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Your search keyword '"Eschbach, Katja"' showing total 6 results
Start Over Author "Eschbach, Katja" Publication Type Academic Journals
6 results on '"Eschbach, Katja"'

1. Temporal and sequential transcriptional dynamics define lineage shifts in corticogenesis

Author

Mukhtar, Tanzila, Breda, Jeremie, Adam, Manal A, Boareto, Marcelo, Grobecker, Pascal, Karimaddini, Zahra, Grison, Alice, Eschbach, Katja, Chandrasekhar, Ramakrishnan, Vermeul, Swen, Okoniewski, Michal, Pachkov, Mikhail, Harwell, Corey C, Atanasoski, Suzana, Beisel, Christian, Iber, Dagmar, Nimwegen, Erik, and Taylor, Verdon

Subjects
Biomedical and Clinical Sciences, Stem Cell Research, Stem Cell Research - Nonembryonic - Non-Human, Regenerative Medicine, Stem Cell Research - Embryonic - Non-Human, Genetics, Neurosciences, Brain Disorders, Intellectual and Developmental Disabilities (IDD), 1.1 Normal biological development and functioning, Underpinning research, Neurological, Animals, Mice, Cell Differentiation, Cell Lineage, Cerebral Cortex, Embryonic Stem Cells, Neural Stem Cells, Neurogenesis, Neurons, cortical development, lineage specification, networks, signaling pathways, transcriptional landscape, Biological Sciences, Information and Computing Sciences, Medical and Health Sciences, Developmental Biology, Biological sciences, Biomedical and clinical sciences
Abstract

The cerebral cortex contains billions of neurons, and their disorganization or misspecification leads to neurodevelopmental disorders. Understanding how the plethora of projection neuron subtypes are generated by cortical neural stem cells (NSCs) is a major challenge. Here, we focused on elucidating the transcriptional landscape of murine embryonic NSCs, basal progenitors (BPs), and newborn neurons (NBNs) throughout cortical development. We uncover dynamic shifts in transcriptional space over time and heterogeneity within each progenitor population. We identified signature hallmarks of NSC, BP, and NBN clusters and predict active transcriptional nodes and networks that contribute to neural fate specification. We find that the expression of receptors, ligands, and downstream pathway components is highly dynamic over time and throughout the lineage implying differential responsiveness to signals. Thus, we provide an expansive compendium of gene expression during cortical development that will be an invaluable resource for studying neural developmental processes and neurodevelopmental disorders.

