Yalçın Özuysal, Özden
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Yalçın, Özden
Ozuysal, Ozden Y.
Özuysal, Özden Y.
Ozuysal, Ozden Yalcin
Özuysal, Özden Yalçın
Yalcin, Ozden
Yalcin-Ozuysal, Ö.
Yalcin Ozuysal, Ozden
Yalcin-Ozuysal, Ozden
Yalcin-Ozuysal, Özden
Yalçın-Özuysal, Özden
Yalçin Özuysal, Özden
Ozuysal, Ozden Y.
Özuysal, Özden Y.
Ozuysal, Ozden Yalcin
Özuysal, Özden Yalçın
Yalcin, Ozden
Yalcin-Ozuysal, Ö.
Yalcin Ozuysal, Ozden
Yalcin-Ozuysal, Ozden
Yalcin-Ozuysal, Özden
Yalçın-Özuysal, Özden
Yalçin Özuysal, Özden
Job Title
Email Address
ozdenyalcin@iyte.edu.tr
Main Affiliation
04.03. Department of Molecular Biology and Genetics
Status
Current Staff
Website
ORCID ID
Scopus Author ID
Turkish CoHE Profile ID
Google Scholar ID
WoS Researcher ID
Sustainable Development Goals
1NO POVERTY
0
Research Products
2ZERO HUNGER
0
Research Products
3GOOD HEALTH AND WELL-BEING
21
Research Products
4QUALITY EDUCATION
1
Research Products
5GENDER EQUALITY
0
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6CLEAN WATER AND SANITATION
0
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7AFFORDABLE AND CLEAN ENERGY
0
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8DECENT WORK AND ECONOMIC GROWTH
0
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9INDUSTRY, INNOVATION AND INFRASTRUCTURE
8
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10REDUCED INEQUALITIES
0
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11SUSTAINABLE CITIES AND COMMUNITIES
0
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12RESPONSIBLE CONSUMPTION AND PRODUCTION
0
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13CLIMATE ACTION
0
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14LIFE BELOW WATER
0
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15LIFE ON LAND
0
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16PEACE, JUSTICE AND STRONG INSTITUTIONS
0
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17PARTNERSHIPS FOR THE GOALS
0
Research Products
Documents
32
Citations
999
h-index
14
Documents
32
Citations
908
Scholarly Output
49
Articles
25
Views / Downloads
126223/15803
Supervised MSc Theses
10
Supervised PhD Theses
2
WoS Citation Count
771
Scopus Citation Count
857
Patents
0
Projects
12
WoS Citations per Publication
15.73
Scopus Citations per Publication
17.49
Open Access Source
38
Supervised Theses
12
| Journal | Count |
|---|---|
| 2020 Medical Technologies Congress (Tiptekno) | 2 |
| Turkish Journal of Biology | 2 |
| Biotechnology and Bioengineering | 2 |
| 9th International Conference on Recent Advances in Space Technologies, RAST 2019 | 1 |
| ACS Nano | 1 |
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49 results
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Now showing 1 - 10 of 49
Article Citation - WoS: 103Citation - Scopus: 112Perinatal Exposure To Bisphenol a Increases Adult Mammary Gland Progesterone Response and Cell Number(The Endocrine Society, 2011) Ayyanan, Ayyakkannu; Laribi, Ouahiba; Schuepbach-Mallepell, Sonia; Schrick, Christina; Gutierrez, Maria; Tanos, Tamara; Lefebvre, Gregory; Rougemont, Jacques; Yalçın Özuysal, Özden; Brisken, CathrinBisphenol A [BPA, 2,2,-bis (hydroxyphenyl) propane] is one of the highest-volume chemicals produced worldwide. It is detected in body fluids of more than 90% of the human population. Originally synthesized as an estrogenic compound, it is currently utilized to manufacture food and beverage containers resulting in uptake with food and drinks. There is concern that exposure to low doses of BPA, defined as less than or equal to 5 mg/kg body weight /d, may have developmental effects on various hormone-responsive organs including the mammary gland. Here, we asked whether perinatal exposure to a range of low doses of BPA is sufficient to alter mammary gland hormone response later on in life, with a possible impact on breast cancer risk. To mimic human exposure, we added BPA to the drinking water of C57/Bl6 breeding pairs. Analysis of the mammary glands of their daughters at puberty showed that estrogen-dependent transcriptional events were perturbed and the number of terminal end buds, estrogen-induced proliferative structures, was altered in a dose-dependent fashion. Importantly, adult females showed an increase in mammary epithelial cell numbers comparable to that seen in females exposed to diethylbestrol, a compound