations

29

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Scholarly Output

2

Articles

2

Views / Downloads

10722/257

Supervised MSc Theses

0

Supervised PhD Theses

0

WoS Citation Count

13

Scopus Citation Count

15

Patents

0

Projects

0

WoS Citations per Publication

6.50

Scopus Citations per Publication

7.50

Open Access Source

1

Supervised Theses

0

JournalCount
Antimicrobial Agents and Chemotherapy1
Journal of Molecular Modeling1
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2019 - 201912020 - 20221

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Scholarly Output Search Results

Now showing 1 - 2 of 2
  • Article
    Citation - WoS: 6
    Citation - Scopus: 6
    Investigation of Interactions of Doxorubicin With Purine Nucleobases by Molecular Modeling
    (Springer, 2022) Akdeniz, Esra Şahin; Selçuki, Cenk
    Doxorubicin, an anthracycline antibiotic with anti-tumor activity, is produced by the bacterium Streptomyces peucetius. The interactions between doxorubicin and genetic material and the details of the intercalation with DNA have been controversial issues. Thus, the interactions of doxorubicin with purine nucleobases were studied by quantum mechanical methods. Initially, conformer analyses of doxorubicin were performed with Spartan 08 software and 319 different conformers from 422 initial structures for doxorubicin were obtained. Geometry optimizations and frequency analyses were performed for each structure using density functional theory (DFT) at B3LYP/6-31G** level using Gaussian 09 software. The most stable 20 conformers of doxorubicin and tautomers of purine nucleobases were optimized again with ɷB97XD/6-31G** level and their interactions were also analyzed at the same level. The Discovery Studio 3.5 Visualizer was used to draw the initial and optimized structures of investigated geometries. The noncovalent interactions (NCIs) were visualized by calculating reduced density gradient (RDG) with Multiwfn program. The color-filled isosurfaces and RDG scatter maps of most stable interaction geometries were plotted by Visual Molecular Dynamics (VMD) software and Gnuplot 5.3 software, respectively. This study showed that adenine, guanine, and hypoxanthine nucleobases interact with doxorubicin by forming strong hydrogen bonds and π-π interactions. Considering the normal cellular conditions, the effect of solvent (water) on the interaction geometries were also analyzed and when compared to gas phase it was determined that the movements of the molecules were restricted and there was a minimal change between initial and optimized structures in the aqueous phase.
  • Article
    Citation - WoS: 7
    Citation - Scopus: 9
    Genomewide Elucidation of Drug Resistance Mechanisms for Systemically Used Antifungal Drugs Amphotericin B, Caspofungin, and Voriconazole in the Budding Yeast
    (American Society for Microbiology, 2019) Balkan, Çiğdem; Ercan, İlkcan; Işık, Esin; Akdeniz, Esra Şahin; Balcıoğlu, Orhan; Kodedova, Marie; Koç, Ahmet
    There are only a few antifungal drugs used systemically in treatment, and invasive fungal infections that are resistant to these drugs are an emerging problem in health care. In this study, we performed a high-copy-number genomic DNA (gDNA) library screening to find and characterize genes that reduce susceptibility to amphotericin B, caspofungin, and voriconazole in Saccharomyces cerevisiae. We identified the PDR16 and PMP3 genes for amphotericin B, the RMD9 and SWH1 genes for caspofungin, and the MRS3 and TRI1 genes for voriconazole. The deletion mutants for PDR16 and PMP3 were drug susceptible, but the other mutants had no apparent susceptibility. Quantitative-PCR analyses suggested that the corresponding drugs upregulated expression of the PDR16, PMP3, SWH1, and MRS3 genes. To further characterize these genes, we also profiled the global expression patterns of the cells after treatment with the antifungals and determined the genes and paths that were up-or downregulated. We also cloned Candida albicans homologs of the PDR16, PMP3, MRS3, and TRI1 genes and expressed them in S. cerevisiae. Heterologous expression of Candida homologs also provided reduced drug susceptibility to the budding yeast cells. Our analyses suggest the involvement of new genes in antifungal drug resistance.