Explore the words cloud of the REBUILDCNS project. It provides you a very rough idea of what is the project "REBUILDCNS" about.
The following table provides information about the project.
DEUTSCHES KREBSFORSCHUNGSZENTRUM HEIDELBERG
|Coordinator Country||Germany [DE]|
|Total cost||2˙000˙000 €|
|EC max contribution||2˙000˙000 € (100%)|
1. H2020-EU.1.1. (EXCELLENT SCIENCE - European Research Council (ERC))
|Duration (year-month-day)||from 2018-06-01 to 2023-05-31|
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|1||DEUTSCHES KREBSFORSCHUNGSZENTRUM HEIDELBERG||DE (HEIDELBERG)||coordinator||2˙000˙000.00|
Over a million different cell types and billions of connections underlie brain function. While the embryonic brain glial progenitors generate this cellular diversity, in the adult brain progenitor competence becomes restricted to generation of few cell types. Thus, any attempt to repair the brain requires knowledge of the rules governing fate decisions within a damaged environment. We have shown that injury activates an inflammatory transcriptional signature in glial progenitors leading to exit from a dormant state. Excitingly, our recent data indicates that injury leads to demethylation of developmental enhancers in these glial progenitors too. In the regenerating zebrafish, activation of enhancers drives a transcriptional regenerative program. Yet, in rodents, despite enhancer demethylation by injury, transcription of a developmental program is missing. The overall goal of this project is to envisage ways to efficiently commission enhancers to re-direct lineage choices of glial progenitors towards re-establishing brain function following injury. Recent technological breakthroughs, including clonal lineage tracing, genome editing, and single cell “omics” combined with mouse genetics and injury models will allow (i) analysis of fate choices in the naïve and injured CNS (ii) study of how the chromatin landscape impacts transcriptional modulation of cell identity (iii) to finally design an integrated manipulation of the epigenome, transcriptome and environment for directed brain repair by endogenous progenitors. We follow a multidisciplinary approach combining cutting edge technology in functional genomics, developmental biology and translational research and leverage on a set of cutting-edge experimental platforms established in my lab and validated protocols that have led to exciting preliminary discoveries. We will provide fundamental knowledge on the mechanisms underlying lineage-decisions of CNS progenitors and open new research lines for treating CNS disorder.
|year||authors and title||journal||last update|
GÃ¼lce S. GÃ¼lcÃ¼ler Balta, Cornelia Monzel, Susanne Kleber, Joel Beaudouin, Emre Balta, Thomas Kaindl, Si Chen, Liang Gao, Meinolf Thiemann, Christian R. Wirtz, Yvonne Samstag, Motomu Tanaka, Ana Martin-Villalba
3D Cellular Architecture Modulates Tyrosine Kinase Activity, Thereby Switching CD95-Mediated Apoptosis to Survival
published pages: 2295-2306.e6, ISSN: 2211-1247, DOI: 10.1016/j.celrep.2019.10.054
|Cell Reports 29/8||2020-02-06|
Avni Baser, Maxim Skabkin, Susanne Kleber, Yonglong Dang, GÃ¼lce S. GÃ¼lcÃ¼ler Balta, Georgios Kalamakis, Manuel GÃ¶pferich, Damian Carvajal IbaÃ±ez, Roman Schefzik, Alejandro Santos Lopez, Enric Llorens Bobadilla, Carsten Schultz, Bernd Fischer, Ana Martin-Villalba
Onset of differentiation is post-transcriptionally controlled in adult neural stem cells
published pages: 100-104, ISSN: 0028-0836, DOI: 10.1038/s41586-019-0888-x
Georgios Kalamakis, Daniel BrÃ¼ne, Srikanth Ravichandran, Jan Bolz, Wenqiang Fan, Frederik Ziebell, Thomas Stiehl, Francisco CatalÃ¡-Martinez, Janina Kupke, Sheng Zhao, Enric Llorens-Bobadilla, Katharina Bauer, Stefanie Limpert, Birgit Berger, Urs Christen, Peter Schmezer, Jan Philipp Mallm, Benedikt Berninger, Simon Anders, Antonio del Sol, Anna Marciniak-Czochra, Ana Martin-Villalba
Quiescence Modulates Stem Cell Maintenance and Regenerative Capacity in the Aging Brain
published pages: 1407-1419.e14, ISSN: 0092-8674, DOI: 10.1016/j.cell.2019.01.040
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