Researcher:
Atak, Dila

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Dila

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Atak

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Atak, Dila

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2019 - 201932020 - 20213

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Now showing 1 - 6 of 6
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    PublicationMetadata only
    The role of chronic stress on mitochondria related neurodegeneration in parkinson's disease
    (Elsevier, 2021) N/A; N/A; N/A; Kuvvet, Yasemin; Atak, Dila; Eser, Hale Yapıcı; Master Student; Master Student; Faculty Member; Koç University Research Center for Translational Medicine (KUTTAM) / Koç Üniversitesi Translasyonel Tıp Araştırma Merkezi (KUTTAM); Graduate School of Health Sciences; Graduate School of Health Sciences; School of Medicine; N/A; N/A; 134359
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    PublicationMetadata only
    Roles of developmentally regulated KIF2A alternative isoforms in cortical neuron migration and differentiation
    (The Company of Biologists, 2021) N/A; N/A; N/A; N/A; N/A; N/A; N/A; Department of Molecular Biology and Genetics; N/A; Akkaya, Cansu; Atak, Dila; Kamacıoğlu, Altuğ; Akarlar, Büşra; Güner, Gökhan; Bayam, Efil; Taşkın, Ali Cihan; Dunn, Gülayşe İnce; PhD Student; PhD Student; Master Student; Other; Master Student; Researcher; Other; Faculty Member; Other; Department of Molecular Biology and Genetics; N/A; Koç University Research Center for Translational Medicine (KUTTAM) / Koç Üniversitesi Translasyonel Tıp Araştırma Merkezi (KUTTAM); Graduate School of Sciences and Engineering; Graduate School of Sciences and Engineering; Graduate School of Sciences and Engineering; N/A; Graduate School of Sciences and Engineering; N/A; N/A; College of Sciences; N/A; N/A; N/A; N/A; N/A; N/A; N/A; 291296; 105301; N/A
    KIF2A is a kinesin motor protein with essential roles in neural progenitor division and axonal pruning during brain development. However, how different KIF2A alternative isoforms function during development of the cerebral cortex is not known. Here, we focus on three Kif2a isoforms expressed in the developing cortex. We show that Kif2a is essential for dendritic arborization in mice and that the functions of all three isoforms are sufficient for this process. Interestingly, only two of the isoforms can sustain radial migration of cortical neurons; a third isoform, lacking a key N-terminal region, is ineffective. By proximity-based interactome mapping for individual isoforms, we identify previously known KIF2A interactors, proteins localized to the mitotic spindle poles and, unexpectedly, also translation factors, ribonucleoproteins and proteins that are targeted to organelles, prominently to the mitochondria. In addition, we show that a KIF2A mutation, which causes brain malformations in humans, has extensive changes to its proximity-based interactome, with depletion of mitochondrial proteins identified in the wild-type KIF2A interactome. Our data raises new insights about the importance of alternative splice variants during brain development.
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    The role of pericytes in the pathophysiology multiple of sclerosis
    (Lippincott Williams & Wilkins, 2019) Tüzün, Erdem; Ulusoy, Canan; Küçükali, Cem; Şekerdağ, Emine; Atak, Dila; Gökyüzü, Aysu Bilge; Zeybel, Müjdat; Çakmak, Özgür Öztop; Vural, Atay; Özdemir, Yasemin Gürsoy; PhD Student; PhD Student; PhD Student; Faculty Member; Faculty Member; Faculty Member; Faculty Member; Koç University Research Center for Translational Medicine (KUTTAM) / Koç Üniversitesi Translasyonel Tıp Araştırma Merkezi (KUTTAM); Graduate School of Health Sciences; Graduate School of Health Sciences; Graduate School of Health Sciences; School of Medicine; School of Medicine; School of Medicine; School of Medicine; N/A; N/A; N/A; 214694; 299358; 182369; 170592
