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Your search keyword '"Özturan, Doğancan' showing total 3 results
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3 results on '"Özturan, Doğancan'

1. Protein scaffold-based multimerization of soluble ACE2 efficiently blocks SARS-CoV-2 infection in vitro and in vivo

Author

Kayabölen, Alişan; Akcan, Uğur; Özturan, Doğancan; Sahin, Gizem Nur; Pınarbaşı Değirmenci, Nareğ; Bayraktar, Canan; Soyler, Gizem; Sarayloo, Ehsan; Nurtop, Elif; Özer, Berna; Güney Esken, Gülen; Barlas, Tayfun; Doğan, Özlem (ORCID 0000-0002-6505-4582 & YÖK ID 170418); Karahüseyinoğlu, Serçin (ORCID 0000-0001-5531-2587 & YÖK ID 110772); Lack, Nathan Alan (ORCID 0000-0001-7399-5844 & YÖK ID 120842); Kaya, Mehmet (ORCID 0000-0001-8318-1350 & YÖK ID 10486); Albayrak, Cem; Can, Füsun (ORCID 0000-0001-9387-2526 & YÖK ID 103165); Solaroğlu, İhsan (ORCID 0000-0002-9472-1735 & YÖK ID 102059); Önder, Tuğba Bağcı (ORCID 0000-0003-3646-2613 & YÖK ID 184359), Ulbegi Polat, Hivda; Yıldırım, İsmail Selim, Koç University Research Center for Translational Medicine (KUTTAM) / Koç Üniversitesi Translasyonel Tıp Araştırma Merkezi (KUTTAM), Koç University Hospital, Graduate School of Health Sciences; School of Medicine, Kayabölen, Alişan; Akcan, Uğur; Özturan, Doğancan; Sahin, Gizem Nur; Pınarbaşı Değirmenci, Nareğ; Bayraktar, Canan; Soyler, Gizem; Sarayloo, Ehsan; Nurtop, Elif; Özer, Berna; Güney Esken, Gülen; Barlas, Tayfun; Doğan, Özlem (ORCID 0000-0002-6505-4582 & YÖK ID 170418); Karahüseyinoğlu, Serçin (ORCID 0000-0001-5531-2587 & YÖK ID 110772); Lack, Nathan Alan (ORCID 0000-0001-7399-5844 & YÖK ID 120842); Kaya, Mehmet (ORCID 0000-0001-8318-1350 & YÖK ID 10486); Albayrak, Cem; Can, Füsun (ORCID 0000-0001-9387-2526 & YÖK ID 103165); Solaroğlu, İhsan (ORCID 0000-0002-9472-1735 & YÖK ID 102059); Önder, Tuğba Bağcı (ORCID 0000-0003-3646-2613 & YÖK ID 184359), Ulbegi Polat, Hivda; Yıldırım, İsmail Selim, Koç University Research Center for Translational Medicine (KUTTAM) / Koç Üniversitesi Translasyonel Tıp Araştırma Merkezi (KUTTAM), Koç University Hospital, and Graduate School of Health Sciences; School of Medicine

Abstract

Soluble ACE2 (sACE2) decoys are promising agents to inhibit SARS-CoV-2, as their efficiency is unlikely to be affected by escape mutations. However, their success is limited by their relatively poor potency. To address this challenge, multimeric sACE2 consisting of SunTag or MoonTag systems is developed. These systems are extremely effective in neutralizing SARS-CoV-2 in pseudoviral systems and in clinical isolates, perform better than the dimeric or trimeric sACE2, and exhibit greater than 100-fold neutralization efficiency, compared to monomeric sACE2. SunTag or MoonTag fused to a more potent sACE2 (v1) achieves a sub-nanomolar IC50, comparable with clinical monoclonal antibodies. Pseudoviruses bearing mutations for variants of concern, including delta and omicron, are also neutralized efficiently with multimeric sACE2. Finally, therapeutic treatment of sACE2(v1)-MoonTag provides protection against SARS-CoV-2 infection in an in vivo mouse model. Therefore, highly potent multimeric sACE2 may offer a promising treatment approach against SARS-CoV-2 infections., Koç University Isbank Center for Infectious Diseases (KUISCID); Koç University Research Center for Transla-tional Medicine (KUTTAM)

Published
2022

2. Androgen receptor-mediated transcription in prostate cancer

Author

Lack, Nathan Alan (ORCID 0000-0001-7399-5844 & YÖK ID 120842); Özturan, Doğancan, Morova, Tunç, Koç University Research Center for Translational Medicine (KUTTAM) / Koç Üniversitesi Translasyonel Tıp Araştırma Merkezi (KUTTAM), School of Medicine, Department of Computer Engineering; Department of Chemical and Biological Engineering, Lack, Nathan Alan (ORCID 0000-0001-7399-5844 & YÖK ID 120842); Özturan, Doğancan, Morova, Tunç, Koç University Research Center for Translational Medicine (KUTTAM) / Koç Üniversitesi Translasyonel Tıp Araştırma Merkezi (KUTTAM), School of Medicine, and Department of Computer Engineering; Department of Chemical and Biological Engineering