Published
2022

3. Establishing standardized immune phenotyping of metastatic melanoma by digital pathology

Author

Sobottka, Bettina, Nowak, Marta, Frei, Anja Laura, Haberecker, Martina, Merki, Samuel, Levesque, Mitchell P., Dummer, Reinhard, Moch, Holger, Koelzer, Viktor Hendrik, Aebersold, Rudolf, Ak, Melike, Al-Quaddoomi, Faisal S., Albinus, Jonas, Alborelli, Ilaria, Andani, Sonali, Attinger, Per-Olof, Bacac, Marina, Baumhoer, Daniel, Beck-Schimmer, Beatrice, Beerenwinkel, Niko, Beisel, Christian, Bernasconi, Lara, Bertolini, Anne, Bodenmiller, Bernd, Bonilla, Ximena, Casanova, Ruben, Chevrier, Stéphane, Chicherova, Natalia, D'Costa, Maya, Danenberg, Esther, Davidson, Natalie, Drăganmoch, Monica-Andreea, Engler, Stefanie, Erkens, Martin, Eschbach, Katja, Esposito, Cinzia, Fedier, André, Ferreira, Pedro, Ficek, Joanna, Frey, Bruno, Goetze, Sandra, Grob, Linda, Gut, Gabriele, Günther, Detlef, Haeuptle, Pirmin, Heinzelmann-Schwarz, Viola, Herter, Sylvia, Holtackers, Rene, Huesser, Tamara, Irmisch, Anja, Jacob, Francis, Jacobs, Andrea, Jaeger, Tim M., Jahn, Katharina, James, Alva R., Jermann, Philip M., Kahles, André, Kahraman, Abdullah, Kuebler, Werner, Kuipers, Jack, Kunze, Christian P., Kurzeder, Christian, Lehmann, Kjong-Van, Lugert, Sebastian, Maass, Gerd, Manz, Markus G., Markolin, Philipp, Mena, Julien, Menzel, Ulrike, Metzler, Julian M., Miglino, Nicola, Milani, Emanuela S., Muenst, Simone, Murri, Riccardo, Ng, Charlotte K.Y., Nicolet, Stefan, Pedrioli, Patrick G.A., Pelkmans, Lucas, Piscuoglio, Salvatore, Prummer, Michael, Ritter, Mathilde, Rommel, Christian, Rosano-González, María L., Rätsch, Gunnar, Santacroce, Natascha, del Castillo, Jacobo Sarabia, Schlenker, Ramona, Schwalie, Petra C., Schwan, Severin, Schär, Tobias, Senti, Gabriela, Singer, Franziska, Sivapatham, Sujana, Snijder, Berend, Sreedharan, Vipin T., Stark, Stefan, Stekhoven, Daniel J., Theocharides, Alexandre P.A., Thomas, Tinu M., Tolnay, Markus, Tosevski, Vinko, Toussaint, Nora C., Tuncel, Mustafa A., Tusup, Marina, Van Drogen, Audrey, Vetter, Marcus, Vlajnic, Tatjana, Weber, Sandra, Weber, Walter P., Wegmann, Rebekka, Weller, Michael, Wendt, Fabian, Wey, Norbert, Wicki, Andreas, Wildschut, Mattheus HE, Wollscheid, Bernd, Yu, Shuqing, Ziegler, Johanna, Zimmermann, Marc, Zoche, Martin, and Zuend, Gregor

Published
2021
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6. TGF-β induces oncofetal fibronectin that, in turn, modulates TGF-β superfamily signaling in endothelial cells.

Author

Ventura, Elisa, Weller, Michael, Macnair, Will, Eschbach, Katja, Beisel, Christian, Cordazzo, Cinzia, Claassen, Manfred, Zardi, Luciano, and Burghardt, Isabel

Subjects
GENETIC engineering, GLIOBLASTOMA multiforme treatment, FIBRONECTINS, THERAPEUTICS
Abstract

Gene splicing profiles are frequently altered in cancer, and the splice variants of fibronectin (FN) that contain the extra-domains A (EDA) or B (EDB), referred to as EDA+FN or EDB+FN, are highly upregulated in tumor vasculature. Transforming growth factor β (TGF-β) signaling has been attributed a pivotal role in glioblastoma, with TGF-β promoting angiogenesis and vessel remodeling. By using immunohistochemistry staining, we observed that the oncofetal FN isoforms EDA+FN and EDB+FN are expressed in glioblastoma vasculature. Ex vivo singlecell gene expression profiling of tumors by using CD31 and α-smooth muscle actin (aSMA) as markers for endothelial cells, and pericytes and vascular smooth muscle cells (VSMCs), respectively, confirmed the predominant expression of FN, EDA+FN and EDB+FN in the vascular compartment of glioblastoma. Specifically, within the CD31- positive cell population, we identified a positive correlation between the expression of EDA+FN and EDB+FN, and of molecules associated with TGF-β signaling. Further, TGF-β induced EDA+FN and EDB+FN in human cerebral microvascular endothelial cells and glioblastoma-derived endothelial cells in a SMAD3- and SMAD4- dependent manner. In turn, we found that FN modulated TGF-β superfamily signaling in endothelial cells via the EDA and EDB, pointing towards a bidirectional influence of oncofetal FN and TGF-β superfamily signaling. [ABSTRACT FROM AUTHOR]

Published
2018
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