    Objective: Our aim was to investigate the impact of pericytes, an important component of the blood brain barrier (BBB), on multiple sclerosis (MS) pathogenesis. Background: Although MS is known as a classical inflammatory demyelinating disorder, the involvement of glial cells in demyelination is increasingly recognized. Vascular pathology has also been recently found to contribute to the pathogenesis of MS. However, the exact mechanisms of this pathology and the influence of pericytes have been scarcely investigated. Design/Methods: Experimental allergic encephalomyelitis (EAE) was induced in C57BL6 mice by myelin oligodendrocyte glycoprotein (MOG) immunization. BBB permeability, number and localization of pericytes were assessed in MS lesions and extracellular matrix components were investigated by immunohistochemical methods. Results: Multiple inflammatory lesions were detected in spinal cord and brain on 40th day of MOG-induced EAE. The lesions contained an abundance of T cells and macrophages and lacked myelin. The BBB permeability increase was shown on EAE lesions by albumin staining. The lesion sites with albumin leakage showed a reduction in PDGFRB+ pericytes and some of the pericytes were found to deviate from the walls of microvessels and be repositioned in the brain parenchyma. Moreover, aSMA+ cells and the extracellular matrix protein content around PDGFRB+ and aSMA+ cells were significantly increased. Conclusions: In this study, we have shown for the first time that EAE lesions show altered pericyte distribution. This alteration is associated with a change in BBB permeability and an increase in extracellular matrix.
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    PublicationOpen Access
    Impact of autoimmune demyelinating brain disease sera on pericyte survival
    (Turkish Neuropsychiatry Association / Türk Nöropsikiyatri Derneği, 2021) Ulusoy, Canan; Yılmaz, Vuslat; Küçükali, Cem İsmail; Karaaslan, Zerrin; Kürtüncü, Murat; Türkoğlu, Recai; Tüzün, Erdem; Şekerdağ, Emine; Gökyüzü, Aysu Bilge; Atak, Dila; Vural, Atay; Özdemir, Yasemin Gürsoy; PhD Student; Researcher; Faculty Member; Koç University Research Center for Translational Medicine (KUTTAM) / Koç Üniversitesi Translasyonel Tıp Araştırma Merkezi (KUTTAM); Graduate School of Health Sciences; School of Medicine; N/A; N/A; N/A; 182369; 170592
    Introduction: multiple sclerosis (MS) is an autoimmune disease of the central nervous system (CNS) characterized by demyelination and brain pericyte dysfunction might be involved in MS pathogenesis Our aim was to evaluate whether the factors in serum affect pericyte survival. Method: C57BL/6 female mice were immunized with myelin oligodendrocyte glycoprotein (MOG) to induce experimental autoimmune encephalomyelitis (EAE). To confirm the animal model, the sera level of anti-MOG antibody in mice and platelet-derived growth factor-BB (PDGF-BB) in patients was measured by ELISA. Human brain vascular pericytes (HBVP) cell lines were incubated with sera of EAE mice and primer progressive MS (PPMS), seconder progressive MS (SPMS) and relapsing-remitting MS (RRMS) patients. The viability of HBVP is measured with Annexin V-FITC/propidium iodide staining with flow cytometry. Results: annexin V-FITC/propidium iodide staining with flow cytometry showed increased ratios of early apoptosis and decreased survival following incubation with sera of EAE and progressive MS. Levels of platelet-derived growth factor-BB were identical in serum and cerebrospinal fluids of patients with different forms of MS. Conclusion: our results suggest that serum factors might contribute to progressive MS pathogenesis via pericyte dysfunction. / Amaç: multipl skleroz (MS) merkezi sinir sisteminin (MSS) otoimmün demiyelinizan hastalığıdır. Son yıllardaki bulgular beyin perisit disfonksiyonunun MS patogenezinde yol oynayabileceğini göstermiştir. Bu çalışmada amacımız MS’nin perisit sağkalımına etkilerini ortaya koymaktır. Yöntem: MS hayvan modeli olan deneysel otoimmün ensefalomiyelit (DOE) modelini oluşturmak için, 8–10 haftalık C57BL/6 dişi fareler miyelin oligodendrosit glikoprotein (MOG) ile immünize edildi. Deneysel hayvan modelinin başarılı bir şekilde oluştuğunu doğrulamak için fareler klinik olarak gözlemlendi ve kanları alınarak