Doğan, Hülya

Profile URL
https://hdl.handle.net/11147/15960
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Email Address
Main Affiliation
01. Izmir Institute of Technology
Status
Current Staff
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Scopus Author ID
Turkish CoHE Profile ID
Google Scholar ID
WoS Researcher ID

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Scholarly Output

3

Articles

1

Views / Downloads

3018/534

Supervised MSc Theses

1

Supervised PhD Theses

0

WoS Citation Count

29

Scopus Citation Count

19

Patents

0

Projects

0

WoS Citations per Publication

9.67

Scopus Citations per Publication

6.33

Open Access Source

1

Supervised Theses

1

JournalCount
European Journal of Cell Biology1
Handbook of Food Engineering1
Current Page: 1 / 1

Scopus Quartile Distribution

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Author of Publication: search.filters.isAuthorOfPublication.c7e5ce9a-9849-4ccf-95d6-a49d045aeb88

Scholarly Output Search Results

Now showing 1 - 3 of 3
  • Book Part
    Citation - WoS: 12
    Linear and Non-Linear Rheological Properties of Foods
    (Taylor & Francis, 2019) Doğan, Hülya; Doğan, Hülya; Çağlar Duvarcı, Özlem; Çağlar Duvarcı, Özlem; Doğan, Hülya; Kokini, Jozef L.; 03.02. Department of Chemical Engineering; 01. Izmir Institute of Technology; 03. Faculty of Engineering
    [No abstract available]
  • Master Thesis
    Role of Human Aprataxin Protein in P53-Related Cellular Processes in Breast Cells
    (01. Izmir Institute of Technology, 2021) Doğan, Hülya; Yalçın Özuysal, Özden; Yalçın Özuysal, Özden; Yalçın Özuysal, Özden; 01. Izmir Institute of Technology; 04.03. Department of Molecular Biology and Genetics; 04. Faculty of Science
    Aprataxin encoded by APTX, which is the human homolog of yeast HNT3, reverses adenylation damages emerged from abortive DNA ligation during ribonucleotide and base excision repair. Thus, it corrects AMP-modified nucleic acid termini and protects genome integrity as a DNA ligase "proofreader". Role of HNT3, which is a candidate p53-related gene, against DNA oxidative and alkylating damage indicates its antioxidant importance. Besides, previous studies demonstrated that absence of Aprataxin gives rise to ROS generation and oxidative stress in addition to mitochondrial dysfunction. Also, role of Aprataxin in drug and radiotherapy sensitivity was shown in many cancer. Since conformation of cysteine residues in p53 DNA-binding domain can be modified by oxidizing environment, functionality can be influenced by defective APTX. Although p53-Aprataxin interaction has been shown by co-immunoprecipitation, effects of APTX on p53 pathway were not studied. Aim of this study is to investigate Aprataxin-driven changes in p53-regulated processes in p53 wild-type cells through. According to results, Aprataxin overexpression leads to cell cycle arrest in low stress levels. However, it triggers cell death against induced stress in MCF10A cells. Moreover, apoptotic assay on MCF10A APTX Crispr cells indicated elevated level of basal cell death. Also, expression analysis of p53 targets in APTX knockdown MCF7 cells revealed that extrinsic apoptosis pathway might be induced. Consequently, these results help us to gain insight into how Aprataxin affects activity of p53 pathway. Further investigation providing stress accumulation based assays and protein level analysis is needed to figure out whether resulting changes are p53-dependent or not.
  • Article
    Citation - WoS: 17
    Citation - Scopus: 19
    Pro-Metastatic Functions of Notch Signaling Is Mediated by Cyr61 in Breast Cells
    (Elsevier, 2020) Küçükköse, Cansu; Yalçın Özuysal, Özden; Efe, Eda; Doğan, Hülya; Günyüz, Zehra Elif; Fıratlıgil Yıldırır, Burcu; Fıratlıgil, Burcu; Efe, Eda; Doğan, Hülya; Yalçın Özuysal, Özden; İlhan, Mustafa; 01. Izmir Institute of Technology; 04.03. Department of Molecular Biology and Genetics; 04. Faculty of Science
    Metastasis is the main cause of cancer related deaths, and unfolding the molecular mechanisms underlying metastatic progression is critical for the development of novel therapeutic approaches. Notch is one of the key signaling pathways involved in breast tumorigenesis and metastasis. Notch activation induces pro-metastatic processes such as migration, invasion and epithelial to mesenchymal transition (EMT). However, molecular mediators working downstream of Notch in these processes are not fully elucidated. CYR61 is a secreted protein implicated in metastasis, and its inhibition by a monoclonal antibody suppresses metastasis in xenograft breast tumors, indicating the clinical importance of CYR61 targeting. Here, we aimed to investigate whether CYR61 works downstream of Notch in inducing pro-metastatic phenotypes in breast cells. We showed that CYR61 expression is positively regulated by Notch activity in breast cells. Notch1-induced migration, invasion and anchorage independent growth of a normal breast cell line, MCF10A, were abrogated by CYR61 silencing. Furthermore, upregulation of core EMT markers upon Notch1-activation was impaired in the absence of CYR61. However, reduced migration and invasion of highly metastatic cell line, MDA MB 231, cells upon Notch inhibition was not dependent on CYR61 downregulation. In conclusion, we showed that in normal breast cell line MCF10A, CYR61 is a mediator of Notch1-induced pro-metastatic phenotypes partly via induction of EMT. Our results imply CYR61 as a prominent therapeutic candidate for a subpopulation of breast tumors with high Notch activity.