Abstract

Androgen receptor (AR)-mediated transcription is critical in almost all stages of prostate cancer (PCa) growth and differentiation. This process involves a complex interplay of coregulatory proteins, chromatin remodeling complexes, and other transcription factors that work with AR at cis-regulatory enhancer regions to induce the spatiotemporal transcription of target genes. This enhancer-driven mechanism is remarkably dynamic and undergoes significant alterations during PCa progression. In this review, we discuss the AR mechanism of action in PCa with a focus on how cis-regulatory elements modulate gene expression. We explore emerging evidence of genetic variants that can impact AR regulatory regions and alter gene transcription in PCa. Finally, we highlight several outstanding questions and discuss potential mechanisms of this critical transcription factor., Scientific and Technological Research Council of Turkey (TÜBİTAK); TÜBİTAK 1001; U.S. Department of Defense Prostate Cancer Research Program Idea Development Award

Published
2022

3. Functional mapping of androgen receptor enhancer activity

Author

Özturan, Doğancan; Altıntaş, Berkay Umut; Gökbayrak, Bengül; Lack, Nathan Alan (ORCID 0000-0001-7399-5844 & YÖK ID 120842), Huang, Flora Chia-Chi; Morova, Tunç; Hu, Eugene; Yu, Lok Pak Ivan; Linder, Simon; Hoogstraat, M.; Stelloo, Suzan; Sar, Funda; Van der Poel, Henk; Saffarzadeh, Mohammadali; Le Bihan, Stephane; McConegy, Brian; Y Feng, Felix; Gleave, E. Martin; Bergman, M. Andries; Collins, Colin; Hach, Faraz; Zwart, Wilbert; Emberly, Eldon, Koç University Research Center for Translational Medicine (KUTTAM) / Koç Üniversitesi Translasyonel Tıp Araştırma Merkezi (KUTTAM), Graduate School of Health Sciences; Graduate School of Sciences and Engineering, Department of Computational Sciences and Engineering; Department of Molecular Biology and Genetics, Özturan, Doğancan; Altıntaş, Berkay Umut; Gökbayrak, Bengül; Lack, Nathan Alan (ORCID 0000-0001-7399-5844 & YÖK ID 120842), Huang, Flora Chia-Chi; Morova, Tunç; Hu, Eugene; Yu, Lok Pak Ivan; Linder, Simon; Hoogstraat, M.; Stelloo, Suzan; Sar, Funda; Van der Poel, Henk; Saffarzadeh, Mohammadali; Le Bihan, Stephane; McConegy, Brian; Y Feng, Felix; Gleave, E. Martin; Bergman, M. Andries; Collins, Colin; Hach, Faraz; Zwart, Wilbert; Emberly, Eldon, Koç University Research Center for Translational Medicine (KUTTAM) / Koç Üniversitesi Translasyonel Tıp Araştırma Merkezi (KUTTAM), Graduate School of Health Sciences; Graduate School of Sciences and Engineering, and Department of Computational Sciences and Engineering; Department of Molecular Biology and Genetics

Abstract

Background: androgen receptor (AR) is critical to the initiation, growth, and progression of prostate cancer. Once activated, the AR binds to cis-regulatory enhancer elements on DNA that drive gene expression. Yet, there are 10-100x more binding sites than differentially expressed genes. It is unclear how or if these excess binding sites impact gene transcription. Results: to characterize the regulatory logic of AR-mediated transcription, we generated a locus-specific map of enhancer activity by functionally testing all common clinical AR binding sites with Self-Transcribing Active Regulatory Regions sequencing (STARRseq). Only 7% of AR binding sites displayed androgen-dependent enhancer activity. Instead, the vast majority of AR binding sites were either inactive or constitutively active enhancers. These annotations strongly correlated with enhancer-associated features of both in vitro cell lines and clinical prostate cancer samples. Evaluating the effect of each enhancer class on transcription, we found that AR-regulated enhancers frequently interact with promoters and form central chromosomal loops that are required for transcription. Somatic mutations of these critical AR-regulated enhancers often impact enhancer activity. Conclusions: using a functional map of AR enhancer activity, we demonstrated that AR-regulated enhancers act as a regulatory hub that increases interactions with other AR binding sites and gene promoters., KWF Dutch Cancer Society; Scientific and Technological Research Council of Turkey (TÜBİTAK); 1001 Projects; NSERC; Prostate Cancer Foundation BC; Astellas Pharma Inc.

Published
2021

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