Researcher: Özçimen, Burcu
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Özçimen, Burcu
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Publication Metadata only NLRP7's key role in primate trophoblast differentiation(Amer Soc Cell Biology, 2017) Garipcan, A.; Özören, Nesrin; N/A; Özçimen, Burcu; Önder, Tamer Tevfik; Phd Student; Faculty Member; Graduate School of Sciences and Engineering; School of Medicine; 316273; 42946N/APublication Metadata only Transgene-free disease-specific iPSC generation from fibroblasts and peripheral blood mononuclear cells(Humana Press Inc, 2016) Ebrahimi, Ayyub; N/A; N/A; N/A; N/A; Fidan, Kerem; Bozlak, Özlem Hilal Çağlayan; Özçimen, Burcu; Önder, Tamer Tevfik; Master Student; Undergraduate Student; Phd Student; Faculty Member; Graduate School of Sciences and Engineering; School of Medicine; Graduate School of Sciences and Engineering; School of Medicine; N/A; 296433; 316273; 42946Induced pluripotent stem cells (iPSCs) offer great promise as tools for basic biomedical research, disease modeling, and drug screening. In this chapter, we describe the generation of patient-specific, transgene-free iPSCs from skin biopsies and peripheral blood mononuclear cells through electroporation of episomal vectors and growth under two different culture conditions. The resulting iPSC lines are characterized with respect to pluripotency marker expression through immunostaining, tested for transgene integration by PCR, and assayed for differentiation capacity via teratoma formation.Publication Metadata only Leptin treatment of in vitro cultured embryos increases outgrowth rate of inner cell mass during embryonic stem cell derivation(Springer, 2019) Ebrahimi, Ayyub; N/A; N/A; N/A; N/A; N/A; N/A; N/A; Taşkın, Ali Cihan; Kocabay, Ahmet; Karahüseyinoğlu, Serçin; Şahin, Gizem Nur; Özçimen, Burcu; Ruacan, Ayşe Arzu; Önder, Tamer Tevfik; Other; Other; Faculty Member; PhD Student; PhD Student; Faculty Member; Faculty Member; Koç University Research Center for Translational Medicine (KUTTAM) / Koç Üniversitesi Translasyonel Tıp Araştırma Merkezi (KUTTAM); N/A; N/A; School of Medicine; Graduate School of Health Sciences; Graduate School of Sciences and Engineering; School of Medicine; School of Medicine; 291296; N/A; 110772; N/A; 316273; 38250; 42946Leptin, a metabolic hormone, regulates the reproductive functions responding to both nutritional and body conditions. Embryonic stem cells play important roles in reproductive technology, but their derivation can be challenging. In this study, we evaluated the derivation rates of mouse embryonic stem cell (mESC) line from blastocysts developing in embryo culture media supplemented with different leptin concentrations. The results showed that addition of leptin into the embryo culture medium supported the in vitro development of mouse embryo. The mESC line derivation rates for media treated with 0, 10, 50, and 100ng/ml of leptin were 61.24 % (54/88), 84.96 % (42/50), 81.79 % (61/76), and 85.78 % (56/67), respectively. In addition, leptin treatment of blastocysts upregulated the expression levels of the trophectoderm marker Cdx2, whereas inner cell mass markers Oct-4 and Nanog were not affected. mESC lines derived after leptin treatment demonstrated hallmarks of pluripotency, such as alkaline phosphatase activity, expression of, OCT4, NANOG, and SSEA1, as well as the ability to form embryoid bodies and well-differentiated teratomas. In conclusion, leptin has a positive effect on the derivation rate of mouse embryonic stem cell lines which may be, in part, due to its effects on the development of the trophectoderm cell lineage in the embryo.Publication Open Access Generation of transgene-free iPSC lines from three patients with Friedreich's ataxia (FRDA) carrying GAA triplet expansions in the first intron of FXN gene(Elsevier, 2021) Kelekçi, Simge; Uğurlu Çimen, Deniz; Demir, Ata Berk; Özçimen, Burcu; Yıldız, Abdullah Burak; Karakuş, Mehmet Batuhan; Börklü Yücel, Esra; Önder, Tamer Tevfik; PhD Student; Undergraduate Student; Other; Faculty Member; Graduate School of Health Sciences; School of Medicine; Koç University Hospital; N/A; N/A; N/A; N/A; N/A; N/A; N/A; 42946Friedreich's ataxia (FRDA) is a rare neurodegenerative disorder which is caused by triplet repeat expansion (GAA) in the first intron of FXN gene. In this present study, we generated induced pluripotent stem cells (iPSC) lines from fibroblasts of three unrelated FRDA patients using integration-free episomal vectors. All iPSC lines express the pluripotency markers such as OCT4 and SSEA4, display normal karyotypes and can differentiate into all three germ layers via in vivo teratoma formation assay.Publication Open Access Robust, long-term culture of endoderm-derived hepatic organoids for disease modeling(Cell Press, 2019) Akbari, Soheil; Ersoy, Nevin; Başak, Onur; Kaplan, Kübra; Bağrıyanık, Alper; Arslan, Nur; Erdal, Esra; Department of Molecular