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17 results on '"Serçin, Özdemirhan"'

2. High‐resolution transcriptomic and epigenetic profiling identifies novel regulators of COPD

Author

Schwartz, Uwe, Llamazares Prada, Maria, Pohl, Stephanie T, Richter, Mandy, Tamas, Raluca, Schuler, Michael, Keller, Corinna, Mijosek, Vedrana, Muley, Thomas, Schneider, Marc A, Quast, Karsten, Hey, Joschka, Heußel, Claus P, Warth, Arne, Winter, Hauke, Serçin, Özdemirhan, Karmouty‐Quintana, Harry, Jyothula, Soma SK, Patel, Manish K, Herth, Felix, Koch, Ina, Petrosino, Giuseppe, Titimeaua, Alexandru, Mardin, Balca R, Weichenhan, Dieter, Jurkowski, Tomasz P, Imbusch, Charles D, Brors, Benedikt, Benes, Vladimir, Jung, Birgit, Wyatt, David, Stahl, Heiko F, Plass, Christoph, and Jurkowska, Renata Z

Published
2023
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8. High-resolution transcriptomic and epigenetic profiling identifies novel regulators of COPD phenotypes in human lung fibroblasts

Author

Schwartz, Uwe, primary, Prada, Maria Llamazares, additional, Pohl, Stephanie T., additional, Richter, Mandy, additional, Tamas, Raluca, additional, Schuler, Michael, additional, Keller, Corinna, additional, Mijosek, Vedrana, additional, Muley, Thomas, additional, Schneider, Marc A., additional, Quast, Karsten, additional, Hey, Joschka, additional, Heußel, Claus P., additional, Warth, Arne, additional, Winter, Hauke, additional, Serçin, Özdemirhan, additional, Karmouty-Quintana, Harry, additional, Herth, Felix, additional, Koch, Ina, additional, Petrosino, Giuseppe, additional, Mardin, Balca R., additional, Weichenhan, Dieter, additional, Jurkowski, Tomasz P., additional, Imbusch, Charles D., additional, Brors, Benedikt, additional, Benes, Vladimir, additional, Jung, Brigit, additional, Wyatt, David, additional, Stahl, Heiko, additional, Plass, Christoph, additional, and Jurkowska, Renata Z., additional

Published
2022
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12. A solid‐phase transfection platform for arrayed CRISPR screens [Corrigendum]

Author

Serçin, Özdemirhan, Reither, Sabine, Roidos, Paris, Ballin, Nadja, Palikyras, Spyridon, Baginska, Anna, Rein, Katrin, Llamazares, Maria, Halavatyi, Aliaksandr, Winter, Hauke, Muley, Thomas, Jurkowska, Renata Z., Abdollahi, Amir, Zenke, Frank T., Neumann, Beate, and Mardin, Balca R.

Subjects
animal structures
Abstract

Since the publication of this study, it has come to our attention that a citation to the study by Bulkescher et al (2017) was omitted from the Introduction. The following sentence should have been included in the introduction: “A previously reported solid‐phase reverse transfection method for proteins (Bulkescher et al , 2017) was used for the delivery of RNPs for three endogenous genes suggesting the potential of solid‐phase reverse transfection for CRISPR/Cas9‐based gene editing, despite its low efficiency”.\ud\udWe apologise for any inconvenience this omission may have caused.

Published
2020

15. Transient PLK4 overexpression accelerates tumorigenesis in p53-deficient epidermis

Author

Serçin, Özdemirhan, Larsimont, Jean-Christophe, Karambelas, Andrea E., Marthiens, Veronique, Moers, Virginie, Boeckx, Bram, Le Mercier, Marie, Lambrechts, Diether, Basto, Renata, and Blanpain, Cédric

Abstract

Aneuploidy is found in most solid tumours, but it remains unclear whether it is the cause or the consequence of tumorigenesis. Using Plk4 overexpression (PLK4OE) during epidermal development, we assess the impact of centrosome amplification and aneuploidy on skin development and tumorigenesis. PLK4OE in the developing epidermis induced centrosome amplification and multipolar divisions, leading to p53 stabilization and apoptosis of epidermal progenitors. The resulting delayed epidermal stratification led to skin barrier defects. Plk4 transgene expression was shut down postnatally in the surviving mice and PLK4OE mice never developed skin tumours. Concomitant PLK4OE and p53 deletion (PLK4OE/p53cKO) rescued the differentiation defects, but did not prevent the apoptosis of PLK4OE cells. Remarkably, the short-term presence of cells with supernumerary centrosomes in PLK4OE/p53cKO mice was sufficient to generate aneuploidy in the adult epidermis and triggered spontaneous skin cancers with complete penetrance. These results reveal that aneuploidy induced by transient centrosome amplification can accelerate tumorigenesis in p53-deficient cells.

Published
2016
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16. The interplay of DNA repair context with target sequence predictably biases Cas9-generated mutations.

Author

Pallaseni A, Peets EM, Girling G, Crepaldi L, Kuzmin I, Moor M, Muñoz-Subirana N, Schimmel J, Serçin Ö, Mardin BR, Tijsterman M, Peterson H, Kosicki M, and Parts L

Abstract

Mutagenic outcomes of CRISPR/Cas9-generated double-stranded breaks depend on both the sequence flanking the cut and cellular DNA damage repair. The interaction of these features has been largely unexplored, limiting our ability to understand and manipulate the outcomes. Here, we measured how the absence of 18 repair genes changed frequencies of 83,680 unique mutational outcomes generated by Cas9 double-stranded breaks at 2,838 synthetic target sequences in mouse embryonic stem cells. This large scale survey allowed us to classify the outcomes in an unbiased way, generating hypotheses about new modes of double-stranded break repair. Our data indicate a specialised role for Prkdc (DNA-PKcs protein) and Polm (Polμ) in creating 1bp insertions that match the nucleotide on the proximal side of the Cas9 cut with respect to the protospacer-adjacent motif (PAM), a variable involvement of Nbn (NBN) and Polq (Polθ) in the creation of different deletion outcomes, and a unique class of uni-directional deletion outcomes that are dependent on both end-protection gene Xrcc5 (Ku80) and the resection gene Nbn (NBN). We used the knowledge of the reproducible variation across repair milieus to build predictive models of the mutagenic outcomes of Cas9 scission that outperform the current standards. This work improves our understanding of DNA repair gene function, and provides avenues for more precise modulation of CRISPR/Cas9-generated mutations., Competing Interests: B.M. is an employee of Merck Healthcare, Darmstadt, Germany. O.S. is an employee of BioMed X Institute (GmbH), Heidelberg, Germany, which receives research grants from Merck KGaA. L.P. Receives remuneration and stock options from ExpressionEdits. We would like to acknowledge Allan Bradley and Frances Steward for providing us with the mouse embryonic stem cell DNA damage knock-out library and feeder cells, and for helpful suggestions; Juliane Weller for suggestions on the design of the web tool; and Uku Raudvere for technical guidance.

Published
2024
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