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Elif Damla Arisan
Researcher at Gebze Institute of Technology
Publications - 92
Citations - 1019
Elif Damla Arisan is an academic researcher from Gebze Institute of Technology. The author has contributed to research in topics: Apoptosis & Autophagy. The author has an hindex of 15, co-authored 77 publications receiving 706 citations. Previous affiliations of Elif Damla Arisan include Istanbul Kültür University & Sabancı University.
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The Prediction of miRNAs in SARS-CoV-2 Genomes: hsa-miR Databases Identify 7 Key miRs Linked to Host Responses and Virus Pathogenicity-Related KEGG Pathways Significant for Comorbidities.
Elif Damla Arisan,Alwyn Dart,Guy H. Grant,Serdar Arisan,Songul Cuhadaroglu,Sigrun Lange,Pinar Uysal-Onganer +6 more
TL;DR: KEGG pathway analysis revealed a number of critical pathways linked to the seven identified miRs that may provide insight into the interplay between the virus and comorbidities, and miRNAs may constitute potential and effective therapeutic approaches in COVID-19 and its pathological consequences.
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Inhibition of PI3K signaling triggered apoptotic potential of curcumin which is hindered by Bcl-2 through activation of autophagy in MCF-7 cells
Yunus Akkoc,Özge Berrak,Elif Damla Arisan,Pinar Obakan,Ajda Coker-Gurkan,Narcin Palavan-Unsal +5 more
TL;DR: The hypothesis that blocking the PI3K/Akt pathway may further increasedCurcumin-induced apoptosis and overcome forced Bcl-2 expression level mediated autophagic responses against curcumin treatment in MCF-7 cells is supported.
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The inhibition of PI3K and NFκB promoted curcumin-induced cell cycle arrest at G2/M via altering polyamine metabolism in Bcl-2 overexpressing MCF-7 breast cancer cells
Özge Berrak,Yunus Akkoc,Elif Damla Arisan,Ajda Coker-Gurkan,Pınar Obakan-Yerlikaya,Narcin Palavan-Unsal +5 more
TL;DR: The results indicated that curcumin induced cell cycle arrest at G2/M phase by downregulation of cyclin B1 and Cdc2 and inhibited colony formation in MCF-7wt cells, but Bcl-2 overexpression prevented the inhibition of cell cycle associated proteins afterCurcumin treatment.
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Small inhibitor of Bcl-2, HA14-1, selectively enhanced the apoptotic effect of cisplatin by modulating Bcl-2 family members in MDA-MB-231 breast cancer cells
TL;DR: The results suggest that the potentiating effect of HA14-1 is drug and cell type specific and may not only depend on the inhibition of Bcl-2, and alteration of other pro-APoptotic or anti-apoptotic B cl-2 family members may dictate the apoptotic response when HA14 -1 is combined with chemotherapeutic drugs.
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Cisplatin overcomes Bcl-2-mediated resistance to apoptosis via preferential engagement of Bak: critical role of Noxa-mediated lipid peroxidation
TL;DR: It is shown that cisplatin triggers a Bak-dependent pathway to induce apoptosis in Bcl-2-overexpressing MCF-7 cells, which requires preferential activation of Bak and p53-mediated upregulation of Noxa protein levels and lipid peroxidation.