exposure to which was previously linked to increased breast cancer risk. Molecularly, the mRNAs encoding Wnt-4 and receptor activator of nuclear factor kB ligand, two key mediators of hormone function implicated in control of mammary stem cell proliferation and carcinogenesis, showed increased induction by progesterone in the mammary tissue of exposed mice. Thus, perinatal exposure to environmentally relevant doses of BPA alters long-term hormone response that may increase the propensity to develop breast cancer. © 2011 by The Endocrine Society.Conference Object Detection and Restoration Pipeline for Phase Contrast Microscopy Time Series Images(IEEE, 2022) Iheme, Leonardo O.; Uçar, Mahmut; Önal, Sevgi; Yalçın Özuysal, Özden; Pesen Okvur, Devrim; Töreyin, Behçet U.; Ünay, DevrimWe propose a pre-processing pipeline for the de-tection and restoration of distorted frames in phase-contrast microscopy time-series images. The analysis is based on the average intensity values of the frames within any given time- series image. The extent of the correction of intensity variation in frames is determined by the normalization of the difference between the current frame's average intensity and the median of average intensity of all frames. Our restoration algorithm preserves regional trans-passing pixels, does not cause new distortions, and increases the histogram similarity between the distorted and non-distorted frames. The algorithm was validated on 15,395 time-series image frames from 27 experiments and the results were found to be visually and quantitatively accurate.Conference Object Citation - Scopus: 1A Preliminary Study on Cell Motility Analysis From Phase-Contrast Microscopy Image Series(IEEE, 2020) Kayan, Emre; Kavuşan, Tarık; Önal, Sevgi; Pesen Okvur, Devrim; Yalçın Özuysal, Özden; Töreyin, Behçet Uğur; Ünay, DevrimAnalyses of morphology, polarity, and motility of cells is important for cell biology research such as metastatic and invasive capacity of cells, wound healing, and embryonic development. Automation of such analyses using image series of phase-contrast optical microscopy, which allows label-free imaging of live cells in their living environment, is a need. With this purpose, in this study image series of a cell motility experiment is manually annotated, and an automation algorithm realizing motion and shape analyses of cells using the annotated data is developed. In addition, due to the low number of annotated data at hand, a U-Net based solution is devised for automated segmentation of the cells and its performance is evaluated.Master Thesis Role of Human Aprataxin Protein in P53-Related Cellular Processes in Breast Cells(01. Izmir Institute of Technology, 2021) Doğan, Hülya; Doğan, Hülya; Yalçın Özuysal, Özden; Yalçın Özuysal, ÖzdenAprataxin 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: 17Citation - Scopus: 19Pro-Metastatic Functions of Notch Signaling Is Mediated by Cyr61 in Breast Cells(Elsevier, 2020) Küçükköse, Cansu; Efe, Eda; Günyüz, Zehra Elif; Fıratlıgil, Burcu; Doğan, Hülya; Yalçın Özuysal, Özden; İlhan, MustafaMetastasis 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.Master Thesis Investigating the Effect of Human Sacm1l Gene in the P53 Wild Type Breast Epithelial Mcf10a and Breast Cancer Mcf7 Cells(01. Izmir Institute of Technology, 2021) Efe, Eda; Efe, Eda; Yalçın Özuysal, Özden; Yalçın Özuysal, Özdenp53, tumor suppressor protein, plays role in the regulation of many cellular processes. Thus, p53 activity is controlled by a series of mechanisms, one of which is a redox reaction. However, redox regulation of p53 is not well defined in the literature. As a candidate of antioxidant, Sac1 gene mutation resulted in decreased levels of human p53 protein in transformed yeast, but the human homolog of Sac1 (SACM1L) has not been studied yet. SACM1L is known to function as a phosphoinositide phosphatase, hydrolyzes PI4P in the Golgi and ER. Previous studies demonstrated SACM1L depletion in HeLa cells led to decreased viability and arrest at the G2/M phase. However, no data were found on the association between the SACM1L and either directly p53 or p53 mediated cellular processes. We aimed to investigate the role of SACM1L in p53 controlled cellular processes like cell cycle and apoptosis in p53 wild type (wt) breast epithelial cells MCF10A and breast cancer cells MCF7 