Biology and Genetics; Department of Molecular Biology and Genetics; Önder, Tamer Tevfik; Sevinç, Gülben Gürhan; Özçimen, Burcu; Enüstün, Eray; Şengün, Berke; Özel, Erkin; Sevinç, Kenan; Faculty Member; PhD Student; Undergraduate Student; School of Medicine; Graduate School of Health Sciences; 42946; N/A; N/A; N/A; N/A; N/A; N/AOrganoid technologies have become a powerful emerging tool to model liver diseases, for drug screening, and for personalized treatments. These applications are, however, limited in their capacity to generate functional hepatocytes in a reproducible and efficient manner. Here, we generated and characterized the hepatic organoid (eHEPO) culture system using human induced pluripotent stem cell (iPSC)-derived EpCAM-positive endodermal cells as an intermediate. eHEPOs can be produced within 2 weeks and expanded long term (>16 months) without any loss of differentiation capacity to mature hepatocytes. Starting from patient-specific iPSCs, we modeled citrullinemia type 1, a urea cycle disorder caused by mutations in the argininosuccinate synthetase (ASST) enzyme. The disease-related ammonia accumulation phenotype in eHEPOs could be reversed by the overexpression of the wild-type ASS1 gene, which also indicated that this model is amenable to genetic manipulation. Thus, eHEPOs are excellent unlimited cell sources to generate functional hepatic organoids in a fast and efficient manner.Publication Open Access NLRP7 plays a functional role in regulating BMP4 signaling during differentiation of patient-derived trophoblasts(Springer Nature, 2020) Alici-Garipcan, Aybüke; Suder, İlke; Ülker, Volkan; Özören, Nesrin; Önder, Tamer Tevfik; Özçimen, Burcu; Faculty Member; PhD Student; School of Medicine; 42946; N/AComplete hydatidiform mole (HM) is a gestational trophoblastic disease resulting in hyperproliferation of trophoblast cells and absence of embryo development. Mutations in the maternal-effect gene NLRP7 are the major cause of familial recurrent complete HM. Here, we established an in vitro model of HM using patient-specific induced pluripotent stem cells (iPSCs) derived trophoblasts harboring NLRP7 mutations. Using whole transcriptome profiling during trophoblast differentiation, we showed that impaired NLRP7 expression results in precocious downregulation of pluripotency factors, activation of trophoblast lineage markers, and promotes maturation of differentiated extraembryonic cell types such as syncytiotrophoblasts. Interestingly, we found that these phenotypes are dependent on BMP4 signaling and BMP pathway inhibition corrected the excessive trophoblast differentiation of patient-derived iPSCs. Our human iPSC model of a genetic placental disease recapitulates aspects of trophoblast biology, highlights the broad utility of iPSC-derived trophoblasts for modeling human placental diseases and identifies NLRP7 as an essential modulator of key developmental cell fate regulators.Publication Open Access AF10 (MLLT10) prevents somatic cell reprogramming through regulation of DOT1L-mediated H3K79 methylation(BioMed Central, 2021) Philpott, Martin; Oppermann, Udo; Department of Molecular Biology and Genetics; Department of Molecular Biology and Genetics; Önder, Tamer Tevfik; Uğurlu Çimen, Deniz; Sevinç, Kenan; Küçük, Nazlı Ezgi Özkan; Özçimen, Burcu; Demirtaş, Deniz; Enüstün, Eray; Faculty Member; Faculty Member; PhD Student; Koç University Research Center for Translational Medicine (KUTTAM) / Koç Üniversitesi Translasyonel Tıp Araştırma Merkezi (KUTTAM); School of Medicine; College of Sciences; Graduate School of Sciences and Engineering; Graduate School of Health Sciences; 42946; 105301; N/A; N/A; N/A; N/A; N/A; N/A; N/A; N/ABackground: the histone H3 lysine 79 (H3K79) methyltransferase DOT1L is a key chromatin-based barrier to somatic cell reprogramming. However, the mechanisms by which DOT1L safeguards cell identity and somatic-specific transcriptional programs remain unknown. Results: we employed a proteomic approach using proximity-based labeling to identify DOT1L-interacting proteins and investigated their effects on reprogramming. Among DOT1L interactors, suppression of AF10 (MLLT10) via RNA interference or CRISPR/Cas9, significantly increases reprogramming efficiency. In somatic cells and induced pluripotent stem cells (iPSCs) higher order H3K79 methylation is dependent on AF10 expression. In AF10 knock-out cells, re-expression wild-type AF10, but not a DOT1L binding-impaired mutant, rescues overall H3K79 methylation and reduces reprogramming efficiency. Transcriptomic analyses during reprogramming show that AF10 suppression results in downregulation of fibroblast-specific genes and accelerates the activation of pluripotency-associated genes. Conclusions: our findings establish AF10 as a novel barrier to reprogramming by regulating H3K79 methylation and thereby sheds light on the mechanism by which cell identity is maintained in somatic cells.