Researcher:
Ebrahimi, Ayyub A.

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Researcher

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Ayyub A.

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Ebrahimi

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Ebrahimi, Ayyub A.

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2014 - 20195

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    Epigenetic modifications of androgen receptor signaling in castration resistant prostate cancer (CRPC)
    (Elsevier Sci Ltd, 2014) Saraç, Hilal; Toparlak, Ömer Duhan; Kaplan, Anıl; Ebrahimi, Ayyub A.; Önder, Tuğba Bağcı; Önder, Tamer Tevfik; Lack, Nathan Alan; PhD Student; Other; Undergraduate Student; Researcher; Faculty Member; Faculty Member; Faculty Member; Graduate School of Sciences and Engineering; School of Medicine; School of Medicine; School of Medicine; School of Medicine; School of Medicine; School of Medicine; N/A; N/A; N/A; 381072; 184359; 42946; 120842
    Introduction: Prostate cancer is one of the most common forms of cancer in Turkish and European men. For those patients with late-stage prostate cancer, androgen depletion therapy is current standard treatment. While initially successful, almost all patients eventually develop resistance against this treatment. Once the cancer reaches this advanced, progressive form, it is termed castration resistant prostate cancer (CRPC). Whereas the progression mechanisms of CRPC are poorly understood, it has been shown that in CRPC patients, the androgen receptor (AR) is still active despite undetectable androgen levels. Since AR signaling is important in the progression and growth of prostate cancer, understanding how AR mediated signaling occurs in CRPC is critical to more efficient treatment of this recurrent disease. Material and Methods: There are several possible causes for this conversion from androgen-sensitive to androgen-independent prostate cancer. Previous work has demonstrated that epigenetic modifiers such as EZH2 and LSD1 can mediate the sensitization of androgen receptor in CRPC. However, only a small subset of epigenetic modifiers has been characterized. To better understand the role of histone modification on CRPC, we conducted a large scale shRNA screen of epigenetic modifying enzymes to identify those genes that prevent androgen-independent growth. Results and Discussion: From this screen several hit genes have been found that cause a reversion of androgen-independent to androgen-dependent prostate cancer. The shRNA knock-down of these hit genes was confirmed by western blot and qRT-PCR. We are currently characterizing how these epigenetic modifiers affect androgen-receptor mediated signalling. Conclusion: These results will offer new insight into the role of epigenetic modifiers in nuclear receptor signalling.
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    Effects of histone H3 lysine 9 inhibition on gene expression profile in tobacco (Nicotiana tabacum L.)
    (Wiley-Blackwell, 2016) Arı, Şule; Tombul, Nazrin; Şahin, Önder; Ebrahimi, Ayyub A.; Researcher; School of Medicine; 381072
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    Effect of leptin on derivation rate of mouse embryonic stem (ES) cell line
    (Springer, 2016) N/A; N/A; N/A; N/A; Taşkın, Ali Cihan; Kocabay, Ahmet; Önder, Tamer Tevfik; Ebrahimi, Ayyub A.; Other; Other; Faculty Member; Researcher; N/A; N/A; School of Medicine; School of Medicine; Koç University Research Center for Translational Medicine (KUTTAM) / Koç Üniversitesi Translasyonel Tıp Araştırma Merkezi (KUTTAM); Koç University Research Center for Translational Medicine (KUTTAM) / Koç Üniversitesi Translasyonel Tıp Araştırma Merkezi (KUTTAM); N/A; N/A; 291296; N/A; 42946; 381072
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    Bromodomain inhibition of the coactivators CBP/EP300 facilitate cellular reprogramming
    (Nature Publishing Group (NPG), 2019) Cribbs, Adam P.; Philpott, Martin; Dunford, James E.; Ari, Sule; Oppermann, Udo; N/A; N/A; N/A; N/A; Department of Molecular Biology and Genetics; N/A; N/A; Önder, Tamer Tevfik; Ebrahimi, Ayyub A.; Sevinç, Kenan; Sevinç, Gülben Gürhan; Uyulur, Fırat; Morova, Tunç; Göklemez, Sencer; Faculty Member; Researcher; PhD Student; PhD Student; Undergraduate Student; Master Student; Undergraduate Student; Department of Molecular Biology and Genetics; School of Medicine; School of Medicine; Graduate School of Sciences and Engineering; Graduate School of Health Sciences; College of Sciences; Graduate School of Sciences and Engineering; School of Medicine; 42946; 381072; N/A; N/A; N/A; N/A; N/A
    Silencing of the somatic cell type-specific genes is a critical yet poorly understood step in reprogramming. To uncover pathways that maintain cell identity, we performed a reprogramming screen using inhibitors of chromatin factors. Here, we identify acetyl-lysine competitive inhibitors targeting the bromodomains of coactivators CREB (cyclic-AMP response element binding protein) binding protein (CBP) and E1A binding protein of 300 kDa (EP300) as potent enhancers of reprogramming. These inhibitors accelerate reprogramming, are critical during its early stages and, when combined with DOT1L inhibition, enable efficient derivation of human induced pluripotent stem cells (iPSCs) with OCT4 and SOX2. In contrast, catalytic inhibition of CBP/EP300 prevents iPSC formation, suggesting distinct functions for different coactivator domains in reprogramming. CBP/EP300 bromodomain inhibition decreases somatic-specific gene expression, histone H3 lysine 27 acetylation (H3K27Ac) and chromatin accessibility at target promoters and enhancers. The master mesenchymal transcription factor PRRX1 is one such functionally important target of CBP/EP300 bromodomain inhibition. Collectively, these results show that CBP/EP300 bromodomains sustain cell-type-specific gene expression and maintain cell identity.
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    PublicationOpen Access
    Generation of integration-free induced pluripotent stem cells from a patient with Familial Mediterranean Fever (FMF)
    (Elsevier, 2015) Gül, Ahmet; Department of Molecular Biology and Genetics; Fidan, Kerem; Kavaklıoğlu, Gülnihal; Ebrahimi, Ayyub A.; Özlü, Can; Ay, Nur Zeynep; Ruacan, Ayşe Arzu; Önder, Tamer Tevfik; Master Student; Faculty Member; Faculty Member; Department of Molecular Biology and Genetics; School of Medicine; Graduate School of Sciences and Engineering; N/A; N/A; N/A; N/A; N/A; 38250; 42946
    Fibroblasts from a Familial Mediterranean Fever (FMF) patient were reprogrammed with episomal vectors by using the Neon Transfection System for the generation of integration-free induced pluripotent stem cells (iPSCs). The resulting iPSC line was characterized to determine the expression of pluripotency markers, proper differentiation into three germ layers, the presence of normal chromosomal structures as well as the lack of genomic integration. A homozygous missense mutation in the MEFV gene (p.Met694Val), which lead to typical FMF phenotype, was shown to be present in the generated iPSC line.