in the presence or absence of SACM1L gene. We demonstrated that SACM1L knockout MCF7 cells were arrested in the G1 phase, and number of proliferating cells was reduced, whereas overexpression of SACM1L did not change the proliferation, and cell cycle. Further, the rate of apoptosis was increased in SACM1L overexpressing and knockout MCF10A and MCF7 cells, supported by the findings of transcriptional analysis for p53 target genes. In conclusion, the greatest effect of SACM1L was observed in the apoptosis, but the underlying mechanisms are still unclear and must be further studied.Article Citation - WoS: 22Citation - Scopus: 24Scaffold-Free Biofabrication of Adipocyte Structures With Magnetic Levitation(John Wiley and Sons Inc., 2021) Sarıgil, Öykü; Yalçın Özuysal, Özden; Anıl İnevi, Müge; Meşe Özçivici, Gülistan; Fıratlıgil Yıldırır, Burcu; Fıratlıgil Yıldırır, Burcu; Ünal, Yağmur Ceren; Ünal, Yağmur Ceren; Yalçın Özuysal, Özden; Özçivici, Engin; Meşe, Gülistan; Sarıgil, Öykü; Özçivici, Engin; Anıl İnevi, Müge; Meşe Özçivici, GülistanTissue engineering research aims to repair the form and/or function of impaired tissues. Tissue engineering studies mostly rely on scaffold-based techniques. However, these techniques have certain challenges, such as the selection of proper scaffold material, including mechanical properties, sterilization, and fabrication processes. As an alternative, we propose a novel scaffold-free adipose tissue biofabrication technique based on magnetic levitation. In this study, a label-free magnetic levitation technique was used to form three-dimensional (3D) scaffold-free adipocyte structures with various fabrication strategies in a microcapillary-based setup. Adipogenic-differentiated 7F2 cells and growth D1 ORL UVA stem cells were used as model cells. The morphological properties of the 3D structures of single and cocultured cells were analyzed. The developed procedure leads to the formation of different patterns of single and cocultured adipocytes without a scaffold. Our results indicated that adipocytes formed loose structures while growth cells were tightly packed during 3D culture in the magnetic levitation platform. This system has potential for ex vivo modeling of adipose tissue for drug testing and transplantation applications for cell therapy in soft tissue damage. Also, it will be possible to extend this technique to other cell and tissue types.Master Thesis Identification of Novel Notch Target Genes That Are Mediators of Notch in Inducing Epithelial To Mesenchymal Transition and Migration/Invasion(Izmir Institute of Technology, 2016) Küçükköse, Cansu; Yalçın Özuysal, Özden; Yalçın Özuysal, ÖzdenNotch signaling has first been described in murine mammary gland by the proviral integration of mouse mammary tumor virus (MMTV) into the Notch4 locus (Int3 locus) which resulted expression of constitutively active form of Notch4 and transformation of mammary epithelial cells. Notch1 is highly expressed in breast cancer and constitutively active form of Notch1 induces neoplasm. In breast cancer, overexpression of active Notch1 receptor (NICD) promotes epithelial-mesenchymal transition (EMT) via Snail induction which demonstrates the role of Notch signaling in induction of metastasis through EMT. However, the downstream mediators of Notch in EMT, migration and invasion processes are still elusive. In this study, we hypothesized that Notch signaling induces EMT and migration via regulating one or more of the seven candidate genes that are SEMA6D, SEMA3C, CXCR7, CXCL14, CCL20, HMGA2 and CYR61 which were shown to be differentially regulated by Notch signaling in breast cells in microarray data. The candidate genes are involved in EMT and migration in different cell types and tissues. We showed that Notch1 activation in normal breast epithelial cell line MCF10A significantly increased both mRNA and protein expressions of SEMA6D and CYR61 while it significantly reduced SEMA3C and HMGA2 mRNA levels. Notch inhibition led to significant reduction in mRNA expression of CYR61, CCL20 and HMGA2 and protein expression of CYR61 only, while the rest of candidate genes were affected slightly in breast cancer cell line, MDA-MB-231. We chose SEMA6D for further investigation because there is no data indicating the role of SEMA6D in breast cancer in the literature. SEMA6D could be mediator of Notch