serumlarında anti-MOG antikoru taraması yapıldı. Hücre kültürü ortamında, insan beyin damarsal perisit (İBDP) ile DOE fare ve insan MS hastası serumları (yineleyici MS, sekonder progresif MS ve primer progresif MS hastaları dâhil edilmiştir.) Yirmi dört saat inkübe edildi. Perisitlerin hücresel canlılık durumu Annexin V-FITC/ propidiyum iyodid (PI) ile akım sitometrisinde değerlendirildi. Ayrıca MS hastaları serumunda perisitlerin fonksiyonu için önemli olan trombosit kaynaklı büyüme faktörü düzeyi ELISA yöntemi ile ölçüldü. Bulgular: DOE ve progresif tip MS serumları ile inkübe olan perisitlerin diğer gruplara göre anlamlı derecede yüksek oranlarda erken apoptoza girdiği ve buna bağlı olarak canlılık yüzdelerinin düştüğü görülmüştür. Farklı MS tiplerine sahip hasta ve sağlıklı kontrollerin serum ve beyin omurilik sıvılarındaki trombosit-kaynaklı büyüme faktörü seviyeleri açısından anlamlı bir fark bulunmadı. Sonuç: elde ettiğimiz bulgular progresif tip MS hastalarının serumlarındaki birtakım faktörlerin perisit disfonksiyonuna sebep olarak MS patogenezine katkı yaptığını düşündürmektedir.
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    PublicationOpen Access
    Terminal neuron localization to the upper cortical plate is controlled by the transcription factor NEUROD2
    (Nature Publishing Group (NPG), 2019) Department of Molecular Biology and Genetics; Department of Physics; Akkaya, Cansu; Atak, Dila; Güzelsoy, Gizem; Dunn, Cory David; Dunn, Gülayşe İnce; Kabakçıoğlu, Alkan; Master Student; Faculty Member; Faculty Member; Faculty Member; Department of Molecular Biology and Genetics; Department of Physics; Koç University Research Center for Translational Medicine (KUTTAM) / Koç Üniversitesi Translasyonel Tıp Araştırma Merkezi (KUTTAM); Graduate School of Sciences and Engineering; College of Sciences; N/A; N/A; N/A; N/A; 105301; N/A; 49854
    Excitatory neurons of the mammalian cerebral cortex are organized into six functional layers characterized by unique patterns of connectivity, as well as distinctive physiological and morphological properties. Cortical layers appear after a highly regulated migration process in which cells move from the deeper, proliferative zone toward the superficial layers. Importantly, defects in this radial migration process have been implicated in neurodevelopmental and psychiatric diseases. Here we report that during the final stages of migration, transcription factor Neurogenic Differentiation 2 (Neurod2) contributes to terminal cellular localization within the cortical plate. In mice, in utero knockdown of Neurod2 resulted in reduced numbers of neurons localized to the uppermost region of the developing cortex, also termed the primitive cortical zone. Our ChIP-Seq and RNA-Seq analyses of genes regulated by NEUROD2 in the developing cortex identified a number of key target genes with known roles in Reelin signaling, a critical regulator of neuronal migration. Our focused analysis of regulation of the Reln gene, encoding the extracellular ligand REELIN, uncovered NEUROD2 binding to conserved E-box elements in multiple introns. Furthermore, we demonstrate that knockdown of NEUROD2 in primary cortical neurons resulted in a strong increase in Reln gene expression at the mRNA level, as well as a slight upregulation at the protein level. These data reveal a new role for NEUROD2 during the late stages of neuronal migration, and our analysis of its genomic targets offers new genes with potential roles in cortical lamination.
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    PublicationOpen Access
    The role of pericytes in the pathophysiology multiple of sclerosis
    (Lippincott Williams and Wilkins (LWW), 2019) Tüzün, Erdem; Ulusoy, Canan; Küçükali, Cem; N/A; N/A; Şekerdağ, Emine; Atak, Dila; Gökyüzü, Aysu Bilge; Zeybel, Müjdat; Çakmak, Özgür Öztop; Özdemir, Yasemin Gürsoy; Vural, Atay; PhD Student; Researcher; Faculty Member; Faculty Member; Koç University Research Center for Translational Medicine (KUTTAM) / Koç Üniversitesi Translasyonel Tıp Araştırma Merkezi (KUTTAM); School of Medicine; N/A; N/A; N/A; 214694; N/A; 170592; 182369