signaling to induce EMT because it partially rescues negative effect of Notch inhibition on EMT markers. Notch independent effect of SEMA6D suggested that SEMA6D may be involved in inhibiting EMT whereas, it induced migration and cell viability in MDA-MB-231 cell line.Further analysis is required to reveal the role of SEMA6D in EMT and migration.Master Thesis Molecular Characterization of Adult Stem Cells' Adaptations To Mechanical Signals During Adipogenic Commitment(Izmir Institute of Technology, 2015) Baskan, Öznur; Özçivici, Engin; Baskan, Öznur; Yalçın Özuysal, Özden; Özçivici, Engin; Yalçın, ÖzdenPrevalence of obesity have increased across the years based on technological developments that supported nutritional availability and sedentary lifestyles. Restoring mechanical activity with physical exercise suppresses obesity, and mechanical loading can also be delivered passively with whole body vibrations with high frequency and low magnitude. Anabolic effects of high frequency low magnitude mechanical vibrations on adult stem cells are well identified whereas sensing mechanism of cells and their response to mechanical stimuli is largely unknown. Here, we hypothesed that daily bouts of low intensity vibrations will affect molecular, physical and ultrastructural profile of the cells and the effect will interact with the adipogenic induction. To test this hypothesis mouse bone marrow stem cell line D1 ORL UVA were subjected to mechanical vibrations (0.15g, 90 Hz, 15min/d) for 7 days to both during quiescence and adipogenic commitment. Ultrastructural changes were identified on cellular and molecular levels. Atomic force microscopy was used to characterize the changes on cell surface and significant increase was observed in cell surface height. Moreover, in order to identify the changes in cytoskeleton structure and physical properties, actin were stained with phalloidin and imaged with inverted microscope. To quantify phalloidin amount, signal intensities and physical features of the cells were measured. It was observed that mechanical stimulation and adipogenic induction affect actin content and the physical structure of the cells significantly. Molecular level analysis of cytoskeleton elements and adipogenic markers were performed with Real time PCR. Dramatic increases in adipogenic markers were detected with adipogenic induction. These results indicate that mesenchymal stem cells responds to mechanical vibrations by altering their molecular and ultrastructure during both quiescence and adipogenesis.Master Thesis Role of Irf6 in Notch Regulated Apoptosis, Cell Cycle and Differentiation in Breast Epithelial Cells(Izmir Institute of Technology, 2015) Ekinci, Burcu; Yalçın Özuysal, ÖzdenNotch pathway, an evolutionarily conserved signaling, controls development, differentiation and proliferation. Notch1 and Notch4 activation caused mammary tumor formation showing an oncogenic effect. Overexpression of Notch1 can also supress proliferation in breast epithelial cells depending on dosage and cell type. Thus, Notch can act as an oncogene or tumor suppressor in breast. IRF6, a member of interferon regulatory factor family, has a role in development and differentiation of the epidermis, downstream of Notch signaling. IRF6 overexpression induces cell cycle arrest in breast cancer cells showing a tumor suppressor role. It was recently identified that IRF6 is a mediator of Notch in proliferation and transformation of breast epithelial cells. In this study, it was aimed to identify whether IRF6 has any effect on cell cycle regulation, apoptosis and breast cancer stem cell population (BCSCs) under Notch and whether IRF6 has a role in expression of luminal and basal markers in breast cell lines. Our results showed that IRF6 knockdown in normal breast epithelial cell line, MCF10A, reduced percentage of cells in S-phase, which was increased by Notch activation. IRF6 knockdown induced early apoptosis and reduced BCSCs, however it has no effect downstream of Notch in these processes. On the other hand, IRF6 did not play an essential role on expression of luminal and basal markers. In conclusion, our previous observation was supported that IRF6 is a mediator of Notch in cell proliferation. Furthermore, these data showed that IRF6 has a novel role on early apoptosis and stem cell population independent of Notch signaling.